Archive for the ‘Gene Therapy Research’ Category

COLUMBIA, Md.--(BUSINESS WIRE)--

Osiris Therapeutics, Inc. (OSIR), announced today it has received consent from New Zealand to market its first-in-class stem cell therapy Prochymal (remestemcel-L), for the treatment of acute graft-vs-host disease (GvHD) in children. With this decision New Zealand joins Canada, which last month became the worlds first internationally recognized regulatory authority to grant approval to a stem cell drug. Prochymal is also the first therapy approved for GvHD - a devastating complication of bone marrow transplantation that kills up to 80 percent of children affected, many within just weeks of diagnosis.

"With each of our approvals it becomes clearer that the time for life-saving stem cell therapies in the practice of medicine has arrived, and we are humbled to have a leading role, said C. Randal Mills, Ph.D., President and Chief Executive Officer of Osiris. I would like to thank the professionals at Medsafe for their thoughtful and expeditious review of this complex application. I would also like to thank the team at Osiris that continues to do an outstanding job of making Prochymal available to children around the world suffering from the devastating effects of GvHD."

Osiris submitted a New Medicine Application (NMA) to Medsafe(New Zealand's medical regulatory agency) in May of 2011, and was granted Priority Review in June of 2011. Priority review provides expedited review for new drugs which offer a significant clinical advantage over current treatment options. Prochymal was granted provisional consent under Section 23 of the Medicines Act 1981.

"The incidence of GvHD is likely to rise as the demographic profile of our transplant population evolves," said Hans Klingemann, M.D., Ph.D., a Professor of Medicine and the Director of the Bone Marrow & Hematopoietic Stem Cell Transplant Program at Tufts University School of Medicine. "Effective strategies to manage the often lethal consequences of GvHD reduce the overall risk to transplantation and provide the transplant physician with better options when approaching their most difficult cases.

Clinical trials have shown that Prochymal is able to induce an objective, clinically meaningful response in 61-64 percent of children with GvHD that is otherwise refractory to treatment. Furthermore, treatment response with Prochymal resulted in a statistically significant improvement in survival.

As a mother who watched my son Christian suffer and die from the horrifying effects of GvHD, while waiting for the regulatory approvals necessary to allow him access to Prochymal, words cannot express how happy I am that significant progress is finally being made, said Sandy Barker, President and Co-founder of the Gold Rush Cure Foundation. We are proud to stand side-by-side with Osiris in this historic battle for our children around the world. Our motto is 'not one more child, not one more family' and when it comes to GvHD mortality, zero is the only acceptable number.

Prochymal is now approved in Canada and New Zealand, and is currently available in seven other countries including the United States under an Expanded Access Program (EAP). It is expected that Prochymal will be commercially available in New Zealand later this year.

About GvHD

GvHD represents a major unmet medical need with no approved treatment until Prochymal. GvHD is the leading cause of transplant related mortality, in which immune cells contained within the transplanted marrow recognize the recipient as foreign and mount an immunologic attack. Severe GvHD can cause blistering of the skin, intestinal hemorrhage and liver failure. Severe GvHD is extremely painful and fatal in up to 80 percent of cases. Currently, steroids are used as first-line therapy with a success rate of only 30-50 percent. When steroids fail, treatment options are limited to immunosuppressive agents used off-label with little benefit and significant toxicities.

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Osiris Receives Second Approval for Life-Saving Stem Cell Drug; Prochymal Granted Marketing Consent by New Zealand

BLOOMFIELD HILLS, MI--(Marketwire -06/14/12)- Arizona-based algae producer Health Enhancement Products (HEPI) has named Scott Freeman, MD to the post of Chief Science Officer as the Company continues to build out its senior management team. Dr. Freeman will help guide the Company through product development initiatives and compliance requirements.

Dr. Freeman's expertise encompasses all therapeutic areas in clinical drug development including oncology, infectious disease, women's health, gastrointestinal, autoimmune, metabolic, and neurological disorders. Dr. Freeman served as Vice President of Clinical Development at Onyx Pharmaceutical (2001-2006) and was head of both clinical development and operations, which executed the clinical trials for renal cell, melanoma, liver, lung, and colorectal cancer. The Phase 1, 2 and 3 trials in kidney and liver cancer were successfully performed and led to NDA approval of Nexavar. Further, Dr. Freeman was a key leader in the regulatory strategy that led to FDA approval of Nexavar for renal cell and liver cancer.

As Clinical Project Director at Schering-Plough Research Institute (1998-2001), his clinical projects included Phase 1, 2 and 3 trials for an anti-estrogen program, a breast cancer treatment, and a P53 gene therapy program. He was Associate Professor at Tulane University (1992-1998) and also served as the Medical Director for the Blood Center. At that time, he also conducted a basic research and clinical research program which focused on gene therapy for cancer and neurological diseases.

Dr. Freeman developed an HSV-TK gene therapy program to treat ovarian cancer, which genetically modified patients' ovarian tumor cells to sensitize the cells to the anti-viral drug ganciclovir. He served as Adjunct Associate Professor at the University of Rochester (1992-1998) and as a clinical investigator on the seminal human gene therapy studies performed at the National Institutes of Health (NIH) in the late 1980's for cancer and metabolic diseases.

Dr. Freeman has authored sixty-four scientific publications. He earned his BA from the University of Colorado in 1978 and received his MD from the University of Nevada in 1983. Dr. Freeman completed an internship and residency at the University of Minnesota in pediatrics and clinical pathology, respectively.

"We're pleased that Dr. Freeman is able to join the senior management team," states Andrew Dahl, HEPI President & CEO. "Finding and recruiting the ideal candidate with the requisite skills, experience and availability is an involved process in its own right. His expertise and experience will hasten the progress being made on several fronts. He's already engaged in a review of current and prior research, and will be directly involved in shaping the R&D work moving forward. Of particular value is Dr. Freeman's intimate knowledge of clinical trials and compliance strategy, as this will also influence food ingredient, supplement and medical food applications, and provide a competitive advantage."

About Health Enhancement Products, Inc. Health Enhancement Products, Inc. (HEPI) is a health & wellness company engaged in the development of natural products derived from algae cultures for use as dietary supplements and food ingredients. These natural products are extracted from living algae grown in purified water.

Safe Harbor Statement

Except for any historical information, the matters discussed in this press release contain forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. These forward-looking statements involve risks and uncertainties. A number of factors could cause actual results to differ from those indicated in the forward-looking statements, including the timing of completion of a trial, actual future clinical trial results being different than the results the company has obtained to date, and the company's ability to secure funding. Such statements are subject to a number of assumptions, risks and uncertainties. Readers are cautioned that such statements are not guarantees of future performance and those actual results or developments may differ materially from those set forth in the forward-looking statements. The company undertakes no obligation to publicly update or revise forward-looking statements, whether as a result of new information or otherwise.

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Health Enhancement Products, Inc. Names New Chief Science Officer

Public release date: 14-Jun-2012 [ | E-mail | Share ]

Contact: Jessa Netting jnetting@ccny.cuny.edu 212-650-7615 City College of New York

In recent years it became clear that people with diabetes face an ominous prospect a far greater risk of developing Alzheimer's disease. Now researchers at The City College of New York (CCNY) have shed light on one reason why. Biology Professor Chris Li and her colleagues have discovered that a single gene forms a common link between the two diseases.

They found that the gene, known to be present in many Alzheimer's disease cases, affects the insulin pathway. Disruption of this pathway is a hallmark of diabetes. The finding could point to a therapeutic target for both diseases. The researchers report their finding in the June 2012 issue of the journal "Genetics." (http://www.genetics.org/)

"People with type 2 diabetes have an increased risk of dementia. The insulin pathways are involved in many metabolic processes, including helping to keep the nervous system healthy," said Professor Li, explaining why the link is not far-fetched.

Although the cause of Alzheimer's is still unclear, one criterion for diagnosis of the disease after death is the presence of sticky plaques of amyloid protein in decimated portions of patients' brains.

