Researchers built up portrait from finger-bone fragment of Denisovan who lived and died in a Siberian cave

Scientists have reconstructed the entire genetic makeup of a girl who lived and died in a Siberian cave more than 50,000 years ago. The young woman belonged to a long extinct group of humans called Denisovans their existence known only from meagre fossil remains uncovered at the Denisova cave in the Altai mountains in 2008. They are thought to have occupied much of Asia tens of thousands of years ago. Previous tests on the remains found they were more closely related to Neanderthals than modern humans.

Writing in the journal Science, researchers in the U.S. and Germany describe how they sequenced the girls genome with an accuracy once considered impossible with such ancient specimens. The final sequence matched the quality of modern genetic tests on living people.

They sequenced single strands of DNA taken from a little finger bone found at the scene. The bone fragments, and two fossilised teeth, are the only remains of the Denisovans.

Studies on the girls genes suggest she had dark skin, brown hair and brown eyes, but other genetic factors help shed light on the Denisovans more broadly. Comparison of genetic material inherited separately from the girls mother and father points to a population with very low genetic diversity, probably a consequence of the Denisovans starting off as a small group of pioneers and expanding rapidly.

Svante Paabo, at the Max Planck Institute for Evolutionary Anthropology in Leipzig, said there was now no difference in what we can learn genetically about a person that lived 50,000 years ago and from a person today, provided that we have well-enough preserved bones.

The team from Leipzig and Harvard Medical School in Boston compared the Denisovan genome with similar sequences from Neanderthals and 11 modern humans from around the world. This revealed evidence for inbreeding, with Denisovan DNA living on in some populations alive today. Its clear that Denisovan material has contributed three to five per cent of the genomes of people in Australia and New Guinea and aboriginal people from the Philippines, and some of the islands nearby, said David Reich, a Harvard geneticist who worked on the study. The research highlighted scores of gene variants that are found in modern humans but not in Denisovans. Eight mutations that have arisen since our ancestors split from Denisovans are involved in brain function and nerve connectivity, for example.

This is perhaps, in the long term for me, the most fascinating thing about this: what it will tell us in the future about what makes us special in the world, relative to the Denisovans and Neanderthals, said Mr. Paabo.

Another 34 mutations found only in modern humans are associated with diseases, including four that affect the skin and eyes. Guardian Newspapers Limited, 2012

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Genetics of 50,000-year-old girl reconstructed

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 1, 2012) Flying high, or down in the dumps -- individuals suffering from bipolar disorder alternate between depressive and manic episodes. Researchers from the University of Bonn and the Central Institute of Mental Health in Mannheim have now discovered, based on patient data and animal models, how the NCAN gene results in the manic symptoms of bipolar disorder.

The results have been published in the current issue of The American Journal of Psychiatry.

Individuals with bipolar disorder are on an emotional roller coaster. During depressive phases, they suffer from depression, diminished drive and often, also from suicidal thoughts. The manic episodes, however, are characterized by restlessness, euphoria, and delusions of grandeur. The genesis of this disease probably has both hereditary components as well as psychosocial environmental factors.

The NCAN gene plays a major part in how manias manifest

"It has been known that the NCAN gene plays an essential part in bipolar disorder," reports Prof. Dr. Markus M. Nthen, Director of the Institute of Human Genetics at the University of Bonn. "But until now, the functional connection has not been clear." In a large-scale study, researchers led by the University of Bonn and the Central Institute of Mental Health in Mannheim have now shown how the NCAN gene contributes to the genesis of mania. To do so, they evaluated the genetic data and the related descriptions of symptoms from 1218 patients with differing ratios between the manic and depressive components of bipolar disorder.

Comprehensive data from patients and animal models

Using the patients' detailed clinical data, the researchers tested statistically which of the symptoms are especially closely related to the NCAN gene. "Here it became obvious that the NCAN gene is very closely and quite specifically correlated with the manic symptoms," says Prof. Dr. Marcella Rietschel from the Central Institute of Mental Health in Mannheim. According to the data the gene is, however, not responsible for the depressive episodes in bipolar disorder.

Manic mice drank from sugar solution with abandon

A team working with Prof. Dr. Andreas Zimmer, Director of the Institute of Molecular Psychiatry at the University of Bonn, examined the molecular causes effected by the NCAN gene. The researchers studied mice in which the gene had been "knocked out." "It was shown that these animals had no depressive component in their behaviors, only manic ones," says Prof. Zimmer. These knockout mice were, e.g., considerably more active than the control group and showed a higher level of risk-taking behavior. In addition, they tended to exhibit increased reward-seeking behavior, which manifested itself by their unrestrained drinking from a sugar solution offered by the researchers.

Lithium therapy also effective against hyperactivity in mice

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Flying high: Researchers decipher manic gene

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/9fkkzb/cell_therapy_tec) has announced the addition of Jain PharmaBiotech's new report "Cell Therapy - Technologies, Markets and Companies" to their offering.

This report describes and evaluates cell therapy technologies and methods, which have already started to play an important role in the practice of medicine. Hematopoietic stem cell transplantation is replacing the old fashioned bone marrow transplants. Role of cells in drug discovery is also described. Cell therapy is bound to become a part of medical practice.

Stem cells are discussed in detail in one chapter. Some light is thrown on the current controversy of embryonic sources of stem cells and comparison with adult sources. Other sources of stem cells such as the placenta, cord blood and fat removed by liposuction are also discussed. Stem cells can also be genetically modified prior to transplantation.

Cell therapy technologies overlap with those of gene therapy, cancer vaccines, drug delivery, tissue engineering and regenerative medicine. Pharmaceutical applications of stem cells including those in drug discovery are also described. Various types of cells used, methods of preparation and culture, encapsulation and genetic engineering of cells are discussed. Sources of cells, both human and animal (xenotransplantation) are discussed. Methods of delivery of cell therapy range from injections to surgical implantation using special devices.

Cell therapy has applications in a large number of disorders. The most important are diseases of the nervous system and cancer which are the topics for separate chapters. Other applications include cardiac disorders (myocardial infarction and heart failure), diabetes mellitus, diseases of bones and joints, genetic disorders, and wounds of the skin and soft tissues.

Regulatory and ethical issues involving cell therapy are important and are discussed. Current political debate on the use of stem cells from embryonic sources (hESCs) is also presented. Safety is an essential consideration of any new therapy and regulations for cell therapy are those for biological preparations.

The cell-based markets was analyzed for 2011, and projected to 2021. The markets are analyzed according to therapeutic categories, technologies and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer and cardiovascular disorders. Skin and soft tissue repair as well as diabetes mellitus will be other major markets.

The number of companies involved in cell therapy has increased remarkably during the past few years. More than 500 companies have been identified to be involved in cell therapy and 284 of these are profiled in part II of the report along with tabulation of 274 alliances. Of these companies, 154 are involved in stem cells. Profiles of 70 academic institutions in the US involved in cell therapy are also included in part II along with their commercial collaborations. The text is supplemented with 55 Tables and 11 Figures. The bibliography contains 1,050 selected references, which are cited in the text.

Key Topics Covered:

Continue reading here:
Research and Markets: Cell Therapy - Technologies, Markets and Companies - Updated 2012 Report

Recommendation and review posted by Bethany Smith

-- Roche to hold investors meeting in London on Wednesday

-- Personalized Medicine, mid-stage pipeline, R&D spending in focus

-- Updates expected on growth strategy in emerging markets

By Marta Falconi

ZURICH--Roche Holding AG (ROG.VX) will tell investors attending a research-and-development presentation in London next week how it expects to grow by making increased use of its diagnostics unit to develop targeted medicines.

At the London meeting Wednesday, the Swiss drug maker will also showcase highlights from its mid-stage development pipeline, talk about growth in emerging markets and try to reassure investors that it isn't overspending on drug development.

