Archive for the ‘Gene Therapy Research’ Category

By Jack Kaskey - 2012-08-21T12:14:41Z

Noah Berger/Bloomberg

A tomato breeder displays varieties grown at the Monsanto Co. facility in Woodland, California.

Doug Heath, a tomato breeder for Monsanto Co. (MON), offers visitors juicy slices of Cherokee Purple, a delicate variety with a sweetness and acidity hes trying to replicate in hardier commercial fruit.

We want to see these in the stores more than one month a year, Heath told visitors this month at his research plot in Woodland, California. He gave out the tomato slices at Field Days, an annual gathering for farmers and distributors to see new crops from Monsantos Seminis vegetable seed unit.

Monsanto is accelerating its push to identify thousands of genetic markers in fruits and vegetables as it brings the tools of biotechnology to conventional breeding, giving Heath the ability to select for everything from taste to disease- resistance. Its also allowing the worlds biggest vegetable- seed producer to develop new varieties in two to four years, down from as many as 10 years. Using the markers is like having X-ray glasses that let breeders peer inside a leaf clipping or seed to find what will grow, Heath said.

His efforts are gathering momentum at the St. Louis-based company, which bought Seminis for $1.4 billion in 2005 and is looking to expand its market share. Monsanto has identified about 5,000 genetic markers in peppers, more than 4,000 in tomatoes and thousands more in melons, cauliflower, broccoli, cucumbers and beans, according to an Aug. 14 investor presentation. The company plans to identify more vegetable markers this year than in the past 20 years combined.

Syngenta AG (SYNN), the second-biggest vegetable seed producer, and other companies are also identifying the markers. Syngenta has more than 250,000 genetic markers to help with vegetable breeding, including about 50,000 in melon, 25,000 in tomato and 10,000 in peppers, according to an e-mail from Paul Minehart, a spokesman for the Basel, Switzerland-based company.

Monsanto is unrivaled in integrating genetic data into breeding decisions, Chief Technology Officer Robb Fraley said in an interview. The company declined to disclose its total vegetable markers.

Using genetic markers to guide breeding decisions will improve the appeal and nutrition of tomatoes and 20 other fruits and vegetables, helping people eat healthier and propelling vegetables to Monsantos third-most-profitable business, surpassing cotton in the next three years, Fraley said.

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Monsanto Genetic ’X-Ray Glasses’ Speed Tastier Tomatoes

ScienceDaily (Aug. 21, 2012) Numerous viruses are used in the service of science today. They serve as gene taxis to transfer therapeutic genes into body cells or as therapeutic viruses targeted to infect and destroy cancer cells. For such applications, the viruses are often equipped with additional genes, such as for immune mediators or for proteins inducing programmed cell death. However, these gene products can harm the body if they are released at the wrong moment or at excessive levels. "Ideally, we want to be able to turn on and off the transferred genes at a specific time," says Dr. Dirk Nettelbeck, a virologist from DKFZ.

To this end, Patrick Ketzer of Nettelbeck's group experimented, jointly with colleagues from Konstanz University, with what are called RNA switches. In order to construct such a switch, the researchers inserted synthetic segments of DNA into the viral genetic material in the direct vicinity of the transferred gene. In the infected cell, this construct is transcribed together with the transferred gene into a single messenger RNA (mRNA) molecule. The switch is operated using an agent which is added to cells infected with the virus. The substance is precisely fitted to bind to the RNA molecule and induces it to cut itself up. Thus, the potentially dangerous protein cannot be produced. The researchers copied this regulation mechanism from bacteria which use RNA switches to regulate production of numerous proteins.

The DKFZ virologists first constructed an RNA switch that is kept in permanent "off" position by the substance. The production of the foreign protein does not start as long as substance is added. "This was a first proof that RNA switches work in viruses at all. But it is just as well possible to construct switches that do not allow production of the protein until the substance is added," Dirk Nettelbeck explains.

In cells, it has been possible for many years now to specifically turn on and off genes. To do so, scientists modified specific natural regulatory regions called promoters in the cellular genetic material. As a result, addition of the antibiotic tetracycline causes mRNA production to be turned on or off.

"However, this type of switch is too big and complex to be used in viruses or doesn't work there," says Dirk Nettelbeck. "The RNA switches, in contrast, are only 100 base pairs long." Using the RNA switches, the researchers managed to increase the production of the therapeutic gene by ten times. "But there is still room for a lot more," Nettelbeck explains. "The construction of RNA switches is extremely variable. Once the technology is fully developed, we will be able to better equip and regulate viruses for many therapeutic applications." Nettelbeck and his team are convinced that the useful RNA switches will become established for many other uses in research and medicine.

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Viruses with integrated gene switch

ADMIXTURE and STRUCTURE tests arent formal mixture tests. Yes! In fact, in the open science community this issue is repeated over and over and over, because people routinely get confused (our audience does not consist of population geneticists and phylogeneticists by and large). So sometimes it is necessary to lay it out in detail as in the post above. The key point to always remember is that population genetic & phylogenetic statistics and visualizations are a reduction and summary of reality in human palatable form. They tell us something, but they do not tell us everything. A common issue is that for purposes of mental digestion it is useful to label ancestral elements European, or on PCA refer to a European-Asian cline, as if the population genetic abstractions themselves are the measure of what European or Asian is. But European and Asian are themselves human constructions, and subject to debate (e.g., do Turks count as Europeans? Indians as Asians?) The population genetic statistics are not themselves subjective, but the meanings we give them are.