Mutations in the human "amyloid precursor protein" (APP) gene, or in genes that process APP, show up in cases of Alzheimer's that run in families. In the study, Professor Li and her colleagues scrutinized a protein called APL-1, made by a gene in the worm Caenorhabditis elegans (C. elegans ) that happens to be a perfect stand-in for the human Alzheimer's disease gene.

"What we found was that mutations in the worm-equivalent of the APP gene slowed their development, which suggested that some metabolic pathway was disrupted," said Professor Li. "We began to examine how the worm-equivalent of APP modulated different metabolic pathways and found that the APP equivalent inhibited the insulin pathway."

This suggested that the human version of the gene likely plays a role in both Alzheimer's disease and diabetes.

They also found that additional mutations in the insulin pathway reversed the defects of the APP mutation. This helped explain how these genes are functionally linked.

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Gene may link diabetes and Alzheimer's, CCNY researchers find

ScienceDaily (June 14, 2012) The first U.S. population prevalence study of mutations in the gene that causes fragile X syndrome, the most common inherited form of intellectual disability, suggests the mutation in the gene -- and its associated health risks -- may be more common than previously believed.

Writing this month (June 2012) in the American Journal of Medical Genetics, a team of Wisconsin researchers reports that the cascade of genetic amino acid repeats, which accumulate over generations and culminate in the mutation of a single gene causing fragile X, is occurring with more frequency among Americans than previously believed. The study also shows that as the genetic basis for the condition is passed from generation to generation and amplified, risks to neurological and reproductive health emerge in many carriers.

"The premutation of this condition is much more prevalent than we previously thought and there are some clinical risks associated with that," explains Marsha Mailick Seltzer, director of the University of Wisconsin-Madison Waisman Center, who led the new study.

Fragile X is caused by the unexplained runaway expansion of a set of amino acid repeats in a single X chromosome gene known as FMR1. When fully mutated, the gene fails to express and produce a protein that's required for healthy brain development. The syndrome, which is more common in boys, results in a spectrum of intellectual disability.

However, before the gene fully mutates, carriers of the faulty gene exhibit a smaller number of elevated repeats, which expand as the gene is passed from generation to generation. Normal FMR1 genes exhibit anywhere from five to 40 repeats. Carriers with a premutation may have anywhere from 55 to 200. Those with between 45 and 54 repeats are characterized as falling into a "gray zone." Carriers of gray zone expansions often pass the mutation on to their children who themselves are at greater risk of having the premutation, and in subsequent generations the risk of a full mutation causing fragile X syndrome is high.

The goal of the new study was to calculate the prevalence in a U.S. population of the premutation and the gray zone. The research was based on data from the Wisconsin Longitudinal Study (WLS), also known as the "Happy Days study," which for more than 50 years has tracked the careers, family life, health and education of more than 10,000 graduates of Wisconsin's high school class of 1957.

Using genetic samples from 6,747 WLS participants, the team led by Seltzer, an expert on developmental disability and family life, found that 1 in 151 females and 1 in 468 males carry the fragile X premutation while 1 in 35 females and 1 of every 42 males fall into the gray zone.

"The prevalence is high, the second highest reported in the world literature," says Seltzer, noting that the incidence of fragile X varies by population and is higher in some places such as Israel, and lower in others like Asia.

The expansion of the FMR1 gene is known to vary across ethnic groups. The sample in the WLS study is primarily white and of northern European descent.

People with the premutation are more likely to have a child with disability; to have neurological symptoms such as numbness, dizziness and faintness; and, for women, to experience early menopause. Although these symptoms have been recognized previously in clinical studies, the WLS data represent an unbiased sample and supports those observations.

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Fragile X gene's prevalence suggests broader health risk

ScienceDaily (June 14, 2012) In recent years it became clear that people with diabetes face an ominous prospect -- a far greater risk of developing Alzheimer's disease. Now researchers at The City College of New York (CCNY) have shed light on one reason why. Biology Professor Chris Li and her colleagues have discovered that a single gene forms a common link between the two diseases.

They found that the gene, known to be present in many Alzheimer's disease cases, affects the insulin pathway. Disruption of this pathway is a hallmark of diabetes. The finding could point to a therapeutic target for both diseases. The researchers report their finding in the June 2012 issue of the journal Genetics.

"People with type 2 diabetes have an increased risk of dementia. The insulin pathways are involved in many metabolic processes, including helping to keep the nervous system healthy," said Professor Li, explaining why the link is not far-fetched.

Although the cause of Alzheimer's is still unclear, one criterion for diagnosis of the disease after death is the presence of sticky plaques of amyloid protein in decimated portions of patients' brains.

Mutations in the human "amyloid precursor protein" (APP) gene, or in genes that process APP, show up in cases of Alzheimer's that run in families. In the study, Professor Li and her colleagues scrutinized a protein called APL-1, made by a gene in the worm Caenorhabditis elegans (C. elegans ) that happens to be a perfect stand-in for the human Alzheimer's disease gene.

"What we found was that mutations in the worm-equivalent of the APP gene slowed their development, which suggested that some metabolic pathway was disrupted," said Professor Li. "We began to examine how the worm-equivalent of APP modulated different metabolic pathways and found that the APP equivalent inhibited the insulin pathway."

This suggested that the human version of the gene likely plays a role in both Alzheimer's disease and diabetes.

They also found that additional mutations in the insulin pathway reversed the defects of the APP mutation. This helped explain how these genes are functionally linked.

The APL-1 is so important, they found, that "when you knock out the worm-equivalent of APP, the animals die," Li explained. "This tells us that the APP family of proteins is essential in worms, as they are essential in mammals," like us.

Professor Li and her colleagues hope that this new insight will help focus research in ways that might lead to new therapies in the treatment of both Alzheimer's disease and diabetes.

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Gene may link diabetes and Alzheimer's

Newswise Bethesda, MDJune 14, 2012 Listed below are the selected highlights for the June 2012 issue of the Genetics Society of Americas journal, GENETICS. The June issue is available online at http://www.genetics.org/content/current. Please credit GENETICS, Vol. 191, JUNE 2012, Copyright 2012.

Please feel free to forward to colleagues who may be interested in these articles.

ISSUE HIGHLIGHTS

APL-1, the Alzheimers amyloid precursor protein in Caenorhabditis elegans, modulates multiple metabolic pathways throughout development, pp. 493507 Collin Y. Ewald, Daniel A. Raps, and Chris Li A hallmark of Alzheimers disease is the deposition of senile plaques, whose major component is the beta-amyloid peptide, which is a cleavage product of the amyloid precursor protein (APP). The function of APP and its cleavage products is still unclear. This article reports that the Caenorhabditis elegans APP-related protein APL-1 has multiple functions during development, including modulating the insulin pathway.

Population genetics models of local ancestry, pp. 607619 Simon Gravel Genomes are mosaics of chromosomal tracts that originate from a finite number of ancestors. These mosaics, which are shaped by historical migration patterns, are key to understanding genomic diversity in complex populations. This article presents gene flow models for inferring migration history using such patterns. When applied to HapMap African-American (ASW) data, a two-epoch migration model agrees with the data better than the commonly used single-migration model.

Synaptic polarity depends on phosphatidylinositol signaling regulated by myo-inositol monophosphatase in Caenorhabditis elegans, pp. 509521 Tsubasa Kimata, Yoshinori Tanizawa, Yoko Can, Shingo Ikeda,Atsushi Kuhara, and Ikue Mori Lithium relieves bipolar disorder by inhibiting the evolutionarily conserved enzyme myo-inositol monophosphatase (IMPase), which is essential for polarized localization of synaptic molecules. These authors show that mutations in two enzymes that degrade membrane phosphatidylinositol 4,5-bisphosphate (PIP2) suppress the synaptic defects of IMPase mutants and confer resistance to lithium treatment. These results provide the first in vivo evidence that lithium impairs neuronal PIP2 synthesis through inhibition of IMPase.