Roche, based in Basel, is the world's sixth-largest pharmaceutical company by sales, according to the latest 2011 figures by pharmaceutical market research company IMS Health Inc. In contrast to many of its peers, sales aren't particularly vulnerable to competition from cheap generics. That is in part because several of its Top 10 drugs are still relatively new, while others are difficult-to-replicate biochemical drugs.

The Swiss drug maker is a darling of analysts, with 17 out of 20 surveyed by Factset giving it a buy rating or equivalent, and only three giving it a hold rating.

Still, Roche needs to convince investors that there is growth beyond the loss of one key patent, that for its third- best selling drug Herceptin, which has become the standard treatment for a certain type of breast cancer. Analysts expect sales of Herceptin to start decreasing from 2015, when the treatment will lose patent protection in Europe. In the U.S., it will lose it in 2019.

Roche has been focusing on developing new drugs to defend its franchise in the treatment of breast cancer, working on products such as Perjeta and T-DM1. Roche is also developing follow-ons to other key cancer drugs, such as Avastin and Rituxan.

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Roche to Showcase Personalized Medicine, Mid-Stage Pipeline

Recommendation and review posted by sam

Public release date: 31-Aug-2012 [ | E-mail | Share ]

Contact: Gillian Shasby gshasby@thejns.org 434-924-5555 Journal of Neurosurgery Publishing Group

Charlottesville, VA (August 31, 2012). The Journal of Neurosurgery (JNS) Publishing Group is proud to announce publication of the NACTN/AOSNA Focus Issue on Spinal Cord Injury, a supplement to the September issue of the Journal of Neurosurgery: Spine, which is sponsored by AOSpine North America available in print and online. The online version of the supplement is available free to the public. The focus of this special supplement, which was spearheaded by Dr. Michael Fehlings, Professor of Neurosurgery at the University of Toronto and Medical Director of the Krembil Neuroscience Centre at the Toronto Western Hospital, is the development of cutting-edge translational research in the treatment of spinal cord injury (SCI), an often devastating injury that affects 2.5 million people worldwide, many of whom are first faced with it in early adulthood. The topic is addressed in a variety of forms in 17 articles and several editorials.

Many of the studies were conducted by members of the North American Clinical Trials Network (NACTN) for the Treatment of SCI, a consortium of 10 neurosurgery departments supplemented by a data management center and a pharmacological center. The principal investigator for the NACTN is Dr. Robert Grossman, Chairman, Department of Neurosurgery, The Methodist Hospital, Houston. Funded by the Christopher and Dana Reeve Foundation and the US Department of Defense, the NACTN was established to move molecular- and cell-based discoveries in the protection and regeneration of neuronal pathways from the laboratory to the clinical setting.

The supplement brings together papers focused on a variety of subjects related to identifying and evaluating different types of SCI, as well as developing therapeutic strategies for dealing with the disabilities that attend the injury. Graded assessments used to define the scope and extent of injury are presented and reviewed. Clinical and imaging predictors of neurological and functional outcomes, complications, and survival after SCI are identified and assessed. Original clinical studies and review articles on current and potential drug-based therapies are presented. Issues surrounding quality of life in patients with SCI are addressed. The cost-effectiveness of surgery in injured patients is examined and validated. Finally, the goals and progress of the NACTN in the transition of therapeutic strategies from preclinical to clinical settings are described.

Some interesting papers include the following:

Spinal cord injuries arise from a two-fold assault. First, there is the initial mechanical injury to the spinal cord, which kills neural cells in the immediate vicinity of the injury and breaks neuronal pathways between the brain and other parts of the body. Second, there is a cascade of new biochemical, cellular, and vascular events that damage axons and lead to the death of previously uninjured neural cells, expanding the area of injury and leading to further neurological compromise. This special supplement to the Journal of Neurosurgery: Spine offers a unique look into current research involving the diagnosis, assessment, and treatment of patients with SCI.

###

NACTN/AOSNA Focus Issue on Spinal Cord Injury, supplement to the Journal of Neurosurgery: Spine, Volume 17, published September 1, 2012, in print and online.

Disclosure: AOSpine North America sponsored publication of this supplement to the Journal of Neurosurgery: Spine. Funding for studies described in the supplement was provided by the Christopher and Dana Reeve Foundation and the US Department of Defense among other organizations. Sponsors of individual studies are listed with each article.

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Therapies for spinal cord injury: On the cutting edge of clinical translation

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Research and MarketsPosted on:31 Aug 12

Research and Markets (http://www.researchandmarkets.com/research/9fkkzb/cell_therapy_tec) has announced the addition of Jain PharmaBiotech's new report "Cell Therapy - Technologies, Markets and Companies" to their offering.

This report describes and evaluates cell therapy technologies and methods, which have already started to play an important role in the practice of medicine. Hematopoietic stem cell transplantation is replacing the old fashioned bone marrow transplants. Role of cells in drug discovery is also described. Cell therapy is bound to become a part of medical practice.

Stem cells are discussed in detail in one chapter. Some light is thrown on the current controversy of embryonic sources of stem cells and comparison with adult sources. Other sources of stem cells such as the placenta, cord blood and fat removed by liposuction are also discussed. Stem cells can also be genetically modified prior to transplantation.

Cell therapy technologies overlap with those of gene therapy, cancer vaccines, drug delivery, tissue engineering and regenerative medicine. Pharmaceutical applications of stem cells including those in drug discovery are also described. Various types of cells used, methods of preparation and culture, encapsulation and genetic engineering of cells are discussed. Sources of cells, both human and animal (xenotransplantation) are discussed. Methods of delivery of cell therapy range from injections to surgical implantation using special devices.

Cell therapy has applications in a large number of disorders. The most important are diseases of the nervous system and cancer which are the topics for separate chapters. Other applications include cardiac disorders (myocardial infarction and heart failure), diabetes mellitus, diseases of bones and joints, genetic disorders, and wounds of the skin and soft tissues.

Regulatory and ethical issues involving cell therapy are important and are discussed. Current political debate on the use of stem cells from embryonic sources (hESCs) is also presented. Safety is an essential consideration of any new therapy and regulations for cell therapy are those for biological preparations.

The cell-based markets was analyzed for 2011, and projected to 2021. The markets are analyzed according to therapeutic categories, technologies and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer and cardiovascular disorders. Skin and soft tissue repair as well as diabetes mellitus will be other major markets.

The number of companies involved in cell therapy has increased remarkably during the past few years. More than 500 companies have been identified to be involved in cell therapy and 284 of these are profiled in part II of the report along with tabulation of 274 alliances. Of these companies, 154 are involved in stem cells. Profiles of 70 academic institutions in the US involved in cell therapy are also included in part II along with their commercial collaborations. The text is supplemented with 55 Tables and 11 Figures. The bibliography contains 1,050 selected references, which are cited in the text.

Key Topics Covered:

Link:
Press Release

Recommendation and review posted by simmons

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/9fkkzb/cell_therapy_tec) has announced the addition of Jain PharmaBiotech's new report "Cell Therapy - Technologies, Markets and Companies" to their offering.

This report describes and evaluates cell therapy technologies and methods, which have already started to play an important role in the practice of medicine. Hematopoietic stem cell transplantation is replacing the old fashioned bone marrow transplants. Role of cells in drug discovery is also described. Cell therapy is bound to become a part of medical practice.

Stem cells are discussed in detail in one chapter. Some light is thrown on the current controversy of embryonic sources of stem cells and comparison with adult sources. Other sources of stem cells such as the placenta, cord blood and fat removed by liposuction are also discussed. Stem cells can also be genetically modified prior to transplantation.

Cell therapy technologies overlap with those of gene therapy, cancer vaccines, drug delivery, tissue engineering and regenerative medicine. Pharmaceutical applications of stem cells including those in drug discovery are also described. Various types of cells used, methods of preparation and culture, encapsulation and genetic engineering of cells are discussed. Sources of cells, both human and animal (xenotransplantation) are discussed. Methods of delivery of cell therapy range from injections to surgical implantation using special devices.