Lets illustrate this with a concrete example. The Cape Coloured population of South Africa is a compound of Khoisan, Bantu, South Asian, Southeast Asian, and Northern European ancestry. But if you use a basic summary statistic which measured genetic distance, such as Fst,they turn out to exhibit the lowest value with South Asians. Whats going on here? This is a real result, but Fst is blind to extraneous information of demographic history. If you used ADMIXTURE or STRUCTURE with only African and European populations you would overestimate the European ancestry of the Cape Coloureds. Why? Because the non-European and non-African component would probably collapse into the European element. The algorithms work fine, given the conditions you start it out with. Adding in South and Southeast Asians as reference populations allows these components to fall out. We expect such a division based on history, but recall that South Asians themselves are an admixed population! But for the purposes of understanding the ethnogenesis of the Cape Coloureds, which dates to the past 400 years, an admixture event ~3,000 years before the present is not relevant. In other words, how misleading the result from a given tool is is contingent upon the questions were asking. If we are trying to extract answers which are inappropriate to the tools, then well get inappropriate answers.

For the purposes of human population genetics and phylogenetics the main issue is the historical and cognitive bias toward Platonism and types. Instead of European being a convenient label for pragmatic purposes, we imbue European with the essences of value of an ideal type. Once we make this transition hilarity ensues. For example, using classic Platonic typology the Caucasian race was defined using as a measure the exemplar of that race, the Georgian people of the Caucasus. The classic meaning of Caucasian naturally included the people of Europe and West Asia, with some more expansive definitions inclusive of most South Asians. But in the American context Caucasian has transformed into white European Westerner. This means that there are debates whether genuine Caucasians, such as Armenians, are actually Caucasian! What was once a convenient word used to illustrate a clear and distinct concept has transmuted itself so as to generate confusion and diminish clarity.

But I think the current wave of human population and phylogenetics unmasks an even deeper problem. The extant races of modern humans may themselves be recent syntheses of a very different human phylogenetic tree as recently as ~15,000 years ago. For example, nearly every single indigenous resident of South Asia seems to exhibit some level of admixture between two very distinct branches of the human tree within the last 10,000 years. The Indian race, as we understand it, is definitely a feature of near prehistory at the earliest (the Neolithic), and perhaps as late as the Indo-Aryan migrations ~4,000 years before the present. And now there are suggestive clues that the same applies to Europe. The people of Europe have roots in the Ice Age inhabitants of the continent, but also the Neolithic peoples of West Asia. And, due to the limitations of demography-blind model based clustering algorithms they may even have more exotic affinities to East Asia which have long been masked! The last may even be an Ice Age era admixture (see the comment at the first link on the relationship to First Americans).

One of the realities of trying to reconstruct the past from what we have in the present is that the past becomes a jigsaw puzzle using pieces of the present. This is informative, but there are limitations. Because the reality is is that the present is a jigsaw puzzle constructed out of the past. Obviously we cant run an experiment from the past to the present. We have to go backwards, rather than forwards. These are the constraints which bound and shade our understanding. They should not lead us down the path of pure skepticism. Rather, they should instill in us the importance of constant critique, and evaluation of our premises. In fact, one of the things which seem clear from the latest wave of paleogenetic research is that empirical results themselves can overturn premises.

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On phylogenetic instrumentalism | Gene Expression

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/58n7cj/toxicology_and_epi) has announced the addition of John Wiley and Sons Ltd's new book "Toxicology and Epigenetics" to their offering.

Epigenetics is the study of both heritable and non-heritable changes in the regulation of gene activity and expression that occur without an alteration in the DNA sequence. This dynamic and rapidly developing discipline is making its impact across the biomedical sciences, in particular in toxicology where epigenetic differences can mean that different individuals respond differently to the same drug or chemical.

Toxicology and Epigenetics reflects the multidimensional character of this emerging area of toxicology, describing cutting-edge molecular technologies to unravel epigenetic changes, the use of in vivo and in vitro models, as well as the potential use of toxicological epigenetics in regulatory environments. An international team of experts consider the interplay between epigenetics and toxicology in a number of areas, including environmental, nutritional, pharmacological, and computational toxicology, nanomaterials, proteomics and metabolomics, and cancer research.

Toxicology and Epigenetics is an essential insight into the current trends and future directions of research in this rapidly expanding field for investigators, toxicologists, risk assessors and regulators in academia, industry and government.

Key Topics Covered:

1 Introduction

2 Environment, Epigenetics, and Diseases 5

3 DNA Methylation and Toxicogenomics 25

4 Chromatin at the Intersection of Disease and Therapy 51

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Research and Markets: Toxicology and Epigenetics

17 August 2012 Last updated at 08:29 ET

A court in the US has again backed a biotech company's right to patent genes which have been isolated from the human body.

Myriad Genetics has patents on the BRCA1 and BRCA2 genes, which are strongly linked to breast and ovarian cancer.

Patents on genes have been repeatedly contested in the courts.

The latest decision by the Federal Circuit Court of Appeals sided in favour of the company.

The patents are valuable as they give the owners exclusive rights to diagnostic tests for the genes. One of the questions in the case was whether isolating a gene makes it different to one still in the body.

Circuit Judge Alan Lourie said: "Everything and everyone comes from nature, following its laws, but the compositions here are not natural products.

"They are the products of man, albeit following, as all materials do, laws of nature."

The decision was welcomed in a statement from the president of Myriad Genetics Peter Meldrum: "We are very pleased with the favourable decision the court rendered today which again confirmed that isolated DNA is patentable.

"Importantly, the court agreed with Myriad that isolated DNA is a new chemical matter with important utilities which can only exist as the product of human ingenuity."

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Gene patents upheld in US court

ALAMEDA, Calif.--(BUSINESS WIRE)--

BioTime, Inc. (NYSE MKT: BTX) and BioTimes subsidiary OncoCyte Corporation today announced the publication of a scientific report on the gene COL10A1 and its potential as a marker for numerous types of human cancers. The paper, published in the peer-reviewed journal Future Oncology and available online today, describes the microarray-based approach used to identify COL10A1 as a pan-cancer biomarker with significantly elevated expression in diverse malignant tumor types including cancers of the breast, stomach, colon, lung, bladder, pancreas, and ovaries. In addition, the protein was shown to be specifically localized within tumor vasculature. Combined, these findings will be an important basis for the development and application of new diagnostic and therapeutic strategies, including the measurement of Collagen Type X in the blood as a screen for the presence of cancer, the use of antibodies that recognize and bind to the protein to visualize and locate tumors in the body, and the targeted delivery of tumor-destroying agents.