Analysis of Cryptococcus neoformans sexual development reveals rewiring of the pheromone-response network by a change in transcription factor identity, pp. 435449 Emilia K. Kruzel, Steven S. Giles, and Christina M. Hull Gene regulatory networks evolve, sometimes radically. This article describes the pheromone response network of the human pathogen Cryptococcus neoformans. The authors map transcriptional regulatory changes that occur during sexual development leading to the discovery of a key cis-regulatory element and its binding protein. The resulting regulatory architecture could not have been predicted based on comparative sequence analyses.

A non-Mendelian MAPK-generated hereditary unit controlled by a second MAPK pathway in Podospora anserina, pp. 419433 Herv Lalucque, Fabienne Malagnac, Sylvain Brun, Sbastien Kicka,and Philippe Silar There are many ways to produce a prion, and this article describes yet another one. The Podospora anserina PaMpk1 MAP kinase signaling pathway can generate C, a hereditary unit resembling prions. These authors show that another MAP kinase pathway, PaMpk2, controls the generation of C by activating PaMpk1, revealing unexpectedly complex regulation of a prion-like trait.

Allopolyploidization lays the foundation for evolution of distinct populations: Evidence from analysis of synthetic Arabidopsis allohexaploids, pp. 535547 Starr C. Matsushita, Anand P. Tyagi, Gerad M. Thornton, J. Chris Pires, and Andreas Madlung Allopolyploidycarrying complete chromosome sets of at least two different specieshas been seen as a mechanism for instant speciation. This article shows that different somatic cells of the same neoallopolyploid individual can exhibit different karyotypes, and that somatic mosaics can persist in subsequent generations. The authors characterize and quantify aneuploidy over seven generations in several sibling lines of a synthetic allopolyploid. Their results suggest that this phenomenon has the potential to lead not only to instant speciation but also to instant radiation.

The nearly neutral and selection theories of molecular evolution under the Fisher geometrical framework: Substitution rate, population size, and complexity, pp. 523534 Pablo Razeto-Barry, Javier Daz, and Rodrigo A. Vsquez This article puts forth that nearly neutral evolution cannot explain the high rate of fixations driven by positive selection found in DNA sequences. The authors use Fishers geometrical model (FGM) to simulate evolution from biologically interpretable distributions of mutations. They find that nearly neutral and selection scenarios predict molecular patterns different from previous models. In a selective scenario in the FGM, evolutionary rate depends not on population size, but rather on the complexity of organisms and mutation size.

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Genetics Society of America's GENETICS Journal Highlights

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today announced updated survival data from a pivotal clinical trial of single-agent ADCETRIS (brentuximab vedotin) in patients with relapsed or refractory Hodgkin lymphoma (HL) after autologous stem cell transplant (ASCT) showing that the median overall survival has not been reached after a 26.5 month median follow-up. The data will be reported during an oral presentation at the 17th European Hematology Association (EHA) Annual Meeting being held June 14-17, 2012 in Amsterdam, Netherlands. ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30.

Heavily pretreated Hodgkin lymphoma patients who relapse following autologous stem cell transplant often have a poor prognosis and there is a high unmet medical need for effective treatment options, said Scott Smith M.D., Ph.D., Loyola University Medical Center. These updated overall survival results from the pivotal trial are encouraging and demonstrate that ADCETRIS may play an important role in the treatment of patients with relapsed or refractory disease.

Long-term Follow-up Results of an Ongoing Pivotal Study of Brentuximab Vedotin in Patients with Relapsed or Refractory Hodgkin Lymphoma

A pivotal trial was conducted in 102 patients with relapsed or refractory HL after ASCT. The primary endpoint was objective response rate (ORR) per independent review. The secondary endpoints were complete remission (CR) rate, duration of response, progression-free survival (PFS), overall survival (OS), and safety and tolerability. At the time of the long-term follow-up analysis, the median observation time from first dose was 26.5months. Data, to be presented by Dr. Smith, include:

Patients received 1.8milligrams per kilogram of ADCETRIS every 3 weeks as a 30-minute outpatient intravenous infusion for up to 16cycles. Patients received a median of nine cycles of ADCETRIS while on trial. The median age of patients in the pivotal trial was 31 years. Enrolled patients had received a median of 3.5 (range 113) prior cancer-related systemic therapies, excluding ASCT. Seventy-one percent of patients had primary refractory disease, defined in the study protocol as patients who relapsed within three months of attaining CR or failed to achieve a CR, and 42 percent had not responded to their most recent prior therapy.

Details of the oral presentation are as follows:

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) for two indications: (1) the treatment of patients with Hodgkin lymphoma after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates, and (2) the treatment of patients with systemic anaplastic large cell lymphoma (sALCL) after failure of at least one prior multi-agent chemotherapy regimen. The indications for ADCETRIS are based on response rate. There are no data available demonstrating improvement in patient-reported outcomes or survival with ADCETRIS.

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Seattle Genetics Highlights Updated Survival Data from ADCETRIS® Pivotal Trial in Patients with Relapsed or Refractory ...

SACRAMENTO, Calif., June 13, 2012 /PRNewswire/ --Leading scientists and academics today issued a statement in response to the qualification of a measure on California's November ballot that would require mandatory labels of food grown or produced using genetic engineering. Like the overwhelming majority of scientific and medical experts and the U.S. Food and Drug Administration, these scientists believe that foods made with the benefit of modern biotechnology are safe and that labeling them as "genetically engineered" would mislead consumers by creating the false impression that foods containing GE ingredients are less safe than foods made without the benefit of biotechnology.

Bob Goldberg, Distinguished Professor of Molecular, Cell & Developmental Biology at UCLA, Member, National Academy of Sciences: "As a scientist who has spent the better part of my career studying and utilizing biotechnology, or genetic engineering, I am extremely concerned about qualification of this ballot measure. It's a Trojan Horse, promising the 'Right to Know' but really only serving to mislead Californians about the safety of their food. Foods made using modern biotechnology are thoroughly tested and proven safe. Labels are misleading and unnecessary."

Nina Federoff, Ph.D., Recipient of National Medal of Science, Distinguished Professor, King Abdullah University of Science and Technology (KAUST); Evan Pugh Professor, Huck Institutes of the Life Sciences, Penn State University: "Foods made with the benefit of modern biotechnology are some of the safest and most thoroughly-tested food to ever enter our food supply. I'm passionately opposed to labeling for the sake of labeling without providing any health or safety benefits, as this measure does, because the cost burden for doing so falls on those who can least afford it."

Martina Newell-McGloughlin, DSc. Executive Director Strategic Research Initiatives, University of California Davis: "Mandatory labeling can only be scientifically justified when based on the characteristics of the food product, not on the processes used in their development. But there are no material differences between crops that have been genetically modified using modern techniques and other crops, and they have routinely been found to be as safe. Unfortunately, it is easy to sell fear and doubt, which is exactly what the proponents are doing with this measure."

Roger N. Beachy, Ph.D., President Emeritus, Donald Danforth Plant Science Center; Former Director National Institute of Food and Agriculture, USDA; Member, National Academy of Science; Laureate, Wolf Prize in Agriculture: "Modern biotechnology offers important tools to increase agricultural productivity, protect crops from insects, pests and diseases, reduce the use of pesticides and water and increase the nutritional benefits of certain foods. GE foods have been studied for 25 years and been found to be safe. It would be really unfortunate if this measure passed because it would erroneously call into question the safety of these foods and their value to solve many global environmental and hunger problems."

Paid for by the Coalition Against the Costly Food Labeling Proposition, sponsored by farmers and food producers, major funding by Council for Biotechnology Information and Grocery Manufacturers Association. 1121 L. Street, #803, Sacramento, CA 95814| 1-800-331-0850| http://www.StopCostlyFoodLabeling.com

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Coalition Against the Deceptive and Costly Food Labeling Proposition says Scientists and Academic Community Oppose ...