Cell therapy has applications in a large number of disorders. The most important are diseases of the nervous system and cancer which are the topics for separate chapters. Other applications include cardiac disorders (myocardial infarction and heart failure), diabetes mellitus, diseases of bones and joints, genetic disorders, and wounds of the skin and soft tissues.

Regulatory and ethical issues involving cell therapy are important and are discussed. Current political debate on the use of stem cells from embryonic sources (hESCs) is also presented. Safety is an essential consideration of any new therapy and regulations for cell therapy are those for biological preparations.

The cell-based markets was analyzed for 2011, and projected to 2021. The markets are analyzed according to therapeutic categories, technologies and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer and cardiovascular disorders. Skin and soft tissue repair as well as diabetes mellitus will be other major markets.

The number of companies involved in cell therapy has increased remarkably during the past few years. More than 500 companies have been identified to be involved in cell therapy and 284 of these are profiled in part II of the report along with tabulation of 274 alliances. Of these companies, 154 are involved in stem cells. Profiles of 70 academic institutions in the US involved in cell therapy are also included in part II along with their commercial collaborations. The text is supplemented with 55 Tables and 11 Figures. The bibliography contains 1,050 selected references, which are cited in the text.

Key Topics Covered:

Read more:
Research and Markets: Cell Therapy - Technologies, Markets and Companies - Updated 2012 Report

Recommendation and review posted by simmons

Public release date: 30-Aug-2012 [ | E-mail | Share ]

Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the United States and is thought to affect almost three million people in the UK. New research published in BioMed Central's open access journal Genome Medicine has identified genes whose activity is altered with increasing lung damage and, using a database of drug effects on gene activity (the Connectivity Map), finds that the compound Gly-His-Lys (GHK) affects the activity of these genes. When tested on human cells from lungs damaged by emphysema, GHK was able to restore normal gene activity and repair cell function.

The strongest cause of COPD is smoking, and at least 25% of smokers will develop this disease. Tobacco smoke and other irritants cause oxidative stress and chronic inflammation, which over time results in emphysema, the destruction of lung alveolar cells. Without these cells, the lungs are not able to efficiently exchange oxygen for carbon dioxide, leaving the patient continuously short of breath and with low levels of oxygen in their blood.

In a ground breaking, multi-centre, study funded by the National Institute of Health (NIH), researchers used cells taken from lungs donated by patients undergoing double lung transplant, whose own lungs were irrevocably damaged by COPD. Profiling of these samples showed that 127 genes had changes in activity that was associated with worsening disease severity within the lung. As would be expected from the nature of the disease, several genes associated with inflammation, such as the genes involved in signalling to B-cells (the immune system cells which make antibodies), showed increased activity.

In contrast genes involved in maintaining cellular structure and normal cellular function, along with the growth factors TGF and VEGF, were down-regulated and showed decreased activity. This included genes which control the ability of the cells to stick together (cell adhesion), produce the protein matrix which normally surrounds the cells, and which promote the normal association between lung cells and blood vessels.

Dr Avrum Spira and Dr Marc Lenburg, who co-led this study from the Boston University School of Medicine, explained, "When we searched the Connectivity Map database, which is essentially a compendium of experiments that measure the effect of therapeutic compounds on every gene in the genome, we found that how genes were affected by the compound GHK, a drug known since the 1970s, was the complete opposite of what we had seen in the cells damaged by emphysema."

Dr Joshua Campbell explained, "What got us especially excited was that previous studies had shown that GHK could accelerate wound repair when applied to the skin. This made us think that GHK could have potential drug's as a therapy for COPD."

Prof James Hogg, from the University of British Columbia continued, "When we tested GHK on cells from the damaged lungs of smokers with COPD, we saw an improvement in the structure of their actin cytoskeleton and in cell adhesion, especially to collagen. GHK also restored the ability of cells to reorganise themselves to repair wounds and construct the contractile filaments essential for alveolar function."

GHK is a natural peptide found in human plasma, but the amount present decreases with age. While more testing needs to be done on its effects in COPD, these early results are very promising. Therapeutic studies with GHK in animal models of COPD are now underway with the ultimate goal of moving this compound into clinical trials. As more gene activity signatures are discovered, this method of matching drug to disease may provide a rapid method for discovering potential uses for existing drugs and compounds.

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How gene profiling in emphysema is helping to find a cure

Recommendation and review posted by Bethany Smith

Latest Mental Health News

WEDNESDAY, Aug. 29 (HealthDay News) -- A "happy" gene that affects females but not males may explain why women are often happier than men, research suggests.

In the new study, researchers analyzed data from 193 women and 152 men who were assessed for happiness and underwent DNA testing as part of a long-term study of mental health.

The team focused on the "monoamine oxidase A" (MAOA) gene, which regulates an enzyme that breaks down brain neurotransmitters such as serotonin and dopamine, "feel-good" chemicals targeted by many antidepressants.

One version of the MAOA gene raises levels of monoamine, which allows larger amounts of these neurotransmitters to remain in the brain and boost mood.

The researchers found that women with the low-expression version of the MAOA gene were much happier than other women. Compared to women with no copies of the low-expression version, those with one copy scored higher on the happiness scale and those with two copies scored even higher.

A large number of men carried the low-expression version of the MAOA gene, but they were no happier than those without it, the investigators found.

The study was released online in advance of print publication in the journal Progress in Neuro-Psychopharmacology & Biological Psychiatry.

"This is the first happiness gene for women," lead author Dr. Henian Chen, an associate professor in the department of epidemiology and biostatistics in the College of Public Health, at University of South Florida, said in a university news release.

"I was surprised by the result, because low expression of MAOA has been related to some negative outcomes like alcoholism, aggressiveness and antisocial behavior. It's even called the warrior gene by some scientists, but, at least for women, our study points to a brighter side of this gene," Chen said.

Read more from the original source:
Scientists ID 'Happy' Gene in Women

Recommendation and review posted by Bethany Smith

ScienceDaily (Aug. 30, 2012) Two papers led by scientific teams from the Cancer Genetics Program at Beth Israel Deaconess Medical Center (BIDMC) shed new light on the genetic mechanisms underlying cellular energy and metabolism and, at the same time, highlight both the challenges and opportunities of genetic approaches to cancer treatment.

Appearing in the September 2012 issues of The Journal of Clinical Investigation (JCI) and Nature Medicine, the new findings reveal surprising insights into how PML regulates metabolism via the fatty acid oxidation (FAO) pathway and, in the process, uncover paradoxical roles for this tumor suppressor gene.

"The real story lies in the juxtaposition of these two papers, the way they jointly illuminate the braided function of PML in the FAO pathway," says the papers' senior author Pier Paolo Pandolfi, MD, PhD, Director of Cancer Genetics at BIDMC and George C. Reisman Professor of Medicine at Harvard Medical School. The Pandolfi laboratory has been studying the PML (promyelocytic leukemia protein) tumor suppressor gene, for more than 20 years.

Fatty-acid oxidation is the fat-burning metabolic process that is of importance to the energy of all cells. The two studies examined the impact of the FAO process in different biomedical situations including obesity, breast cancer and hematopoetic stem cell maintenance. Importantly, both publications determined that the FAO pathway could be a target for pharmacologic treatments.

The JCI paper defines the mechanism by which PML regulates FAO (involving the regulation of peroxisome proliferator-activated receptors or PPARs). According to first author Arkaitz Carracedo, PhD, a former postdoctoral fellow in the Pandolfi laboratory and currently Ikerbasque Research Professor at the research institute CIC bioGUNE, Bizkaia, Spain, the findings demonstrate that alterations in this pathway result in excessive fat accumulation and obesity in genetically engineered mouse models. In other words, when PML is highly expressed, cellular metabolism is enhanced and the mice were able to briskly burn fat and avoid gaining weight. Conversely, when PML was lost, the animals grew obese.