These findings are significant on several levels, said Karen Chapman, PhD, Director of Bioinformatics at OncoCyte and lead author of the report. COL10A1, the gene that encodes Collagen Type X, is normally only expressed in a specific zone within developing bones and is generally not expressed in most adult cells and tissues. This low background expression, taken together with the significant expression that we observed in many tumor types, underscores the potential use of this biomarker as a novel diagnostic and therapeutic target for many cancer types.

As a result of the studies described in todays publication, OncoCyte has generated five proprietary monoclonal antibodies to Collage Type X for use in developing novel cancer diagnostics, imaging agents and targeted therapeutics, said Joseph Wagner, PhD, CEO of OncoCyte and co-author of the study. Given the broad expression of this protein across numerous tumor types and its association with tumor vasculature, characterization of this marker in cancer patients blood samples has become a priority at OncoCyte. Upon validation of their performance in detecting cancers from patient samples, these antibodies are candidates for inclusion in PanC-DxTM, a low-cost, easy-to-use product with broad cancer detection ability slated for launch in 2014.

PanC-DxTM is being developed to detect the presence of a variety of human cancers, including cancers of the breast, lung, bladder, uterus, stomach, and colon, during routine check-ups. By facilitating early non-invasive cancer detection through a blood test, PanC-DxTM could lead to more successful therapeutic outcomes while simultaneously reducing the costs of cancer monitoring and globally increasing the availability of affordable cancer screening. OncoCyte first announced the development of PanC-DxTM during December 2011 and intends to launch the product in Europe in 2014 before seeking the required approval by the Food and Drug Administration to market PanC-DxTM in the United States.

About BioTime, Inc.

BioTime, headquartered in Alameda, California, is a biotechnology company focused on regenerative medicine and blood plasma volume expanders. Its broad platform of stem cell technologies is enhanced through subsidiaries focused on specific fields of application. BioTime develops and markets research products in the field of stem cells and regenerative medicine, including a wide array of proprietary ACTCellerate cell lines, HyStem hydrogels, culture media, and differentiation kits. BioTime is developing Renevia (formerly known as HyStem-Rx), a biocompatible, implantable hyaluronan and collagen-based matrix for cell delivery in human clinical applications. BioTime's therapeutic product development strategy is pursued through subsidiaries that focus on specific organ systems and related diseases for which there is a high unmet medical need. BioTime's majority owned subsidiary Cell Cure Neurosciences Ltd. is developing therapeutic products derived from stem cells for the treatment of retinal and neural degenerative diseases. BioTime's subsidiary OrthoCyte Corporation is developing therapeutic applications of stem cells to treat orthopedic diseases and injuries. Another subsidiary, OncoCyte Corporation, focuses on the diagnostic and therapeutic applications of stem cell technology in cancer, including the diagnostic product PanC-Dx currently being developed for the detection of cancer in blood samples. ReCyte Therapeutics, Inc. is developing applications of BioTime's proprietary induced pluripotent stem cell technology to reverse the developmental aging of human cells to treat cardiovascular and blood cell diseases. BioTime's subsidiary, LifeMap Sciences, Inc., markets GeneCards, the leading human gene database, and is developing an integrated database suite to complement GeneCards that will also include the LifeMap database of embryonic development, stem cell research and regenerative medicine, and MalaCards, the human disease database. LifeMap will also market BioTime research products. BioTime's lead product, Hextend, is a blood plasma volume expander manufactured and distributed in the U.S. by Hospira, Inc. and in South Korea by CJ CheilJedang Corporation under exclusive licensing agreements. Additional information about BioTime can be found on the web at http://www.biotimeinc.com.

About OncoCyte Corporation

OncoCyte Corporation is a majority-owned subsidiary of BioTime, Inc. OncoCyte's mission is to develop novel products for the diagnosis and treatment of cancer in order to improve both the quality and length of life of cancer patients. OncoCyte's molecular diagnostics division is developing products for earlier detection of a variety of cancers. In addition to its diagnostic product line, OncoCyte is developing cellular therapies to treat cancer based on the unique biology of vascular precursor cells. The goal of OncoCyte's therapeutic research efforts is to derive vascular cells that can be engineered to deliver a toxic payload to the developing blood vessels of a malignant tumor to destroy the tumor without killing nearby normal tissues in the body. Additional information on OncoCyte can be found on the web at http://www.oncocyte.com.

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BioTime and OncoCyte Corporation Publish Data on the Gene COL10A1 as a Marker and Potential Diagnostic for a Wide ...

Credit: Tel Aviv University

Published: Aug. 16, 2012 at 5:03 PM

TEL AVIV, Israel, Aug. 16 (UPI) -- Genetics can reveal not only who your ancestors were but where they came from geographically, researchers at Israel's Tel Aviv University report.

Working with researchers from UCLA, they've created a probabilistic model of genetic traits for every coordinate on the globe for determining more precisely the geographical location of a person's ancestral origins.

The method has the potential to reveal the ancestry, origins, and migration patterns of many different human populations, the researchers said.

There are points in the human genome called SNPs that differ among individuals, Tel Aviv researcher Eran Halperin said, and mutated sometime in the past and the mutation was then passed to a large part of the population in a particular geographic region.

The probability of a person possessing these mutations today varies depending on the geographical location of those early ancestors, he said.

The new method is able to pinpoint more specific locations for an individual's ancestors, for example placing an individual's father in Paris and mother in Barcelona, a TAU release said Thursday.