ScienceDaily (June 13, 2012) In the not-too-distant future, scientists may be able to use DNA to grow their own specialized materials, thanks to the concept of directed evolution. UC Santa Barbara scientists have, for the first time, used genetic engineering and molecular evolution to develop the enzymatic synthesis of a semiconductor.

"In the realm of human technologies it would be a new method, but it's an ancient approach in nature," said Lukmaan Bawazer, first author of the paper, "Evolutionary selection of enzymatically synthesized semiconductors from biomimetic mineralization vesicles," published in the Proceedings of the National Academy of Sciences. Bawazer, who was a Ph.D. student at the time, wrote the paper with co-authors at UCSB's Interdepartmental Graduate Program in Biomolecular Science and Engineering; Institute for Collaborative Biotechnologies; California NanoSystems Institute and Materials Research Laboratory; and Department of Molecular, Cellular and Developmental Biology. Daniel Morse, UCSB professor emeritus of biochemistry of molecular genetics, directed the research.

Using silicateins, proteins responsible for the formation of silica skeletons in marine sponges, the researchers were able to generate new mineral architectures by directing the evolution of these enzymes. Silicateins, which are genetically encoded, serve as templates for the silica skeletons and control their mineralization, thus participating in similar types of processes by which animal and human bones are formed. Silica, also known as silicon, is the primary material in most commercially manufactured semiconductors.

In this study, polystyrene microbeads coated with specific silicateins were put through a mineralization reaction by incubating the beads in a water-in-oil emulsion that contained chemical precursors for mineralization: metals of either silicon or titanium dissolved in the oil or water phase of the emulsion. As the silicateins reacted with the dissolved metals, they precipitated them, integrating the metals into the resulting structure and forming nanoparticles of silicon dioxide or titanium dioxide.

With the creation of a silicatein gene pool, through what Bawazer only somewhat euphemistically calls "molecular sex" -- the combination and recombination of various silicatein genetic materials -- the scientists were able to create a multitude of silicateins, and then select for the ones with desired properties.

"This genetic population was exposed to two environmental pressures that shaped the selected minerals: The silicateins needed to make (that is, mineralize) materials directly on the surface of the beads, and then the mineral structures needed to be amenable to physical disruption to expose the encoding genes," said Bawazer. The beads that exhibited mineralization were sorted from the ones that didn't, and then fractured to release the genetic information they contained, which could either be studied, or evolved further.

The process yielded forms of silicatein not available in nature, that behaved differently in the formation of mineral structures. For example, some silicateins self-assembled into sheets and made dispersed mineral nanoparticles, as opposed to more typical agglomerated particles formed by natural silicateins. In some cases, crystalline materials were also formed, demonstrating a crystal-forming ability that was acquired through directed evolution, said Bawazer.

Because silicateins are enzymes, said Bawazer, with relatively long amino acid chains that can fold into precise shapes, there is the potential for more functionality than would be possible using shorter biopolymers or more traditional synthetic approaches. In addition, the process could potentially work with a variety of metals, to evolve different types of materials. By changing the laboratory-controlled environments in which directed evolution occurs, it will be possible to evolve materials with specific capacities, like high performance in an evolved solar cell, for example.

"Here we've demonstrated the evolution of material structure; I'd like to take it a step further and evolve material performance in a functional device," said Bawazer.

Research for this paper was supported by the U.S. Department of Energy.

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Scientists synthesize first genetically evolved semiconductor material

Main Category: GastroIntestinal / Gastroenterology Also Included In: Genetics Article Date: 13 Jun 2012 - 16:00 PDT

Current ratings for: 'Genetic Discovery Will Help Fight Diarrhoea Outbreaks'

Published today in the journal Evolutionary Applications, the findings pave the way for a new gold standard test to distinguish between the waterborne parasite's two main species affecting humans. One species is spread from person to person (Cryptosporidium hominis) but the other is often spread from livestock to people (Cryptosporidium parvum).

"Being able to discriminate quickly between the two species means it is easier to spot an outbreak as it develops, trace the original source, and take appropriate urgent action to prevent further spread," said lead author Dr Kevin Tyler of Norwich Medical School at UEA.

Cryptosporidium is a protozoan parasite that causes outbreaks of diarrhoea across the globe. In the UK, around two per cent of cases of diarrhoea are caused by the organism and many people will be infected at some time in their lives. Symptoms include watery diarrhoea, stomach pain, nausea and vomiting and can last for up to a month, but healthy people usually make a full recovery.

However, in the developing world infection can be serious in malnourished children and a significant cause of death in areas with high prevalence of untreated AIDS.

In the UK, outbreaks have been caused by faulty filtration systems in water supplies and transmission through swimming pools because the parasite is not killed by chlorine disinfection. Outbreaks also occur at open farms and in nurseries. People can also be infected by eating vegetables that have been washed in contaminated water. Hygiene is important in the prevention of spread of Cryptosporidium: people are advised to always wash their hands with warm running water and soap after touching animals, going to the toilet, changing nappies and before preparing, handling or eating food.

In this EU-funded study, the researchers identified the first parasite proteins that are specific to the different species. They found them at the ends of the chromosomes where they had been missed during previous parasite genetic studies.

Dr Tyler said: "Our discovery is an important advance in developing new simple and reliable tests for identifying these two species of parasite. This is the first step in discriminating outbreaks from sporadic cases, local strains from exotic ones, and tracing the source of outbreaks to an individual water supply, swimming pool or farm."

The UEA team worked with colleagues at the UK Cryptosporidium Reference Unit in Swansea, and Barts and the London School of Medicine and Dentistry, part of Queen Mary, University of London. Recently obtained renewed funding from the EU will enable further development towards a diagnostic test for use in the water industry and public health.

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Genetic Discovery Will Help Fight Diarrhoea Outbreaks

MINNEAPOLIS--(BUSINESS WIRE)--

The worlds leading experts in the field of personalized medicine are meeting in Boston, MA September 12th and 13th 2012 for the 4th Annual Personalized Medicine Conference. This conference will tackle the issues driving, as well as restraining, the clinical delivery of personalized medicine, including coding and reimbursement, whole genome sequencing in practice, the economics of personalized medicine, Medicare policy, and market access challenges for companion diagnostics.

Personalized medicine has the potential to revolutionize medical care by utilizing an improved understanding of genetics and molecular biology to allow for better, more precise diagnostic tests, greater predictability of disease course, and improved patient safety.

Speakers and panelists will be answering the following key questions:

Is personalized medicine changing clinical practice? Can personalized medicine improve clinical outcomes? Will insurers fund the genomic revolution? What types of validation requirements are payors looking for?

At this conference, Robert C. Green, MD, MPH, Director, G2P Research Program, Associate Director for Research, Partners Center for Personalized Genetic Medicine, Brigham and Women's Hospital and Harvard Medical School will discuss the impact that whole genome sequencing will have on the practice of medicine, patients, and health care costs, as well as the potential risks associated with its use.

An important question being asked today by the medical community is What genome information is ready for clinical use? Michael Christman, Ph.D., President & CEO, Coriell Institute for Medical Research will be answering this question in a presentation which will outline how the Coriell Personalized Medicine Collaborative (CPMC) is studying the use of genomic information in clinical decision-making.

Bryan Loy, MD, Market Medical Officer, Humana will describe the various perspectives that must be considered when addressing the payment methods for molecular diagnostics. He will discuss the issue of more widely integrating personalized medicine, while keeping the health plan, the consumer, and the provider in mind.

Dora Dias-Santagata, Ph.D., Instructor of Pathology, Harvard Medical School and Co-Director, Translational Research Laboratory at Mass General, will be describing her experience in developing and implementing a clinical platform for broad-base tumor genotyping. She will also outline the challenges that arose in her clinical testing. Her presentation will also include patient cases with clinical follow-up.

Numerous other speakers will be participating. Please visit http://www.personalized-medicine-conference.com for the full list of speakers, a preliminary agenda, and information on how to register to attend.

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Leaders in Personalized Medicine to Discuss Clinical and Market Access Challenges at 4th Annual Personalized Medicine ...