But, the team also made the paradoxical discovery that PML's enhanced cellular metabolism appeared to provide breast cancer cells with the energy needed to survive. These findings are further supported by data showing PML is highly expressed in a subset of breast cancers with poor prognosis, notes Carracedo. Instead of maintaining its function as a tumor suppressor and keeping breast cancer cells under control, PML is providing breast cancer with a survival advantage. These findings aligned with work by other labs that have found a relationship between high PML expression and breast cancers with poor prognosis.

In the second paper, in the September 2012 issue of Nature Medicine, Keisuke Ito, MD PhD, together with co-lead author Arkaitz Carracedo, looked at PML's role in regulating hematopoetic stem cells (HSCs), again through the FAO pathway, and defined for the first time the contribution of lipid metabolism to maintaining the function of HSCs.

HSCs replenish blood cells throughout the lifespan of an organism, and so they are critical to the aging process, explains Ito, also a former postdoctoral fellow in the Pandolfi laboratory and currently a member of the faculty at the Albert Einstein College of Medicine. The authors discovered that inhibition of fatty acid oxidation could represent an effective therapy for leukemia, as well as other forms of cancer -- but that it simultaneously posed a risk to the replenishment of HSCs. "Our results uncover a crucial metabolic requirement involving PPAR-delta signaling and FAO for preservation of the delicate equilibrium between HSC maintenance and function," the authors write. The findings have straightforward therapeutic implications for the improvement of both the efficacy of bone marrow transplantation (BMT) and the treatment of hematological malignancies.

"These two studies highlight both the opportunities and complexities of genetic approaches to human disease," notes Pandolfi. "Our next logical step will be to identify a potential path for therapeutic intervention through the opposing Scylla and Charybdis-like threats and benefits of this pathway," he says, referring to the two sea monsters that sailors of mythology had to navigate. "Through pharmacological dosage and scheduling, we will come up with a way to reap the benefits of PML and FAO regulation, while reducing or even eliminating its risks. The opportunity is there since we have drugs that can modulate both PML levels and FAO, and we have begun testing these concepts right away in our "mouse hospital."

In addition to Pandolfi and Carracedo, coauthors of the JCI paper include BIDMC investigators Dror Weiss, Manoj Bhasin, Andrew C. Adams, Maria Sundvall, Su Jung Song, Keisuke Ito, Ainara Egia, Towia Libermann, and Elefteria Maratos-Flier; Harvard Medical School investigators Vincent C.J. de Boer, Gaelle Laurent, Lydia S. Finley, and Marcia C. Haigis; Dana-Farber Cancer Institute investigators Zachary Gerhart-Hines, and Pere Puigserver; Amy K. Leliaert and Zachary T. Schafer of the University of Notre Dame; and Andrea L. Richardson of Brigham and Women's Hospital.

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Diverse metabolic roles for PML tumor suppressor gene

Recommendation and review posted by Bethany Smith

AARHUS, Denmark--(BUSINESSWIRE)--

CLC bio, the world's leading bioinformatics software developer, has been awarded a share of a EU-funded clinical research grant, PATHSEEK, worth $ 2 million out of a total project budget of $ 10 million.

As part of the grant, CLC bio will develop a user-friendly and computationally efficient solution for pathogen identification, host biomarker identification, pathogen variant characterization and molecular epidemiology in a clinical setting, as well as build a flexible computational back-end.

VP of R&D at CLC bio, Dr. Roald Forsberg, comments, "Current platforms in diagnostic laboratories are limited by the amount of time required for generating a result and by the limited sequence information available for pathogens. To overcome these limitations were going to develop a disruptive diagnostic technological pathogen sequencing platform which utilizes our world-leading bioinformatics expertise to enable scientists to go from a patient sample to a result, in less than 48 hours."

CEO of CLC bio, Thomas Knudsen, adds, "From the start, it has been one of CLC bios core strategies to do active research within the bioinformatics field and letting that research be a primary driver of our software development. We're currently part of and coordinating 10 different research projects, of which half are funded by the EU. This underlines our successful strategy and we plan to be part of even more research grants in the future."

About PATHSEEK

PATHSEEK is a 3-year study led by Professor Judy Breuer at University College London, which will demonstrate the potential of next generation sequencing technologies in clinical microbiology labs, to enable the detection of pathogens directly from clinical samples and the early detection of drug resistant mutations. The study will look at infections with clear unmet clinical needs or which pose a global risk, including, HIV, Mycobacterium tuberculosis, hepatitis B (HBV) and C (HCV) and influenza A. PATHSEEK will also investigate two host pharmacogenomics biomarkers which predict response to therapy for HCV and HIV.

The partners in PATHSEEK include University College London (UK), Erasmus Universitair Medisch Centrum Rotterdam (NL), Oxford Gene Technology (UK), and CLC bio (DK).

About CLC bio

http://www.clcbio.com/about

More here:
CLC bio Part of $ 10M EU PATHSEEK Project

Recommendation and review posted by Bethany Smith

April Flowers for redOrbit.com Your Universe Online

An international consortium of researchers from Uppsala University, Swedish University of Agricultural Sciences and Texas A&M University have discovered a mutation in a single gene in horses that is critical for the ability to perform ambling gaits and pacing that has a major effect on performance in harness racing. The study, published in Nature, is a breakthrough for understanding spinal cord neuronal circuitry and locomotion in vertebrates.

A complex coordination of muscle contractions carried out by neuronal circuits in our spinal cords allow us to walk and run, but how does this work at the level of nerve cells and molecules?

There is a great variability in the pattern of locomotion for horses, including the three naturally occurring gaits: walk, trot and canter/gallop. Some horses, however, have additional gaits such as ambling gaits or pace. For instance, Icelandic Horses can tolt (ambling gait) and flying pace. The team decided to investigate the genetic basis for these locomotive differences.

Gus Cothran, a professor in the Animal Genetic Lab of the College of Veterinary Medicine & Biomedical Sciences at Texas A&M, and the team used a process called whole genome SNP analysis to study the genes of 70 Icelandic horses that had either four gaits or five, with the pace being the fifth gait.

The team sequenced the DMRT3 gene of the test horses and found that in almost every case of gaited horses, there was mutation in the DMRT3 that caused a premature stop codon which causes the protein product of the gene to be terminated before the whole protein is completed. This alters the function of the protein, which leads to the differences associated with the gait.

We suspected a strong genetic component, but were almost shocked when we discovered that a single gene, DMRT3, largely explained the genetic difference between pacers and non-pacers, explains Lisa Andersson one of the PhD students involved in the project.

A separate group of researchers from Uppsala University, led by Klas Kullander, found that this particular gene, DMRT3, is expressed in a previously unknown type of neuron in the spinal cord of mice. The characteristics of these neurons, including their location, suggested that these neurons could take part in the neuronal circuitry that coordinates movement.

When the two groups of scientists compared their data, they realized an important biological finding was imminent.

At that moment, we realized that our discovery did not only extend our understanding of spinal neuronal circuits in mice, but that we had discovered a tangible population of nerve cells that also seemed to be critical for the control of gaits in horses. The new type of nerve cell is dependent on DMRT3, and is tentatively named after this gene, said Kullander.

Read more here:
Single Gene Has Impact On Gait Of Horses And Mice

Recommendation and review posted by Bethany Smith

ScienceDaily (Aug. 30, 2012) The WTX gene is mutated in approximately 30 percent of Wilms tumors, a pediatric kidney cancer. Like many genes, WTX is part of a family. In this case, WTX has two related siblings, FAM123A and FAM123C. While cancer researchers are learning more of WTX and how its loss contributes to cancer formation, virtually nothing is known of FAM123C or FAM123A, the latter of which is a highly abundant protein within neurons, cells that receive and send messages from the body to the brain and back to the body.