Previous methods would "split the difference" and place this origin inaccurately at a site between those two cities, such as Lyon, the release said.

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Genetics pins ancestors to a map location

Public release date: 16-Aug-2012 [ | E-mail | Share ]

Contact: Kim Polacek kim.polacek@moffitt.org 813-745-7408 H. Lee Moffitt Cancer Center & Research Institute

Researchers at Moffitt Cancer Center, working with colleagues in Sweden, the Netherlands and Puerto Rico, have validated a radiosensitivity molecular signature that can lead to better radiation therapy decisions for treating patients with breast cancer.

The results appeared in a recent issue of Clinical Cancer Research, a publication of the American Association for Cancer Research.

The study examined patients with breast cancer who had been treated with radiation therapy and demonstrated that a radiosensitivity molecular signature (RSI) could predict clinical outcomes exclusively in patients treated with radiation therapy. The radiosensitivity molecular signature (RSI) used by the research team had previously been tested and validated for rectal, esophageal, and head and neck cancers. The technology, which identifies radiosensitivity and radioresistance, opens the door to biologically guided radiation therapy and offers the potential for better outcomes.

"Developing a radiosensitivity predictive assay has been a goal of radiation biology for decades," said Javier F. Torres-Roca, M.D., member of the Experimental Therapeutics program at Moffitt. "This effort supports the emphasis on personalized medicine, where the goal is to use molecular signatures to guide therapeutic decisions."

According to Torres-Roca, approximately 60 percent of all cancer patients receive radiation therapy during their treatment. Yet until now, no molecular diagnostic or biomarker of radiosensitivity had been developed to predict its benefit.

The radiosensitivity molecular signature was developed based on gene expression for 10 specific genes and a linear regression algorithm. RSI was developed in 48 cancer cell lines using a systems-biology strategy focused on identifying biomarkers for cellular radiosensitivity.

This study validated RSI's benefit when researchers found that radiosensitive breast cancer patients had an improved five-year, relapse-free survival when compared to radioresistant patients.

"This study validated RSI in 503 patients in two independent data sets," Torres-Roca said. "We have validated RSI in five independent cohorts totaling 621 patients, so this latest validation study, to the best of our knowledge, makes this technology the most extensively validated molecular signature in radiation oncology."

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Moffitt Cancer Center researchers validate molecular signature to predict radiation therapy benefit

SILVER SPRING, Md., Aug. 16, 2012 (GLOBE NEWSWIRE) -- Nuvilex, Inc. (NVLX), an international biotechnology provider of cell and gene therapy solutions, announced today it has contacted several key members of congress, lending its support to the Pancreatic Cancer Research and Education Act (S. 362/H.R. 733).

The legislation being proposed in H.R. 733, calls for an appropriation of $20 Million and requires the Secretary of Health and Human Services "to establish and implement a pancreatic cancer initiative to assist in coordinating activities to address the high mortality rate associated with pancreatic cancer" through establishing an Interdisciplinary Pancreatic Cancer Coordinating Committee and developing a long-term plan with the National Institutes of Health (NIH), the National Cancer Institute (NCI) and the Centers for Disease Control and Prevention (CDC). Research dedicated to providing possible treatments for pancreatic cancer receives only ~2% of the federal funding from NCI. Finally, there is no national plan designed to improve patient survival, which this bill is designed to initiate.

Since its original introduction in 2009 by Congresswoman Anna Eshoo (D,CA) and reintroduction with Leonard Lance (R,NJ) in 2011 followed by introduction of S. 362 by Senator Sheldon Whitehouse (D,RI) to the Senate, the bill has now received 276 cosponsoring members from the House and 58 from the Senate. In addressing the critical need for this legislation in his letters to Congress, Nuvilex's Chief Executive Dr. Robert Ryan, stressed the importance of funding in order to help bring new pancreatic cancer therapies forward to completion, stating, "...the opportunities for bringing treatments such as Nuvilex's for [pancreatic cancer] to fruition are, and will continue to be, limited by the availability of funding." Dr. Ryan added, "Government funding must be made available to small companies who, like Nuvilex, have demonstrated through preclinical and/or early clinical trials the efficacy of their product in treating high-mortality diseases such as pancreatic cancer." One of the bill's sponsors, Senator Isakson (R,GA), emphasized his deep commitment to this bill stating, "...this bill will go a long way in ensuring that the fight against pancreatic cancer receives its fair share of research and resources."

In providing endorsement of this legislation by Nuvilex, its Board and on behalf of its new wholly-owned subsidiary Austrianova Singapore, Dr. Ryan finished by pointing out, "Nuvilex feels it is critical to endorse S. 362/H.R. 733. It's very important that our Congressional leaders receive the recommendations and support from all constituents, including Nuvilex, in order to help support and stimulate passage of the Pancreatic Cancer Research and Education Act. We believe the completed Phase 1/2 pancreatic cancer trial using our Cell-in-a-Box(R) patented technology will provide an important step toward helping change the poor pancreatic cancer survivor statistics. Nuvilex sees this Congressional Initiative as another potentially critical mechanism to help move our technology forward."

Pancreatic Cancer

Statistics directly show pancreatic cancer is the fourth leading cause of cancer death in the United States. Internationally >250,000 people will die from it this year. At present, there are no standard early detection methods, although recent discoveries suggest a new pancreatic cancer detection method may be on the horizon, there are few effective treatment options and there is no cure. As a result, 74 percent of patients die within a year of diagnosis and only six percent survive beyond five years.

About Nuvilex

Nuvilex, Inc. (NVLX) is an international biotechnology provider of live therapeutically valuable, encapsulated cells and services for research and medicine. A great deal of work is ongoing to move Nuvilex, and in particular its Austrianova Singapore subsidiary, forward. Our company's clinical offerings will include cancer, diabetes and other treatments using the company's cell and gene therapy expertise and live-cell encapsulation technology.