Public release date: 13-Jun-2012 [ | E-mail | Share ]

Contact: Simon Dunford s.dunford@uea.ac.uk 44-160-359-2203 University of East Anglia

Researchers at the University of East Anglia (UEA) have discovered unexpectedly large genetic differences between two similar species of the pathogenic Cryptosporidium parasite.

Published today in the journal Evolutionary Applications, the findings pave the way for a new gold standard test to distinguish between the waterborne parasite's two main species affecting humans. One species is spread from person to person (Cryptosporidium hominis) but the other is often spread from livestock to people (Cryptosporidium parvum).

"Being able to discriminate quickly between the two species means it is easier to spot an outbreak as it develops, trace the original source, and take appropriate urgent action to prevent further spread," said lead author Dr Kevin Tyler of Norwich Medical School at UEA.

Cryptosporidium is a protozoan parasite that causes outbreaks of diarrhoea across the globe. In the UK, around two per cent of cases of diarrhoea are caused by the organism and many people will be infected at some time in their lives. Symptoms include watery diarrhoea, stomach pain, nausea and vomiting and can last for up to a month, but healthy people usually make a full recovery.

However, in the developing world infection can be serious in malnourished children and a significant cause of death in areas with high prevalence of untreated AIDS.

In the UK, outbreaks have been caused by faulty filtration systems in water supplies and transmission through swimming pools because the parasite is not killed by chlorine disinfection. Outbreaks also occur at open farms and in nurseries. People can also be infected by eating vegetables that have been washed in contaminated water. Hygiene is important in the prevention of spread of Cryptosporidium: people are advised to always wash their hands with warm running water and soap after touching animals, going to the toilet, changing nappies and before preparing, handling or eating food.

In this EU-funded study, the researchers identified the first parasite proteins that are specific to the different species. They found them at the ends of the chromosomes where they had been missed during previous parasite genetic studies.

Dr Tyler said: "Our discovery is an important advance in developing new simple and reliable tests for identifying these two species of parasite. This is the first step in discriminating outbreaks from sporadic cases, local strains from exotic ones, and tracing the source of outbreaks to an individual water supply, swimming pool or farm."

Original post:
Genetic discovery will help fight diarrhea outbreaks

MANILA, Philippines -- "The Buzz" host Boy Abunda is going to Europe this weekend with his mother, who is suffering from dementia and Alzeimers disease.

In an interview with ABS-CBN News on Tuesday afternoon, Abunda said he will bring his mother to Germany to try stem cell therapy.

"Ako ay pupunta sa Europe hindi para magbakasyon. Dadalhin ko po ang aking ina para magpagamot sa Germany. Ito po 'yung fresh stem cell therapy. Maganda 'yung dini-diretso na dahil napag-uusapan ito," Abunda said.

While Abunda is in Germany, Kris Aquino will take his place on ABS-CBN's entertainment talk show "The Buzz."

In the interview, Abunda also said he's proud of Aquino, who's now open to doing extreme adventures, while continuing to be a good mother to her two sons.

"Ang daming nagbago kay Kris. May mga bagay na hindi ko inakala na gagawin ni Kris like 'yung diving, zipline at marami pang iba. Natutuwa ako that she has become more open to many things. She has become more adventurous. She has retained being the doting mother that she is pero mas malalim ang halakhak niya ngayon sa buhay. She's just so joyful. Natutuwa ako habang pinapanood ko ang kanyang adventure sa 'KrisTV,'" Abunda said.

Abunda said he's also hoping to do a new project with Aquino.

"I'm hoping na someday ay muli kaming magtagpo sa isang palabas dahil marami ang humihiling na kami ay magsama sa isang palabas. Sigurado ako sa puso ko na kami ay gagawa at gagawa dahil magkadugtong ang aming pusod," he said.

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Abunda to try stem cell therapy for mom

Public release date: 12-Jun-2012 [ | E-mail | Share ]

Contact: Bruce Goldman goldmanb@stanford.edu 650-725-2106 Stanford University Medical Center

STANFORD, Calif. A team led by investigators at the Stanford University School of Medicine has found that the most common genetic risk factor for Alzheimer's disease disrupts brain function in healthy older women but has little impact on brain function in healthy, older men. Women harboring the gene variant, known to be a potent risk factor for Alzheimer's disease, show brain changes characteristic of the neurodegenerative disorder that can be observed before any outward symptoms manifest.

Both men and women who inherit two copies (one from each parent) of this gene variant, known as ApoE4, are at extremely high risk for Alzheimer's. But the double-barreled ApoE4 combination is uncommon, affecting only about 2 percent of the population, whereas about 15 percent of people carry a single copy of this version of the gene.

The Stanford researchers demonstrated for the first time the existence of a gender distinction among outwardly healthy older people who carry the ApoE4 variant. In this group, women but not men exhibit two telltale characteristics that have been linked to Alzheimer's disease: a signature change in their brain activity, and elevated levels of a protein called tau in their cerebrospinal fluid.

One implication of the study, which will be published June 13 in the Journal of Neuroscience, is that men revealed by genetic tests to carry a single copy of ApoE4 shouldn't be assumed to be at elevated risk for Alzheimer's, a syndrome afflicting about 5 million people in the United States and nearly 30 million worldwide. The new findings also may help explain why more women than men develop this disease, said Michael Greicius, MD, assistant professor of neurology and neurological sciences and medical director of the Stanford Center for Memory Disorders. Most critically, identifying the prominent interaction between ApoE4 and gender opens a host of new experimental avenues that will allow Greicius' team and the field generally to better understand how ApoE4 increases risk for Alzheimer's disease.

For every three women with Alzheimer's disease, only about two men have the neurodegenerative disorder, said Greicius, the study's senior author. (The first author is Jessica Damoiseaux, PhD, a postdoctoral scholar in Greicius' laboratory. They collaborated with colleagues at the University of California-San Francisco and UCLA.) True, women live longer than men do, on average, and old age is by far the greatest risk factor for Alzheimer's, Greicius said. "But the disparity in Alzheimer's risk persists even if you correct for the difference in longevity," he said. "This disparate impact of ApoE4 status on women versus men might account for a big part of the skewed gender ratio."

Besides age, another well-studied major risk factor is genetic: possession of a particular version of the gene known as ApoE. This gene is a recipe for a protein involved in transporting cholesterol into cells an important job, as cholesterol is a crucial constituent of all cell membranes including those of nerve cells. And nerve cells are constantly responding to experience by developing or enhancing small, bulblike electrochemical contacts to other nerve cells, or diminishing or abolishing them. For all these processes, efficient cholesterol transport is critical.

The ApoE protein comes in three versions, each the product of a slightly differing version of the ApoE gene: E2, E3 or E4. Most people have two copies of the E3 version of ApoE. A small percentage carries one copy of E3 and one of E2, and even fewer two copies of E2. The protein specified by the E4 gene version seems to be somewhat defective in comparison to the one encoded by either E2 or the much more common E3. Thus, while only about 10-15 percent of the population carries one copy of E4 (or, much less commonly, two), more than 50 percent of people who develop Alzheimer's are E4 carriers.

But, as it turns out, the heightened risk E4 imposes may be largely restricted to women.

More here:
Alzheimer's risk gene disrupts brain function in healthy older women, but not men

A gene that's been known for two decades as the largest inheritable risk for developing Alzheimer's disease mostly affects the brains of women, not men, according to a team of researchers from Stanford and the University of California at San Francisco.

The gene variant known as APOE4 is the most common genetic risk factor for Alzheimer's only about 15 percent of people carry the gene, but it's found in more than half of all Alzheimer's patients.

The variant was first connected to Alzheimer's in 1993, but doctors and scientists for the most part have been unaware of any gender differences, despite early studies that showed an increased risk for women with the gene.

The new research, which is being published Wednesday in the Journal of Neuroscience, looked at two biological indicators or biomarkers associated with Alzheimer's disease: decreased activity in a brain network related to memory and increased levels of the tau protein in spinal fluid. Women with the APOE4 gene were more likely to test positive for both markers than men who had the gene and women who didn't have the gene.