A UNC-led team of scientists used sophisticated technologies to identify and describe the protein interactions that distinguish each member of the WTX family. They found that unlike WTX and FAM123C, FAM123A interacts with a specific set of proteins that regulates cell adhesion and migration, processes essential to normal cell functioning and which, when mutated, contribute to human diseases such as cancer or Alzheimer's.

The report is the first to associate a member of the WTX gene family with cell adhesion and migration. Ben Major, PhD, and his research team believe that because FAM123A is so highly expressed in neurons, their findings raise the possibility that FAM123A controls neuron migration and neuronal activity, both of which play critical roles in development, neuro-degeneration and learning. Dr. Major, study senior author, is an assistant professor of cell biology and physiology in the UNC School of Medicine and a member of UNC Lineberger Comprehensive Cancer Center.

Their report appears in the September 4, 2012 online edition of Science Signaling.

The specific set of proteins the scientists discovered within the FAM123A complex are known microtubules-associated proteins. Microtubules, one component of a cell's cytoskeleton, are rigid hollow rods approximately 25 nm in diameter, about 3000 times thinner than a human hair. Microtubules are dynamic structures that undergo continual assembly and disassembly within the cell. They function both to determine cell shape and to control a variety of cell movements, including some forms of cell locomotion.

Dr. Major explains, "Since FAM123A and WTX are closely related proteins, anything we learn about FAM123A helps us know more about WTX, the tumor suppressor gene lost in pediatric kidney cancer. Unlike WTX, FAM123A binds to a specific set of proteins that are famous for regulating microtubules, a critical component within the cell's cytoskeleton or cellular 'scaffolding.' It's important to understand how different cellular cytoskeletal networks communicate and coordinate with each other. This communication is required for normal development and life.

"When the cytoskeleton is not functioning properly, a myriad of diseases arise, including certain cancers and cancer metastases. In cancer, cells can't move to new areas of the body without being able to squeeze between and crawl around surrounding cells and tissues, which ultimately allows the cell to move away from the primary tumor. Such movement requires complicated and intricate coordination between the cytoskeleton and the rest of the cell. Our work shows that FAM123A is critical for this communication."

Dr. Major and his research team use a powerful new technology to study protein complexes. He says, "Proteins never work alone, rather they bind each other to collectively carry out a specific task. An important challenge in cancer research today is determining which of the more than 30,000 proteins in a cell come together to form complexes." Dr. Major and colleagues can purify a specific protein from cancer cells and then, using sophisticated technologies called mass spectrometry, they identify the associated proteins.

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Cancer gene family member functions key to cell adhesion and migration

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The California mouse (Peromyscus californicus) is a species of rodent in the family Cricetidae found in northwestern Mexico and central to southern California. Most rodents are polygamous, but the California mouse pair bonds, making it a model organism for researchers studying the genetics and implications of partner fidelity. Credit: The University of California, Berkeley

In the foothills of the Santa Cruz Mountains two closely related species of mice share a habitat and a genetic lineage, but have very different social lives. The California mouse (Peromyscus californicus) is characterized by a lifetime of monogamy; the deer mouse (Peromyscus maniculatus) is sexually promiscuous.

Researchers at the University of California Berkeley recently showed how these differences in sexual behavior impact the bacteria hosted by each species as well as the diversity of the genes that control immunity. The results were published in the May 2012 edition of PLoS One.

Monogamy is a fairly rare trait in mammals, possessed by only five percent of species. Rarely do two related, but socially distinguishable, species live side-by-side. This makes these two species of mice interesting subjects for Matthew MacManes, a National Institutes of Health-sponsored post-doctoral fellow at UC Berkeley.

Through a series of analyses, MacManes and researchers from the Lacey Lab examined the differences between these two species on the microscopic and molecular levels. They discovered that the lifestyles of the two mice had a direct impact on the bacterial communities that reside within the female reproductive tract. Furthermore, these differences correlate with enhanced diversifying selection on genes related to immunity against bacterial diseases.

Bacteria live on every part of our bodies and have distinctive ecologies. The first step of MacManes project involved testing the bacterial communities that resided in the vaginas of both species of micethe most relevant area for a study about monogamous and promiscuous mating systems.

Next, MacManes performed a genetic analysis on the variety of DNA present, revealing hundreds of different types of bacteria present in each species. He found that the promiscuous deer mouse had twice the bacterial diversity as the monogamous California mouse. Since many bacteria cause sexually transmitted infections (like chlamydia or gonorrhea), he used the diversity of bacteria as a proxy for risk of disease. Results of the study were published in Naturwissenschaften in October 2011.

But this wasn't the end of the exploration.

"The obvious next question was, does the bacterial diversity in the promiscuous mice translate into something about the immune system, or how the immune system functions?" MacManes asked.

MacManes hypothesized that selective pressures caused by generation after generation of bacterial warfare had fortified the genomes of the promiscuous deer mouse against the array of bacteria it hosts.

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Researchers use Ranger supercomputer to identify genetic differences related to social lives of mammals

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Public release date: 30-Aug-2012 [ | E-mail | Share ]

Contact: Bonnie Prescott bprescot@bidmc.harvard.edu 617-667-7306 Beth Israel Deaconess Medical Center

BOSTON -- Two papers led by scientific teams from the Cancer Genetics Program at Beth Israel Deaconess Medical Center (BIDMC) shed new light on the genetic mechanisms underlying cellular energy and metabolism and, at the same time, highlight both the challenges and opportunities of genetic approaches to cancer treatment.

Appearing in the September 2012 issues of The Journal of Clinical Investigation (JCI) and Nature Medicine, the new findings reveal surprising insights into how PML regulates metabolism via the fatty acid oxidation (FAO) pathway and, in the process, uncover paradoxical roles for this tumor suppressor gene.

"The real story lies in the juxtaposition of these two papers, the way they jointly illuminate the braided function of PML in the FAO pathway," says the papers' senior author Pier Paolo Pandolfi, MD, PhD, Director of Cancer Genetics at BIDMC and George C. Reisman Professor of Medicine at Harvard Medical School. The Pandolfi laboratory has been studying the PML (promyelocytic leukemia protein) tumor suppressor gene, for more than 20 years.

Fatty-acid oxidation is the fat-burning metabolic process that is of importance to the energy of all cells. The two studies examined the impact of the FAO process in different biomedical situations including obesity, breast cancer and hematopoetic stem cell maintenance. Importantly, both publications determined that the FAO pathway could be a target for pharmacologic treatments.

The JCI paper defines the mechanism by which PML regulates FAO (involving the regulation of peroxisome proliferator-activated receptors or PPARs). According to first author Arkaitz Carracedo, PhD, a former postdoctoral fellow in the Pandolfi laboratory and currently Ikerbasque Research Professor at the research institute CIC bioGUNE, Bizkaia, Spain, the findings demonstrate that alterations in this pathway result in excessive fat accumulation and obesity in genetically engineered mouse models. In other words, when PML is highly expressed, cellular metabolism is enhanced and the mice were able to briskly burn fat and avoid gaining weight. Conversely, when PML was lost, the animals grew obese.

But, the team also made the paradoxical discovery that PML's enhanced cellular metabolism appeared to provide breast cancer cells with the energy needed to survive. These findings are further supported by data showing PML is highly expressed in a subset of breast cancers with poor prognosis, notes Carracedo. Instead of maintaining its function as a tumor suppressor and keeping breast cancer cells under control, PML is providing breast cancer with a survival advantage. These findings aligned with work by other labs that have found a relationship between high PML expression and breast cancers with poor prognosis.

In the second paper, in the September 2012 issue of Nature Medicine, Keisuke Ito, MD PhD, together with co-lead author Arkaitz Carracedo, looked at PML's role in regulating hematopoetic stem cells (HSCs), again through the FAO pathway, and defined for the first time the contribution of lipid metabolism to maintaining the function of HSCs.