The Nuvilex, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=13494

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Nuvilex Endorses Proposed Congressional Legislation on Pancreatic Cancer Initiative

Published: Aug. 16, 2012 at 7:28 AM

DAVIS, Calif., Aug. 16 (UPI) -- A defective gene causes brain changes that lead to the atypical social behavior characteristic of autism, U.S. researchers said.

Cecilia Giulivi, professor of molecular biosciences at the University of California, Davis School of Veterinary Medicine, and a researcher affiliated with the University of California, Davis MIND Institute, said studies in mice showed abnormal action of just one gene disrupted energy use in neurons.

The harmful changes were coupled with anti-social and prolonged repetitive behavior -- traits found in autism, Giulivi said.

"A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism -- how one gene defect may trigger this type of neurological behavior," Giulivi said in a statement. "Once you understand the mechanism, that opens the way for developing drugs to treat the condition."

The research, published in the journal PLoS ONE, showed, when defective, the gene's protein interacts with the protein of a second gene known as p53 to dampen energy production in neurons.

This severe stress leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus -- brain regions critical for social behavior and cognition, Giulivi said.

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Defective gene linked to autism symptoms

Public release date: 16-Aug-2012 [ | E-mail | Share ]

Contact: Phil Sahm phil.sahm@hsc.utah.edu 801-581-2517 University of Utah Health Sciences

SALT LAKE CITY Scientists have discovered that poxviruses, which are responsible for smallpox and other diseases, can adapt to defeat different host antiviral defenses by quickly and temporarily producing multiple copies of a gene that helps the viruses to counter host immunity. This discovery provides new insight into the ability of large double-stranded DNA viruses to undergo rapid evolution despite their low mutation rates, according to a study published by University of Utah researchers in the Aug. 17, 2012, issue of Cell.

Poxviruses are a group of DNA-containing viruses that are responsible for a wide range of diseases in both humans and animals, including smallpox. Unlike smaller RNA-containing viruses, such as those that cause influenza and HIV, which are able to evade host immune responses through rapid mutation, poxviruses have larger genomes and low mutation rates and little is known about their adaptive strategies against host defenses.

"Poxviruses encode a variety of genes that help them to counter host immune defenses and promote infection," says Nels Elde, Ph.D., assistant professor of human genetics at the University of Utah School of Medicine and first author on the study. "Despite ample evidence that the poxvirus genome can undergo adaptive changes to overcome evolving host defenses, we still don't know that much about the mechanisms involved in that adaptation."

To determine mechanisms of adaptation, Elde and his colleagues studied the vaccinia virus, a type of poxvirus best known for its role as the vaccine used to eradicate smallpox. Previous research has shown that vaccinia virus encodes two genes, known as K3L and E3L, which inhibit host defenses that normally block viral infection. In this study, Elde and his colleagues started with a strain of vaccinia virus that had been altered to delete the E3L gene and repeatedly propagated this E3L-deficient strain in human cells to see how well the virus would replicate. They found that this E3L-deficient strain was quickly able to increase infectious virus production by selectively increasing the number of copies of the K3L gene in its genome.

"This highly specific and rapid gene amplification was unexpected," says Elde. "Our studies show that increasing K3L copy number leads to increased expression of K3L and enhanced viral replication, providing an immediate evolutionary advantage for those viruses that can quickly expand their genome."

Elde and his colleagues also found that, in addition to K3L copy number amplification, some of the E3L-deficient vaccinia strains also acquired a mutation consisting of a single amino acid substitution in the K3L gene. Both the mutation-bearing and multicopy K3L viruses displayed improved viral fitness, or ability to replicate in the host environment, compared to wild-type vaccinia virus. The emergence of this beneficial amino acid substitution suggests that increasing K3L copy number facilitated the appearance of the variant by providing additional mutational targets, despite the virus' otherwise low mutation rate.

"We were able to demonstrate at least two strategies by which poxviruses are able to adapt diverse mechanisms of host immunity," says Elde. "Our observations reveal that, while poxviruses do undergo gene mutation, their first response to a new, hostile host environment can be rapid gene expansion. We also found evidence that the virus genome can contract after acquiring an adaptive mutation, thus alleviating the potential trade-off of having a larger genome, while leaving a beneficial mutation in place."

Although smallpox was officially eradicated by the World Health Organization in 1980, concerns about the use of smallpox as a bioterrorism agent have spurred renewed interest in the study of vaccinia and other poxviruses. In addition, poxvirus infections, such as monkeypox, can be transmitted from animals to humans and the adaptive strategies of poxviruses may be relevant for other infectious organisms.

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Poxviruses defeat antiviral defenses by duplicating a gene

FARMINGTON, Conn., Aug. 16, 2012 /PRNewswire-iReach/ -- "Personalized" cancer care has never had it better, and three drugs have been responsible for confirming their prospects to combat certain common cancers. Of these, two studies have focused on drugs for treating advanced melanoma, and a third study has explored a gene-targeted chemotherapy for a subset of lung cancers. All the three drugs have proved their efficacy in Phase III trials, and tailored medications similar to these are being used in metastasis or cancer settings. Advanced lung cancer and advanced melanoma necessitate targeted therapies that form the standard of care.

(Photo: http://photos.prnewswire.com/prnh/20120816/CG58765)

The past scenario involved doctors administering cancer drugs to patients as a normal course, in the anticipation that response levels in at least some of the patients would be positive. However, with the advent of personalized medicine, this method has taken a back seat, and greater emphasis is being given to patient-centric approaches for targeting therapies towards genetic abnormalities in cancers that are responsible for driving cancer growth.

Global Information, Inc. presents the latest analysis market research published by Industry Experts and the upcoming ADAPT 2012 in Washington, DC.