The findings will not have an immediate clinical impact few people are encouraged to learn their APOE4 status because there is no treatment for Alzheimer's. But the results could open new research possibilities, such as the relationship between hormones and Alzheimer's or other gender differences that could make women with the gene more vulnerable, scientists said.

"We haven't been able to get much insight into how APOE is affecting increased risk. This might be a big clue," said Dr. Michael Greicius, medical director of the Stanford Center for Memory Disorders and senior author of the study.

The older study of the APOE4 gene found that women with one copy of the gene were four times more likely than anyone without the gene to develop Alzheimer's; men with a single copy had no increased risk. Both men and women, however, were as much as 14 times more likely to develop Alzheimer's if they had two copies of the gene. But that's a rare combination only 2 percent of the population has two copies.

The APOE4 gene, along with other genetic risk factors, has become increasingly important in research for treating the disease. Genetic research can help scientists better understand what causes Alzheimer's and it may lead to treatments that target specific biological mechanisms of the disease.

More:
Alzheimer's risk gene mostly affects women

A gene that's been known for two decades as the largest inheritable risk for developing Alzheimer's disease mostly affects the brains of women, not men, according to a team of researchers from Stanford and UCSF.

The gene variant known as APOE4 is the most common genetic risk factor for Alzheimer's - only about 15 percent of people carry the gene, but it's found in more than half of all Alzheimer's patients.

The variant was first connected to Alzheimer's in 1993, but doctors and scientists for the most part have been unaware of any gender differences, despite early studies that showed an increased risk for women with the gene.

The new research, which is being published Wednesday in the Journal of Neuroscience, looked at two biological indicators - or biomarkers - associated with Alzheimer's disease: decreased activity in a brain network related to memory, and increased levels of the tau protein in spinal fluid. Women with the APOE4 gene were more likely to test positive for both markers than men who had the gene and women who didn't have the gene.

The findings will not have any immediate clinical impact - very few people are encouraged to learn their APOE4 status because there is no treatment for Alzheimer's. But the results could open a torrent of new research possibilities, such as studying the relationship between hormones and Alzheimer's, or looking for other gender differences that could be making women with the gene more vulnerable, scientists said.

"We haven't been able to get much insight into how APOE is affecting increased risk. This might be a big clue," said Dr. Michael Greicius, medical director of the Stanford Center for Memory Disorders and senior author of the study.

The older study of the APOE4 gene found that women with one copy of the gene were four times more likely than anyone without the gene to develop Alzheimer's; men with a single copy had no increased risk. Both men and women, however, were up to 14 times more likely to develop Alzheimer's if they had two copies of the gene. But that's a rare combination - only 2 percent of the population has two copies.

The APOE4 gene, along with other genetic risk factors for Alzheimer's, has become increasingly important in research for treating the disease. Genetic research can help scientists better understand what causes Alzheimer's and it may lead to treatments that target specific biological mechanisms of the disease.

For example, scientists might find a connection between sex hormones and the gene or a genetic mutation tied to the X chromosome that interacts with APOE4, Greicius said.

The gene connection also could help scientists identify people who are showing early biological signs of developing Alzheimer's, years before they suffer memory problems. One of the major barriers to developing treatments has been identifying patients in the earliest stages of Alzheimer's, before the disease has caused too much damage to repair.

Originally posted here:
Alzheimer's gene found to affect women over men

Genetic engineering could hold the key to artificially creating semiconductors in a lab.

A team of academics at the University of California, Santa Barbara is looking at ways to create synthetic proteins that could form new structures of silicon dioxide to make computer chips with. These chips would then be used in all kinds of electronics. The proteins could also form titanium dioxide, used in solar cells.

The process is a bit different from regular genetic engineering because it uses synthetic cells made of the randomly combined genes of two related silicateins replete with random mutations, surrounded by a nucleus of minute plastic beads.

The artificial cells are put through the proverbial wringer, killing many along the way. Those that survive the process have their genes cherry picked by the scientists from either the silicon or titanium dioxide-forming proteins.

The results were somewhat surprising, with researchers finding not just the original silicateins used to form the artificial cell in the first place, but also another, different gene.

Tests on the new gene found it contained a silica-forming protein which has been dubbed silicatein X1, which may prove useful in the making of folded sheets of silica-protein fibers.

Silica skeletons of radiolaria in false color.

While that may sound strange and complicated, it's worth noting that even in nature, creatures like marine sponges can produce materials like fiberglass, while ARS notes that some bacteria can even build magnetic nanoparticles.

Now that scientists know it's possible to create entirely different silica proteins, the next step will be to change the conditions in order to achieve things like semiconductor performance.

- Sylvie Barak EE Times

Read more:
Study enables genetically engineered chips

The European Commission would like to relax limits on genetically modified organisms in food. But Germany's agriculture minister supports a no-tolerance policy.

When the Augustinian monk Gregor Johann Mendel crossed a yellow with a green pea 150 years ago, he hardly could have guessed what his experiment would unleash. It was the starting point for a brand new area of science: genetic technology, which polarizes today more than ever.

The latest point of controversy for business, politicians and citizens is the current zero-tolerance policy, which the European Commission would like to relax. Under current regulations, genetically modified organisms (GMO) which have not been approved are not allowed in food products, but regulators would like to change that to allow contamination by up to 0.1 percent.

Germany's Agriculture Minister Ilse Aigner believes the EU's proposal goes too far.

"When we're talking about unapproved GMOs, then security must be given highest priority, especially when it comes to food," Aigner said in an interview with Deutschlandfunk radio.

Consumers seem to agree with her. But questions remain. How dangerous are food products manipulated in this way? And are we not eating them already without knowing it?

Alexander Hissting prefers the zero tolerance approach

A loophole on zero tolerance

The fact that many foods already include GMOs is usually ignored in the debate on the zero-tolerance policy. Organisms with manipulated genes have been used in Germany for about ten years - provided they have been approved by the EU. Consumers often don't know that because approved GMOs don't have to be identified.

"For approved GMOs, we don't have a zero-tolerance policy," said Alexander Hissting of Lebensmittel ohne Gentechnik (Food without Genetic Technology), a group that advocates against genetically modified foods. "The laws permit GMOs that have been checked for safety to be used in products to a certain degree."

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EU may ease genetic engineering rules on food

ScienceDaily (June 12, 2012) University of Texas Medical Branch at Galveston researchers have developed a powerful visual analytical approach to explore genetic data, enabling scientists to identify novel patterns of information that could be crucial to human health.

The method, which combines three different "bipartite visual representations" of genetic information, is described in an article to appear in the Journal of the American Medical Informatics Association. The work won a distinguished paper award when it was presented at the AMIA Summit on Translational Bioinformatics in March 2012.

In the paper, the authors use their technique to analyze data on genetic alterations in humans known as single-nucleotide polymorphisms, or SNPs. Among other things, the frequencies of particular SNPs are associated with an individual's ancestral origins; for the study, the researchers chose to examine SNP data from 60 individuals from Nigeria and 60 individuals from Utah.

"We selected SNPs that we already knew differentiated between the two groups, and then showed that our method can reveal more about the data than traditional methods," said UTMB associate professor Suresh Bhavnani, lead author on the JAMIA paper and a member of UTMB's Institute for Translational Sciences. "This is a fresh way of looking at genetic data, a methodological contribution that we believe can help biologists and clinicians make better sense of a variety of biomarkers."

Like many kinds of biomedical data, Bhavnani said, datasets describing individuals and their SNPs are particularly suited to visual representations that are bipartite: that is, they simultaneously present two different classes of data. In the case of the Utah-Nigeria SNP data, Bhavnani and his colleagues started with what is known as a bipartite network visualization -- an intricate computer-generated arrangement of colored dots and black, gray and white lines.