HSCs replenish blood cells throughout the lifespan of an organism, and so they are critical to the aging process, explains Ito, also a former postdoctoral fellow in the Pandolfi laboratory and currently a member of the faculty at the Albert Einstein College of Medicine. The authors discovered that inhibition of fatty acid oxidation could represent an effective therapy for leukemia, as well as other forms of cancer but that it simultaneously posed a risk to the replenishment of HSCs. "Our results uncover a crucial metabolic requirement involving PPAR-delta signaling and FAO for preservation of the delicate equilibrium between HSC maintenance and function," the authors write. The findings have straightforward therapeutic implications for the improvement of both the efficacy of bone marrow transplantation (BMT) and the treatment of hematological malignancies.

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New research uncovers diverse metabolic roles for PML tumor suppressor gene

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Public release date: 30-Aug-2012 [ | E-mail | Share ]

Contact: Kristen Woodward kwoodwar@fhcrc.org 206-667-5095 Fred Hutchinson Cancer Research Center

SEATTLE African Americans have higher blood levels of a protein associated with increased heart-disease risk than European Americans, despite higher "good" HDL cholesterol and lower "bad" triglyceride levels. This contradictory observation now may be explained, in part, by a genetic variant identified in the first large-scale, genome-wide association study of this protein involving 12,000 African American and Hispanic American women.

Lead researcher Alexander Reiner, M.D., an epidemiologist at Fred Hutchinson Cancer Research Center, and colleagues describe their findings online ahead of the Sept. 7 print issue of the American Journal of Human Genetics.

Specifically, the researchers looked for genetic signposts associated with elevated levels of C-reactive protein, or CRP a marker of inflammation that is linked with increased risk of heart disease, diabetes and some cancers.

"Most previous studies examining the genetic determinants of elevated CRP have focused on tens of thousands of white individuals of European descent," said Reiner, a member of the Hutchinson Center's Public Health Sciences Division. "Since minorities African Americans and Hispanic Americans in particular tend to have higher CRP levels than other U.S. racial and ethnic groups, it's important to understand whether genetic factors might contribute to these differences."

Reiner and colleagues identified several genetic factors linked to CRP that are relatively specific to African Americans. They found a variation in TREM2, a family of genes on chromosome 6p21 that are expressed in white blood cells and appear to be important for regulating the degree of inflammation generated when white blood cells respond to infection or tissue injury.

"TREM genes were recognized relatively recently to be involved in inflammation and autoimmune disorders. Our finding adds further support to the importance of this gene family in generating and regulating inflammatory responses," said Reiner, who is also a professor of epidemiology at the University of Washington School of Public Health.

They also discovered that approximately 20 previously identified genetic factors associated with elevated CRP in whites are also shared among African Americans and Hispanic Americans genes that involve pathways related to innate immunity as well as metabolism of fat and sugar.

Identifying the genetic variants that regulate CRP levels may help researchers settle a point of scientific controversy: whether chronic, low-grade inflammation causes cardiovascular disease or whether it is just a reaction to the disease process of atherosclerosis, also known as hardening of the arteries.

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New genetic risk factor for inflammation identified in African-American women

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Public release date: 30-Aug-2012 [ | E-mail | Share ]

Contact: Quinn Eastman qeastma@emory.edu 404-727-7829 Emory University

Scientists have established a genetic mouse model for primary ovarian insufficiency (POI), a human condition in which women experience irregular menstrual cycles and reduced fertility, and early exposure to estrogen deficiency.

POI affects approximately one in a hundred women. In most cases of primary ovarian insufficiency, the cause is mysterious, although genetics is known to play a causative role. There are no treatments designed to help preserve fertility. Some women with POI retain some ovarian function and a fraction (5-10 percent) have children after receiving the diagnosis.

Having a mouse model could accelerate research on the causes and mechanisms of POI, and could eventually lead to treatments, says Peng Jin, PhD, associate professor of human genetics at Emory University School of Medicine.

The results were published online recently in the journal Human Molecular Genetics.

The paper was the result of a collaboration between researchers at Emory and the Institute of Zoology, Chinese Academy of Sciences in Beijing. Dahua Chen, PhD, associate director of the State Key Laboratory of Reproductive Biology, is the senior author and postdoctoral fellow Cuiling Lu is the first author. Stephanie Sherman, PhD, professor of human genetics at Emory, is a co-author.

The mouse model builds on research on women who are carriers of a "premutation" for fragile X syndrome, a leading cause of inherited intellectual disability.

The mice have a fragment of a human X chromosome from a fragile X premutation carrier. Other non-genetic mouse models used to study menopause include surgical removal of the ovaries, or exposure of mice to a chemical, 4-vinylcyclohexene diepoxide, which depletes the ovaries.

"While the fragile X premutation is a leading cause of POI, I think this model will be useful and relevant for all women with this condition," Jin says.

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Early menopause: A genetic mouse model of human primary ovarian insufficiency

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NEW YORK (GenomeWeb News) Australian molecular diagnostics firm Genetic Technologies has filed a lawsuit against Chicago-based Reproductive Genetics Institute for alleged infringement of a patent covering its non-coding DNA technology.

The suit was filed this week in the US District Court for the Northern District of Illinois Eastern Division and alleges that RGI infringes US Patent No. 5,612,179, entitled, "Intron Sequence Analysis Method for Adjacent Locus Alleles as Haplotypes." Specifically, Genetic Technologies claims that RGI's screening services for cystic fibrosis infringe the patent.

The Australian firm has asked the court for a judgment that RGI is infringing the '179 patent, and it is seeking unspecified damages for that alleged infringement.

The '179 patent has been at the center of several suits that Genetic Technologies has filed against other firms including Applera, Beckman Coulter, Gen-Probe, Interleukin Genetics, Orchid Cellmark, Pioneer Hi-Bred and others. All of those parties have since taken a license to the '179 patent from Genetic Technologies, according to the suit filed this week.

The patent also is the center of a suit filed in May 2011 by Genetic Technologies against Agilent Technologies and nine other firms. Genetic Technologies settled that case with a few of the defendants GeneSeek, Navigenics, Hologic, and Eurofins earlier this year.

Genetic Technologies noted in the suit filed this week that it has secured more than $15 million in licensing revenue since filing its initial action against Beckman Coulter in 2010.

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Genetic Technologies Sues Reproductive Genetics Institute

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SALT LAKE CITY, Aug. 30, 2012 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) announced today that Peter D. Meldrum, President and CEO, is scheduled to present at the Morgan Stanley Global Healthcare Conference, at 1:00 p.m. Eastern Time on Wednesday, September 12, 2012. The conference is being held at The Grand Hyatt New York in New York, New York.

The presentation will be available to interested parties through a live webcast accessible on the investor relations section of Myriad's website at http://www.myriad.com.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com

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Myriad Genetics to Present at the Morgan Stanley Global Healthcare Conference

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Public release date: 29-Aug-2012 [ | E-mail | Share ]

Contact: Kat Snodgrass mediareg@sfn.org Society for Neuroscience

WASHINGTON, D.C. New research about the brain and related disorders will be unveiled at Neuroscience 2012 in New Orleans, Oct. 1317. Findings will include how the brain weighs complex decisions; progress being made in treating Alzheimers disease, spinal cord injury, and traumatic brain injury; and novel understanding of how life experiences, diet, and sleep influence brain health and wellness.

Neuroscience 2012 is the annual meeting of the SfN and with more than 31,000 attendees the worlds largest source of emerging news about brain science and health.

The research presented at Neuroscience 2012 is part of the latest progress in understanding how the brain and nervous system develops and works and how it breaks down, said SfN President Moses Chao. Each year, the meeting showcases new tools and valuable information about the brain from understanding learning and behavior to how the brain adapts or is ravaged by disease and disorders, Chao said.

Renowned artist Chuck Close, noted for his highly inventive techniques used to paint the human face, speaks about his life as a rolling neurological clinic and his artwork during the Dialogues between Neuroscience and Society lecture. A National Medal of Arts awardee, Close produced his iconic portraits while coping with serious impairments of his body and brain.