Market Research: Personalized Medicine - A Global Market Overview

Personalized Medicine product segments analyzed in this study includes Targeted Biologics, Proteomics & Genomics, Genetically Modified (GM) Products, Wellness & Disease Management, Molecular Diagnostics and Self/Other Diagnostics.

Biologics have gained prominence in treating systemic and cutaneous autoimmune diseases, with a design that targets particular components of immune system. Since novel drugs can target proteins in a more precise manner, in addition to having reduced risks of systemic side effects, they offer significant benefits as compared to the erstwhile immunomodulators. For instance, crucial advances have been achieved in developing TNF-alpha blockers for treating psoriasis, psoriatic arthritis, rheumatoid arthritis, Crohn's disease and ankylosing spondylitis in the same manner, B-cell depletion has revolutionized treatment of lupus, pemphigus, certain vasculitides, etc. Having said this, development of these molecules and their clinical usage are as yet in the evolutionary process.

Further categorization of patients' clinical profiles requiring the use of biologics has to reach a culmination point due to the fact that the long-term safety profiles of such agents are largely hidden at present.

Pharmacogenomics is the branch of pharmacology dealing with the influence of genetic variation on drug response in patients through the correlation of gene expression or single-nucleotide polymorphisms with a drug's efficacy or toxicity. This is focused towards developing rational means for optimizing drug therapy relating to the patients' genotype, ensuring maximum efficacy with minimal adverse effects. Pharmacogenomics offers the prospect of advancing personalized medicine to levels where drugs and drug combinations can be optimized for every individual's unique genetic makeup. Pharmacogenomics is the whole genome application of pharmacogenetics, which examines the single gene interactions with drugs.

An Executive Summary of this analysis, full table of contents, and a free sample/whitepaper of the full report are available at http://www.giiresearch.com/report/inde248627-personalized-medicine-global-market-overview.html

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Healthcare IT Accelerates Joint Venture, Contributes to Interpreting Gene Variation

Public release date: 16-Aug-2012 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 16, 2012Every year tribal gaming generates billions of dollars in revenue, creates tens of thousands of jobs, and boosts the economies of many Native American communities. In the state of California alone, tribal gaming has brought in $7.5 billion annually. However, because of the aggressive movement to legalize Internet gambling, which effectively would give states the power to regulate and tax online gambling even on reservations, the financial success of these communities could change. In "Native American Off-Reservation Gaming," an expert roundtable published in Gaming Law Review and Economics, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers, panelists discuss and debate the issues of tribal gaming, focusing on the impactboth positive and negativeon both tribes and their surrounding communities. The full tables of content for Gaming Law Review and Economics are available online.

"Though some tribes have been incredibly successful financially from casino and resort businesses, experts have observed that the Native American gaming revenues are already going flat," says Joseph M. Kelly, PhD, JD, Co-Editor-in-Chief of Gaming Law Review and Economics, professor of business law at SUNY College at Buffalo, and co-author of the article, 'Enforcement of Native American Gambling Debts.' "There is concern amongst many of these tribes that state legalization of online gambling might have a negative impact on their revenues. Many tribal experts instead would prefer federal regulation."

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About the Journal

Gaming Law Review and Economics: Regulation, Compliance, and Policy is the only authoritative peer-reviewed journal covering traditional land-based, Internet, and wireless gaming law in one of the fastest growing economic leisure industries. The Journal provides the latest developments in legislative, regulatory, and judicial decisions affecting gaming at both the state and federal level in the U.S. and in more than 75 countries, as well as coverage of economic issues associated with the exponential growth of casinos and gaming practices. Topics include legal aspects of all forms of gaming, including casino games, lotteries, sports books, and horse racing; new regulations in Internet and wireless gaming; legal restrictions on gaming and advertising; gaming license requirements within and across jurisdictions; legal aspects of credit and collection of debts; litigation in application, citing, and employment issues concerning casino operations; gaming tax issues; and intellectual property. Complete tables of content and a sample issue may be viewed online at the Gaming Law Review and Economics: Regulation, Compliance, and Policy website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science, biomedical research, and law including Election Law Journal and Biotechnology Law Report. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available at the Mary Ann Liebert, Inc., publishers website.

Mary Ann Liebert, Inc. 140 Huguenot Street, New Rochelle, NY 10801 http://www.liebertpub.com Phone: (914) 740-2100 (800) M-LIEBERT Fax (914) 740-2101

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Prosperous Native-American tribes grow anxious about legalization of Internet gambling

15-08-2012 15:37

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USC Institute for Genetic Medicine Art Show - Video

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

Metagenics, Inc., a nutrigenomics and lifestyle medicine company dedicated to helping people live happier, healthier lives by realizing their genetic potential, today announced the relocation of its corporate and Americas region headquarters from San Clemente, Calif. to Aliso Viejo, Calif. The modern, efficiently designed, and LEED-certified facility not only supports Metagenics healthy lifestyle vision and mission, but also provides future space to accommodate the companys growth trend and goals. Metagenics will be relocating to its new headquarters beginning August 20.

This move represents the right choice for us at a time when were making plans for the next phase of growth, said Fred Howard, chief executive officer of Metagenics. The new facility accommodates our growing employee base, enabling us to better serve the needs of our customers. Additionally, it provides an ideal environment that represents the healthy balance we strive for in our professional and personal lives.

The facility, located at 25 Enterprise Parkway, is staged to accommodate the companys current office space with room for future growth. The building is certified for Leadership in Energy and Environmental Design (LEED) for more efficient use of resources, which often also provides a healthier work environment.

We saw an enormous amount of opportunity in this decision, commented Willy Pardias, senior vice president and general manager of Metagenics Americas region. This facility provides an inspiring and energizing atmosphere that further supports our companys mission to living healthier lifestyles.

About Metagenics, Inc.