"In the bipartite network you see both the individuals and their genetic profiles simultaneously, and cognitively that's really important," Bhavnani said. "You can look at the individuals and know immediately which SNPs make them different from others, and conversely you can look at the SNPs to see how they are co-occurring, and with which individuals they are co-occurring. This rich representation enables you to quickly comprehend the complex bipartite relationships in the data"

The bipartite network visualization of the Utah-Nigeria individual-SNP data has distinct clusters on its left and right sides that correspond to the Utah and Nigerian subjects and SNPs. It also accurately portrays a genetic phenomenon called admixture, in which an individual possesses SNPs that are characteristic of individuals from Utah as well as from Nigeria. Admixed individuals are placed on the edges of their clusters, relatively close to the center of the visualization. The identification of admixed individuals, and the implicated SNPs could help in the design of case-control studies where there is a need for the selection of homogenous sets of individual from different ancestral origins.

To produce an even more detailed picture of the individual-SNP information, the researchers applied two other bipartite visualization techniques to the data: the bipartite heat map, and the bipartite Circos ideogram. In the heat map, rectangular cells laid out in a spreadsheet-like arrangement and colored white, gray, or black helped precisely define the boundaries of the clusters by clarifying individual-SNP relationships. In the Circos ideogram, individuals and SNPs placed around the perimeter of a circle and linked with curved lines, enabling the researchers to more closely examine the admixed individuals' ties to SNPs in the clusters associated with both Utah and Nigeria.

"The network representation is very powerful because it gives you the overall structure of the data, but to really understand the complex relationships, you need these additional bipartite representations," Bhavnani said.

The JAMIA paper, according to Bhavnani, represents a proof of concept for the researchers' novel combination of methods, which can be applied to a wide range of biomedical questions. "You can think of anything -- for example you could examine cases and controls in Alzheimer's disease, or you could compare children who are prone to ear infections and those aren't prone," Bhavnani said. "Whatever your disease or trait of interest is, our approach can handle it."

Link:
Powerful new method to analyze genetic data

U.S. researchers say they've created genetically modified mosquitoes incapable of transmitting the deadly disease malaria to humans.

IRVINE, Calif., June 12 (UPI) -- U.S. researchers say they've created genetically modified mosquitoes incapable of transmitting the deadly disease malaria to humans.

Scientists at the University of California, Irvine, say the genetic option of breeding mosquitoes unable to infect people with the malaria parasite could help curb one of the world's most pressing public health issues.

Researchers at the Irvine campus, along with colleagues from the Pasteur Institute in Paris, have produced a model of the Anopheles stephensi mosquito -- a major source of malaria in India and the Middle East -- that impairs the development of the malaria parasite so it cannot transmit the disease through their bites.

"Our group has made significant advances with the creation of transgenic mosquitoes," UCI microbiology Professor Anthony James said in a university release Tuesday.

"But this is the first model of a malaria vector with a genetic modification that can potentially exist in wild populations and be transferred through generations without affecting their fitness."

The genetic modification can be applied to the dozens of different mosquito types that harbor and transmit the Plasmodium falciparum parasite, researchers said.

In the genetically modified mosquitoes antibodies are released that render the parasite harmless to others, they said.

"We see a complete deletion of the infectious version of the malaria parasite," James said. "This blocking process within the insect that carries malaria can help significantly reduce human sickness and death."

Go here to see the original:
Genetics used as weapon against malaria

IRVINE, Calif. | June 12, 2012

U.S. researchers say they've created genetically modified mosquitoes incapable of transmitting the deadly disease malaria to humans.

Scientists at the University of California, Irvine, say the genetic option of breeding mosquitoes unable to infect people with the malaria parasite could help curb one of the world's most pressing public health issues.

created genetically modified mosquitoes incapable of transmitting the deadly disease malaria

Researchers at the Irvine campus, along with colleagues from the Pasteur Institute in Paris, have produced a model of the Anopheles stephensi mosquito -- a major source of malaria in India and the Middle East -- that impairs the development of the malaria parasite so it cannot transmit the disease through their bites.

"Our group has made significant advances with the creation of transgenic mosquitoes," UCI microbiology Professor Anthony James said in a university release Tuesday.

"But this is the first model of a malaria vector with a genetic modification that can potentially exist in wild populations and be transferred through generations without affecting their fitness."

The genetic modification can be applied to the dozens of different mosquito types that harbor and transmit the Plasmodium falciparum parasite, researchers said.

In the genetically modified mosquitoes antibodies are released that render the parasite harmless to others, they said.

"We see a complete deletion of the infectious version of the malaria parasite," James said. "This blocking process within the insect that carries malaria can help significantly reduce human sickness and death."

Read more here:
Genetics used in fight against malaria

SOUTH SAN FRANCISCO, CA and SAN DIEGO, CA--(Marketwire -06/13/12)- Full Spectrum Genetics, Inc., a privately-held biopharmaceutical company, and BioBlocks, Inc., a privately-held small molecule lead discovery company today announced entering a collaboration to demonstrate the advantages of the combination of Full Spectrum Genetics' MapEng protein analysis and engineering platform and BioBlocks' Fragment-to-Lead fragment based drug discovery platform. Combined, these technologies will serve to identify key protein-protein interactions and discover small molecule drug candidates in a more rapid and cost effective manner than traditional methods. Financial details of the collaboration were not disclosed.

"Traditional methods to understand protein-protein interactions that affect disease outcomes often yield incomplete information despite the considerable time and expense involved," said Tom Smart, president and chief executive officer of Full Spectrum Genetics. Smart continued, "Our MapEng platform is designed to generate these insights significantly faster, less expensively and in more detail. We look forward to working with BioBlocks whose strengths in fragment based drug discovery and medicinal chemistry strongly positions them to capitalize on this information to optimize the discovery of small molecule therapeutics."

"In spite of significant recent developments in drug discovery technologies, the identification of high quality leads that are ultimately successful in clinical trials remains a challenge. This process is even more daunting for difficult targets such as protein-protein interactions," said Peter Pallai, Ph.D., president and chief executive officer of BioBlocks. "Our Target-to-Lead platform addresses this problem with a fragment based approach utilizing a dynamic lead development pathway for selection of high quality lead candidates. Working with Full Spectrum Genetics allows us to take advantage of the synergy between our platform and Full Spectrum Genetics' exceptional capabilities in mapping protein functional sites. Our joint capabilities allow us to develop drug candidates for protein-protein interactions, including the cancer target chosen for our collaboration."

About Full Spectrum GeneticsFounded in 2010, Full Spectrum Genetics, Inc. is a privately-held protein analysis and engineering platform and product company. The Company's MapEng platform enables the ultra-high throughput quantification of the effect on binding of every possible single amino acid substitution within a protein binding site. The MapEng platform provides a comprehensive analysis of protein structure-function relationships, with multiple applications for generating better biotherapeutics and diagnostics. For more information on Full Spectrum Genetics and its MapEng platform, visit http://www.fsgene.com.

About BioBlocksFounded in San Diego in 2002, BioBlocks provides medicinal chemistry expertise and high value intermediate products to partners in the drug discovery community. In numerous successful collaborations aided by a results-based lead optimization model, BioBlocks scientists have developed preclinical candidates and reached program milestones. The Company's Target-to-Lead platform addresses fundamental issues in drug discovery -- the high attrition rate and lack of novelty found in typical HTS hits -- by providing an alternative source for high quality tractable leads with multiple possible optimization pathways. For more information on BioBlocks and its lead discovery services please visit http://www.bioblocks.com.

Follow this link:
Full Spectrum Genetics and BioBlocks Enter Collaboration to Discover Novel Small Molecule Therapeutics That Inhibit a ...

Public release date: 12-Jun-2012 [ | E-mail | Share ]

Contact: Jim Kelly jpkelly@utmb.edu 409-772-8791 University of Texas Medical Branch at Galveston

University of Texas Medical Branch at Galveston researchers have developed a powerful visual analytical approach to explore genetic data, enabling scientists to identify novel patterns of information that could be crucial to human health.