Credentialed media receive complimentary registration, access to a working press room, meals, and live streaming of press conferences held Sunday, Oct. 14, through Tuesday, Oct. 16. Press conference topics include:

The Social Brain People make thousands of decisions each day, from simple choices, to social judgments about ethics and morality. Explore new research being released that bridges the gap between social psychology and neuroscience to better decipher how the brain weighs complex social decisions and environments.

Early Interventions for Alzheimers Disease Diagnosing Alzheimers disease currently relies on logging mental decline over time, potentially long after the disease has wreaked havoc on the brain. What if we could detect Alzheimers disease before symptoms start? Learn more about emerging research that is helping spot initial changes in the diseased brain. What critical clues could help diagnose, delay, or prevent disease onset and suggest new avenues to treat the disease?

Adolescence Teenagers experience many emotional, social, and behavioral changes that can feed into great personal growth as well as increased risk for depression, drug experimentation, and impulsivity. Could these attributes be hardwired in the brain? New research investigates how the adolescent brain functions, and how critical development periods can alter brain health and wellness.

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Neuroscience 2012 press program features latest brain science news

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NEWARK, Calif., Aug. 30, 2012 (GLOBE NEWSWIRE) -- StemCells, Inc. (STEM) today announced that Armin Curt, MD, Professor and Chairman of the Spinal Cord Injury Center at Balgrist University Hospital, University of Zurich, and principal investigator for the Company's Phase I/II clinical trial in chronic spinal cord injury, will make an oral presentation on the progress of the trial on Monday, September 3 at the 51st Annual Scientific Meeting of the International Spinal Cord Society (ISCOS), which is being held in London, England, on September 3-5, 2012.

In his presentation, Dr. Curt will present six-month interim data from the first patient cohort in the trial. The three patients in the first cohort all have thoracic (chest-level) spinal cord injury classified as AIS A, in which there is no neurological function below the injury level. The second and third cohorts will be patients classified as AIS B and AIS C, those with less severe injury, in which there is some preservation of sensory or motor function. In addition to assessing safety, the trial will assess preliminary efficacy based on defined clinical endpoints, such as changes in sensation, motor function and bowel/bladder function. The trial is being conducted at Balgrist University Hospital, University of Zurich, a world leading medical center for spinal cord injury and rehabilitation, and is open for enrollment to patients in Europe, Canada and the United States.

StemCells will host a conference call and webcast, which will include Dr. Curt, to discuss the interim data from its spinal cord injury trial on Tuesday, September 4, at 11:30 a.m. Eastern Time (8:30 a.m. Pacific Time). Interested parties are invited to listen to the call over the Internet via the Investors section of the Company's website at http://investor.stemcellsinc.com/phoenix.zhtml?c=86230&p=irol-irhome. Participants should allot extra time before the webcast begins to register and, if necessary, download and install audio software. An archived version of the webcast will be available for replay on the Company's website beginning approximately two hours following the conclusion of the live call and continuing for a period of 30 days.

About StemCells, Inc.

StemCells, Inc. is engaged in the research, development, and commercialization of cell-based therapeutics and tools for use in stem cell-based research and drug discovery. The Company's lead therapeutic product candidate, HuCNS-SC(R) cells (purified human neural stem cells), is currently in development as a potential treatment for a broad range of central nervous system disorders. In a Phase I clinical trial in Pelizaeus-Merzbacher disease (PMD), a fatal myelination disorder in children, the Company has shown preliminary evidence of progressive and durable donor-derived myelination in all four patients transplanted with HuCNS-SC cells. The Company is also conducting a Phase I/II clinical trial in chronic spinal cord injury in Switzerland and has reported positive interim safety data for the first patient cohort. The Company has also initiated a Phase I/II clinical trial in dry age-related macular degeneration (AMD), and is pursuing preclinical studies in Alzheimer's disease. StemCells also markets stem cell research products, including media and reagents, under the SC Proven(R) brand. Further information about StemCells is available at http://www.stemcellsinc.com.

The StemCells, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=7014

Apart from statements of historical fact, the text of this press release constitutes forward-looking statements within the meaning of the Securities Act of 1933, as amended, and the Securities Exchange Act of 1934, as amended, and is subject to the safe harbors created therein. These statements include, but are not limited to, statements regarding the prospect of retaining continued authorization to conduct a clinical trial in Switzerland in chronic spinal cord injury; the prospect for screening and then enrolling patients into the AIS B and AIS C cohorts; the prospect for evaluating trial patients for changes in their sensation, motor function and bowel/bladder function; the potential of the Company's HuCNS-SC cells to treat spinal cord injury and other central nervous system disorders; and the future business operations of the Company, including its ability to conduct clinical trials as well as its other research and product development efforts. These forward-looking statements speak only as of the date of this news release. The Company does not undertake to update any of these forward-looking statements to reflect events or circumstances that occur after the date hereof. Such statements reflect management's current views and are based on certain assumptions that may or may not ultimately prove valid. The Company's actual results may vary materially from those contemplated in such forward-looking statements due to risks and uncertainties to which the Company is subject, including the fact that additional trials will be required to demonstrate the safety and efficacy of the Company's HuCNS-SC cells for the treatment of any disease or disorder; uncertainties regarding the Company's ability to recruit the patients required to conduct its clinical trials or to obtain meaningful results; uncertainties regarding the Company's ability to obtain the increased capital resources needed to continue its current and planned research and development operations; and other factors that are described under the heading "Risk Factors" in the Company's Annual Report on Form 10-K for the year ended December 31, 2011, and in its subsequent reports on Form 10-Q and Form 8-K.

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StemCells, Inc. to Announce Interim Data on Spinal Cord Injury Trial at the 2012 Annual Scientific Meeting of the ...

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The two rice plant rows on the left are bigger and growing much better they have the PSTOL1 gene, whereas the two rice plant rows on the right do not have the PSTOL1 gene and they look smaller. Part of the image collection of the International Rice Research Institute (IRRI).

BARCELONA, Spain - A multinational team headed by Dr. Sigrid Heuer of the International Rice Research Institute (IRRI), has pinpointed a gene that can significantly increase rice harvest grown in phosphorus-deficient soil.

The team, writing in the journal Nature, said that the gene can enhance grain yield by as much as 60% compared to rice varieties which do not have it based on their controlled experiment.

This finding is significant in increasing rice yield for two reasons:

The gene is named PSTOL1 or Phosphorus-starvation tolerance 1.

Its main function, according to the authors, is to regulate the early crown root development and root growth in rice. Hence, rice with an over expression of this gene produces more roots that are also healthier.

This fact also helps rice plants to have higher uptake of other nutrients such as nitrogen and potassium. This may translate to lesser dependency on fertilizers without a reduction in yield.

Jackpot

PSTOL1, phosphorus uptake research team members from right to left are: Sigrid Heuer, Cheryl Dalid, Rico Gamuyao, Matthias Wissuwa and Joong Hyoun Chin. Part of the image collection of the International Rice Research Institute (IRRI).

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Researchers find gene that can raise rice harvest

Recommendation and review posted by Bethany Smith

An August 25, 2012 Washington Post article talked about a superbug outbreak at the NIH. The article highlighted the problem that we are running out of useful antibiotics. Antibiotic resistance is an evolutionary question of great practical importance. I have recently been asked and agreed to sign on to petitions requesting that antibiotic use in animals be banned for the sake of human health.

There is no evolutionary phenomenon we understand better than multiple antibiotic resistance in bacteria. It has been occurring virtually synchronously with the development of molecular genetics for 60 years. For public health as well as scientific reasons, antibiotic resistance was a major focus of the first decades of molecular biology.

Let us use this well-studied phenomenon to disentangle some of the thorny questions raised and debated in my most recent two blogs dealing with evolutionary processes (you can read them here and here). Our knowledge of the underlying cell and molecular biology makes it possible to discuss these questions in terms of specific experimental results rather than abstract principles.