Metagenics, Inc. (www.metagenics.com) is a nutrigenomics and lifestyle medicine company focused on improving health and reversing chronic illness. Founded in 1983, Metagenics serves more than 75,000 healthcare providers worldwide through premium quality, science-based medical foods, nutritional formulas, and lifestyle therapy programs to help their patients achieve a lifetime of good health. Metagenics scientific staffamong the largest in the nutrigenomics industryhas published more than 80 articles in peer-reviewed journals and has been awarded 78 international or domestic patents. The companys educational arm, Metagenics University, collaborates with renowned medical experts to annually deliver more than 200 events designed to help healthcare professionals stay on the leading edge of lifestyle medicine and incorporate nutrition into their clinical practice.

Metagenics will maintain its corporate headquarters in Aliso Viejo, California; R&D headquarters in Gig Harbor, Washington; and operating subsidiaries in Brussels, Belgium and Brisbane, Australia.

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Metagenics to Relocate to New Facility in Aliso Viejo, California

DETROIT Wayne State University researchers are testing a way to determine the status of fetal chromosomes that could lead to healthier outcomes for mothers and their babies.

Supported by a two-year, $418,000 exploratory/developmental grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health, the researchers will capture human fetal cells for genetic study within the first two months of pregnancy using a newly developed, safe, noninvasive retrieval technique similar to a Pap test.

D. Randall Armant, Ph.D., and Michael P. Diamond, M.D., professors of obstetrics and gynecology in Wayne States School of Medicine, are the principal investigators of the study. Susan Land, Ph.D., associate professor of obstetrics and gynecology, is a co-investigator.

Titled Genetic Analysis of Human First Trimester Trophoblast in Ongoing Pregnancies, the project targets cells called trophoblasts, which surround the blastocyst, a cluster of cells that results from successful fertilization. Researchers are particularly interested in invasive trophoblasts, which attach the blastocyst to the uterine wall; the cells become the placenta and the membranes that nourish and protect the developing organism.

Such cells carry genetic material from the fetus. Armants team will gather them through transcervical sampling, a method that uses a cytobrush inserted into the cervix. Researchers believe the technique is less intrusive than previously used methods, yields intact fetal cells and can be done as early as six to 12 weeks; doctors typically must wait 10 to 14 weeks to use other methods, which can carry more risk to mothers and fetuses.

The earlier you get the information, the more time the doctor has to manage whatever problems are coming up during or after the mothers pregnancy, Armant said. It also gives the parents more time to make decisions about the pregnancy.

Researchers will isolate trophoblasts using immunomagnetic nanotechnology, taking advantage of unique proteins on the surface of fetal cells. Highly sensitive genetic tools capable of analyzing single cells will verify the fetal origin of captured cells before their DNA is analyzed for chromosome number.

Armant said that tests based on fetal cells obtained from the cervix eventually could alert doctors to things like ectopic pregnancy, miscarriage, preterm labor, poor fetal growth, preeclampsia, fetal Rh incompatibility and chromosome number disorders, like Down syndrome. It also could help detect inherited genetic diseases, such as muscular dystrophy, sickle cell anemia and hemophilia.

The goal is to determine if placental cells obtained from the cervix accurately represent the chromosomal status of the fetus.

Development of this diagnostic platform for the detection of chromosome number disorders could establish an innovative approach for prenatal genetic testing that would provide immense opportunities for improving the health of mothers and their babies, Armant said. Continued...

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WAYNE COUNTY: New fetal cell collection method could improve genetic analysis, disorder detection, Wayne State ...

WEDNESDAY, Aug. 15 (HealthDay News) -- Dogs may soon become man's best friend on a level that goes far beyond companionship and loyalty.

Researchers report that the canine genome, similar in many ways to the human one, is starting to shed light on a wide range of human diseases.

What makes dogs particularly interesting to scientists is their breed structure -- a type of artificial selection -- which creates distinct and diverse lines of animals that range from the muscular German shepherd to the nervous Chihuahua, from the hard-working collie to the perpetually pampered poodle.

According to a review article published Aug. 16 in the New England Journal of Medicine, the fact that most purebred dogs have descended from small, closely related parentage with large litters means recessive diseases are common among them.

To those interested in genetics, that's exciting.

It makes less common recessive diseases (which can't be seen or expressed unless the responsible gene is carried by both parents) more prevalent in these animals. And that opens the window to understanding the genetic underpinnings of a wide range of conditions that humans and dogs share.

"The dog genome is very similar to humans," said review author Elaine Ostrander, chief of the Cancer Genetics Branch of the National Human Genome Research Institute at the U.S. National Institutes of Health. "It's closer to us than the genomes of mice, rats or fruit flies, which are often used in research. Dogs also live side-by-side in our environments with us; they drink the same water, they breathe the same air, they're exposed to the same pesticides and they often even eat some of the same food."

Ostrander said dogs and humans get almost all of the same diseases, including cancer, arthritis, epilepsy, retinal atrophy, autoimmune disorders such as lupus, and psychological problems such as obsessive-compulsive disorder.

There are 400 different breeds, and many are associated with greater risk of getting particular diseases, Ostrander said. "A particular torsion [twisting] of the intestine is the only thing we see in dogs but not in humans."

Cancer is the number one cause of death in dogs, said Dr. Ned Patterson, an associate professor of veterinary medicine and genetics at the University of Minnesota. "Because the mechanism [of the disease] and the therapies are similar, we can really learn a lot about cancer in both directions, even concurrently," he noted.

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Man's Best Friend Points the Way in Genetic Research

Dog lovers may be interested in an article published this week in the New England Journal of Medicine: It highlights the discoveries scientists are making about diseases that various dog breeds are prone to -- and how those findings can benefit human health as well as that of canines.

Its written by longtime dog genetics researcher Elaine Ostrander of the National Human Genome Research Institute.