The method, which combines three different "bipartite visual representations" of genetic information, is described in an article to appear in the Journal of the American Medical Informatics Association. The work won a distinguished paper award when it was presented at the AMIA Summit on Translational Bioinformatics in March 2012.

In the paper, the authors use their technique to analyze data on genetic alterations in humans known as single-nucleotide polymorphisms, or SNPs. Among other things, the frequencies of particular SNPs are associated with an individual's ancestral origins; for the study, the researchers chose to examine SNP data from 60 individuals from Nigeria and 60 individuals from Utah.

"We selected SNPs that we already knew differentiated between the two groups, and then showed that our method can reveal more about the data than traditional methods," said UTMB associate professor Suresh Bhavnani, lead author on the JAMIA paper and a member of UTMB's Institute for Translational Sciences. "This is a fresh way of looking at genetic data, a methodological contribution that we believe can help biologists and clinicians make better sense of a variety of biomarkers."

Like many kinds of biomedical data, Bhavnani said, datasets describing individuals and their SNPs are particularly suited to visual representations that are bipartite: that is, they simultaneously present two different classes of data. In the case of the Utah-Nigeria SNP data, Bhavnani and his colleagues started with what is known as a bipartite network visualization an intricate computer-generated arrangement of colored dots and black, gray and white lines.

"In the bipartite network you see both the individuals and their genetic profiles simultaneously, and cognitively that's really important," Bhavnani said. "You can look at the individuals and know immediately which SNPs make them different from others, and conversely you can look at the SNPs to see how they are co-occurring, and with which individuals they are co-occurring. This rich representation enables you to quickly comprehend the complex bipartite relationships in the data"

The bipartite network visualization of the Utah-Nigeria individual-SNP data has distinct clusters on its left and right sides that correspond to the Utah and Nigerian subjects and SNPs. It also accurately portrays a genetic phenomenon called admixture, in which an individual possesses SNPs that are characteristic of individuals from Utah as well as from Nigeria. Admixed individuals are placed on the edges of their clusters, relatively close to the center of the visualization. The identification of admixed individuals, and the implicated SNPs could help in the design of case-control studies where there is a need for the selection of homogenous sets of individual from different ancestral origins.

To produce an even more detailed picture of the individual-SNP information, the researchers applied two other bipartite visualization techniques to the data: the bipartite heat map, and the bipartite Circos ideogram. In the heat map, rectangular cells laid out in a spreadsheet-like arrangement and colored white, gray, or black helped precisely define the boundaries of the clusters by clarifying individual-SNP relationships. In the Circos ideogram, individuals and SNPs placed around the perimeter of a circle and linked with curved lines, enabling the researchers to more closely examine the admixed individuals' ties to SNPs in the clusters associated with both Utah and Nigeria.

Go here to see the original:
UTMB researchers create powerful new method to analyze genetic data

SAN MARINO, Calif.--(BUSINESS WIRE)--

Viral Genetics (VRAL.PK) today published a Letter to Shareholders on its website at: http://www.viralgenetics.com/shareholder-letters/Letter-to-Shareholders-Jun-12.PDF.

The Company elected not to issue a May shareholder letter due to the release of the comprehensive 2011 year-end financial statements and Annual Report, and the press release updating the physicians Investigational New Drug (IND) study on drug-resistant cancer to take place at two Texas universities, which together provided extensive updates on the Companys activity through the end of May.

Highlights from Shareholder Letter

About Viral Genetics, Inc.

San Marino, California-based Viral Genetics discovers drug therapies from two platform technologies based on over 60 patents: Metabolic Disruption (MDT) and Targeted Peptides (TPT). Founded in 1994, the biotech company is researching treatments for HIV/AIDS, Lyme Disease, Strep, Staph and drug resistant cancer. A majority-owned subsidiary, VG Energy (www.vgenergy.net), is dedicated to exploring biofuel and agricultural applications for the MDT platform. For more information, visit http://www.viralgenetics.com.

About VG Energy

VG Energy Inc. is an alternative energy and agricultural biotech company that is a majority-owned subsidiary of Viral Genetics Inc., a biotechnology company researching new treatments and methods of detection for diseases including cancer, HIV/AIDS and others. Using its Metabolic Disruption Technology (MDT), Viral Genetics cancer research led to discoveries with major consequences in a wide variety of other industries, including biofuel, vegetable oils and other high value oils and chemicals. VG Energy holds the exclusive worldwide license to the MDT patent rights for use in the increase of production of various plant-derived oils from algae and seeds. These pivotal discoveries promise to allow the biofuel industry to overcome its major obstacle in the area of production efficiency: namely, an increase in production yields leading to feasible economic returns on investment, allowing renewable biodiesel to be competitive with fossil fuels. For more information, please visit http://www.vgenergy.net.

SAFE HARBOR FOR FORWARD-LOOKING STATEMENTS:

This news release contains forward-looking statements that involve risks and uncertainties associated with financial projections, budgets, milestone timelines, clinical development, regulatory approvals, and other risks described by Viral Genetics, Inc. from time to time in its periodic reports, including statements about its VG Energy, Inc. subsidiary. None of Viral Genetics' drug compounds are approved by the US Food and Drug Administration or by any comparable regulatory agencies elsewhere in the world, nor are any non-pharmaceutical products of VG Energy, Inc. commercialized. While Viral Genetics believes that the forward-looking statements and underlying assumptions reasonable, any of the assumptions could be inaccurate, including, but not limited to, the ability of Viral Genetics to establish the efficacy of any of its drug therapies in the treatment of any disease or health condition, the development of studies and strategies leading to commercialization of those drug compounds in the United States, the obtaining of funding required to carry out the development plan, the completion of studies and tests on time or at all, the successful outcome of such studies or tests, or the successful commercialization of VG Energy, Inc.s non-pharmaceutical products. Therefore, there can be no assurance that the forward-looking statements included in this release will prove to be accurate. In light of the significant uncertainties inherent in the forward-looking statements included herein, the forward-looking statements should not be regarded as a representation by Viral Genetics or any other person that the objectives and plans of Viral Genetics will be achieved.

Originally posted here:
Viral Genetics Publishes June 2012 Monthly Letter to Shareholders

In Early Study, Procedure Helps Teens Halt Insulin Injections

June 11, 2012 (Philadelphia) -- In an early study, an experimental stem cell procedure helped 15 teens with type 1 diabetes stay off of insulin injections for about 1.5 years, on average.

The study was very small, and the procedure is not ready for widespread use. "We now have a unique approach with some positive findings, but it's still early. We need to better understand the biology behind the treatment and follow patients for long-term side effects," Robert E. Ratner, MD, chief scientific and medical officer of the American Diabetes Association, tells WebMD.

This is the latest of several stem cell studies to show promising results for the treatment of type 1 diabetes, Ratner notes.

In the new study, 15 of 28 teens with type 1 diabetes who got an experimental treatment using their own stem cells went into remission and did not need insulin injections for an average of about 1.5 years.

The "cocktail treatment" combines stem cell therapy with drugs that suppress the body's immune system. In type 1 diabetes, the immune system attacks and destroys insulin-producing cells within the pancreas.

The experimental treatment is called autologous nonmyeloablative hematopoietic stem cell transplantation (HSCT). It aims to kill the destructive immune system cells and replace them with immature stem cells not programmed to destroy insulin-producing cells.

First, patients are given drugs to stimulate production of blood stem cells. The blood stem cells are then removed from the body and frozen. Then, patients are hospitalized and given drugs to kill the destructive immune system cells. The harvested blood stem cells are then put back into the patient.

Eight teens who took part in the study have remained insulin-free for two years, on average. One patient has gone without insulin injections for 3.5 years.

"All our patients considered the [treatment] to be worthwhile and beneficial, though some patients experienced side effects," study head Weiqiong Gu, MD, of Ruijin Hospital in Shanghai, tells WebMD.

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Experimental Stem Cell Treatment Tested for Type 1 Diabetes