The chief factor in the rapid evolution of multiple antibiotic resistance is the presence of sequences encoding resistance mechanisms on transmissible plasmids (Watanabe 1967). It was my PhD supervisor, Bill Hayes, who first demonstrated the existence of transmissible plasmids. They have proved to be extremely important evolutionary tools in bacteria.

Working under minimalist conditions (Bill initially had to make his own petri dishes by cutting the bottoms off glass vials), he demonstrated that sexual recombination in E. coli required an infectious factor that he called F, for fertility (Hayes 1968). Bill demonstrated that F was independent of the E. coli chromosome by studying the kinetics of its spread in a bacterial population. He found that F could replicate and spread though the population far faster than the 30 minute division time of the bacteria. This kind of autonomously replicating element came to be called a plasmid (Novick 1980).

A graph showing the spread of an antibiotic resistance plasmid in the absence of antibiotic is included in Watanabe's Scientific American article on transmissible antibiotic (Watanabe 1967). This result is significant because it shows how the mobility apparatus of the plasmid can operate to distribute the plasmid and make it spread through an unselected population of bacteria. Later, when antibiotic is applied, a large fraction of the population is already resistant.

In my recent blogs, a number of commentators asserted that the source of variation is immaterial to evolution because natural selection works on any variants that appear. But, as I pointed out in the first blog on superbugs, cells which can only modifying their existing genomes cannot achieve the same high levels of antibiotic resistance as cells that can pick up DNA from outside. Moreover, they are certainly not able to establish a resistant population prior to encountering selection as quickly as cells that have received a resistance plasmid.

Acquiring DNA from other cells, "horizontal transfer," occurs among bacteria most commonly by plasmids. However, bacterial cells can also take DNA up directly from the environment or receive it by viral infection. All these processes have been amply documented to occur in nature.

The F plasmid that Bill Hayes identified did not carry any antibiotic resistance sequences. So it is important to ask how those particular sequences came to be associated with transmissible plasmids. The answer leads us to two intriguing natural genetic engineering systems, transposons and integrons.

Transposons are segments of DNA that have the capacity to move (or "transpose") from one location in a genome to another (Cohen and Shapiro 1980). In order to make an antibiotic resistance sequence itself part of a transposon, it is sufficient to surround it by two copies of an existing transposon. This sometimes occurs normally as part of the transposition process, but other classes of transposons have been found already associated with antibiotic resistance sequences incorporated inside.

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James A. Shapiro: The Distinct Roles of Selection, Horizontal Transfer and Natural Genetic Engineering in Dangerous ...

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MELBOURNE, AUSTRALIA--(Marketwire -08/30/12)- Genetic Technologies Limited (GTG.AX) (GENE) wishes to advise that it has filed a patent infringement suit in respect of its non-coding DNA technologies against Reproductive Genetics Institute Inc. in the US District Court, for the Northern District of Illinois, Eastern Division.

Further details will be released to the Market as appropriate.

About BREVAGenThe BREVAGen breast cancer risk stratification test is a novel genetic test panel that examines a patient's DNA to detect the absence or presence of certain common genetic variations (SNPs) associated with an increased risk for developing breast cancer. The test is designed to help physicians assess aggregate breast cancer risk from these genetic markers, plus factors from a standard clinical assessment based on a patient's family and personal history, thus giving a clearer picture of an individual woman's risk of developing breast cancer. The BREVAGen test may be especially useful for women predisposed to hormone dependant breast cancer, including those who have undergone breast biopsies, as the test will provide information that can help physicians recommend alternative courses of action, such as more vigilant, targeted surveillance or preventive therapy, on a personalized patient-by-patient basis. For more information, please visit http://www.brevagen.com, or http://www.brevagen.com.au

About Genetic Technologies LimitedGenetic Technologies is an established diagnostics company with more than 20 years of experience in commercializing genetic testing, non-coding DNA and product patenting. The Company has operations in Australia and the U.S. and is dual-listed on the ASX (GTG.AX) and NASDAQ (GENE). Genetic Technologies is focused on the commercialization of its patent portfolio through an active out-licensing program and the global expansion of its oncology and cancer management diagnostics assets. Its U.S. subsidiary, Phenogen Sciences, offers novel predictive testing and assessment tools to help physicians proactively manage women's health. Phenogen's lead product, BREVAGen, is a first in class, clinically validated risk assessment test for non-familial breast cancer. For more information, please visit http://www.gtglabs.com, http://www.phenogensciences.com.

Safe Harbor StatementAny statements in this press release that relate to the Company's expectations are forward-looking statements, within the meaning of the Private Securities Litigation Reform Act The Private Securities Litigation Reform Act of 1995 (PSLRA) implemented several significant substantive changes affecting certain cases brought under the federal securities laws, including changes related to pleading, discovery, liability, class representation and awards fees. Since this information may involve risks and uncertainties and are subject to change at any time, the Company's actual results may differ materially from expected results. Additional risks associated with Genetic Technologies' business can be found in its periodic filings with the SEC.

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Genetic Technologies Files Patent Infringement Suit Against Reproductive Genetics Institute Inc. in USA

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IRVINE, Calif. and AMSTERDAM, Aug.29, 2012 /PRNewswire/ --Agendia, an innovative molecular cancer diagnostics company and leader in personalized medicine, conducted one of its premiere thought leadership events, "Present and Future Trends in Breast Cancer Genomics," on Saturday, August 25, 2012. The event was held at The Westin Times Square Hotel in New York City and featured over 200 attendees that included leading medical oncologists, pathologists, surgeons and molecular biologists. The conference is one of several events organized by Agendia throughout the year that brings together research scientists and physicians in clinical practice dedicated to the use and development of molecular diagnostics for cancer treatment.

"Events like these demonstrate why it is an exciting time in the field of medical oncology," said Dr. Stefan Gluck, Chairman of Agendia's Medical Advisory Board. "Breakthrough tools in molecular diagnostics, such as Agendia's MammaPrint, BluePrint and ColoPrint, play an integral role in helping physicians make clinical decisions about how to most effectively treat their patients. Most importantly, these tools are only the beginning of the precision medicine revolution."

The event featured an impressive list of speakers and panels on the following topics:

The Science Behind Genomic Based Analysis of Breast Cancer

Clinical Utility of Molecular Diagnostics

Landmark Clinical Trials

Tumor Round Table Discussion and Case Study Review

"Seventy five percent of cancer therapies today are ineffective," said David Macdonald, CEO of Agendia. "This represents 37 billion dollars spent globally on cancer drugs that do not benefit patients. Today's event further demonstrates Agendia's commitment to the continued development of clinically reliable diagnostics that provide doctors with decision-making tools needed to improve the effectiveness of cancer therapies for their patients."

About Agendia:Agendia is a leading molecular diagnostic company that develops and markets genomic-based diagnostic products, which help support physicians with their complex treatment decisions. Agendia's breast cancer Symphony suite was developed using unbiased gene selection, analyzing the complete human genome, ensuring 100% definitive results for cancer patients. Symphony includes MammaPrint, the first and only FDA-cleared IVDMIA breast cancer recurrence assay, as well as BluePrint, a molecular subtyping assay, TargetPrint, an ER/PR/HER2 expression assay, and TheraPrint, an alternative therapy selection assay. Together, these tests help physicians determine a patient's individual risk for metastasis, which patients will benefit from chemo, hormonal, or combination therapy, and which patients do not require these treatments and can instead be treated with other less arduous and less costly methods.

In addition to the Symphony suite of tests, Agendia has a rich pipeline of genomic products in development. The company collaborates with pharmaceutical companies, leading cancer centers and academic groups to develop companion diagnostic tests in the area of oncology and is a critical partner in the ISPY-2 and MINDACT trials.

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Agendia Brings Together Thought Leaders in Molecular Diagnostics and Medical Oncology

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