The discoveries are possible because of several things: First off, both the human genome and dog genomes have been sequenced. (The breeds chosen for the first round of dog DNA sequencing were a standard poodle and boxer, should you be curious.)

Secondly, dogs have been intensively bred into distinct breeds, and in the case of purebreds (though not my black mutt Nightshade; who knows where she came from?) their pedigrees are very well known. Often, the breeds are descended from just a few animals, so they can be very inbred as well.

The intensive selection over the decades and/or centuries for traits of body shape or hair color has also inadvertently selected for genes that foster diseases. And so Bedlington terriers are prone to copper storage diseases, Doberman pinschers are prone to narcolepsy, and so on.

Here is where some lemonade gets made out of that sad lemon: Its far easier in many cases for scientists to track down genes associated with, say, a cancer or vision disorder in dogs than it is in human beings, Ostrander writes.

Thats especially true when a disease could stem from one of several genetic defects. If you study a bunch of people with the disease, the underlying genes involved will probably be a mix and the results will be too cloudy for scientists to make sense of. But in an inbred dog strain prone to a disorder, the underlying cause is far more likely to be rooted in one specific gene.

And that means scientists can find it. Once theyve found it, they can then go back and see if the same holds true for some human beings.

Some examples Ostrander cites of gene-influenced disorders in dogs shedding light on diseases in human beings:

--A syndrome called RCND that causes kidney cancer and skin growths in German shepherds was pinpointed to versions of a gene called folliculin. That same gene, it turns out, is involved in a human disease called Birt-Hogg-Dube syndrome.

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How dogs can help unravel genetic diseases in people

The technique could help patients with currently untreatable diseases such as Huntington's.

RNA Rx: An Alynlam chemist prepares RNA molecules. Alnylam Pharmaceuticals

A biotech company called Alnylam announced today that a small clinical trial for a genetic therapy based on RNA interference, or RNAi, suggests that the technique can have a powerful effect on its target gene. The therapeutic effect lasted for over a month with just one dose. The company is also working with a medical device maker, Medtronic, on a way to deliver RNAi treatment directly to the brain, in order to treat the degenerative brain disease Huntington's.

The patients in the trial have a genetic disorder that originates in the liver and leads to the buildup of protein deposits in many organs. Alnylam, a Cambridge, Massachusetts-based company, says its RNAi therapeutic, given at its highest dose, reduces the amount of the faulty protein that spurs the disease by almost 94 percent.

The positive results add weight to the notion that RNAi therapeutics could eventually help patients with a range of genetic diseases. RNAi therapy involves researchers producing snippets of RNA, a close relative of DNA, that match a portion of a gene of interest. When administered, this so-called small interfering RNA (siRNA) causes the destruction of that gene's products before it can be turned into a protein. The specificity of RNAi for targeting particular genes has attracted a lot of interest from people who want to use it as a clinical treatment (see "Prescription RNA").

"Today's platforms target the protein that causes the disease and bind to that protein. We stop the protein from being made in the first place," says Barry Greene, president and chief operating officer of Alnylam.

But a recurring challenge for the therapeutic RNAi field is how to deliver the siRNAs to the right place in the body. On their own, the small molecules do not survive long in the bloodstream, so simply injecting a patient with a solution of unprotected siRNAs is not effective. "The key technical hurdle is getting the siRNA [inside] the right cells," says Greene.

For several of its projects, Alnylam uses nanoparticles to protect and deliver its siRNAs, which can then be delivered by injection. But for genetic diseases that originate in the brain, the body's own defenses, namely the blood-brain barrier, complicate delivery further. To circumvent the blood-brain barrier, which prevents most molecules from leaving the bloodstream and entering the brain, Alnylam has looked to a different delivery mechanism: direct dosing of unpackaged siRNAs.

Medtronic, a Minneapolis company that designs and manufactures medical devices, has devised a way to allow this. Together, the companies have developed a treatment that combines Alnylam's RNAi therapeutic with Medtronic's drug delivery technology to treat Huntington's.

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Gene Control, Delivered Directly to the Brain

NEW YORK, Aug. 15, 2012 (GLOBE NEWSWIRE) -- Amorcyte, a company of NeoStem, Inc. (NYSE MKT:NBS) ("NeoStem" or the "Company"), a rapidly emerging market leader in the fast growing cell therapy market, today announced that it received on August 9, 2012 approval to continue its PreSERVE AMI Phase 2 clinical trial following its first interim data and safety review by the Data Safety Monitoring Board (DSMB). The PreSERVE trial is a Phase 2, randomized, placebo controlled, double-blind study expected to include 160 patients at more than 40 clinical sites. The trial's product candidate, AMR-001, is designed to prevent major adverse cardiac events following acute myocardial infarction (AMI). Patient enrollment for the PreSERVE trial began in January 2012 and the Company anticipates completing enrollment in 2013 with six months initial data readout near the end of 2013.

"We are pleased that, similar to our Phase 1 trial, the first external review of our Phase 2 trial data confirms that there are no safety signals that would preclude the trial from continuing as planned," said Andrew L. Pecora, M.D. FACP CPE, Chief Medical Officer of NeoStem. "The PreSERVE AMI study to date indicates that multiple National Study sites are capable of acquiring the necessary volume of bone marrow to create the AMR-001 product five to seven days after an AMI in a safe and practical manner, and once created the product can be delivered and administered without a safety signal."

NeoStem management believes that cell therapy is a disruptive technology in the $50 billion worldwide regenerative medicine market. Many key opinion leaders in the scientific, medical and investment communities consider AMR-001 to be best in class. Peak annual worldwide sales of AMR-001 for this indication could exceed $1 billion based upon a conservative market penetration of its qualified target patient population. AMR-001 is protected by two issued and multiple pending U.S. patents with corresponding patent coverage in selected markets around the world. The Amorcyte AMR-001 product development program also extends to congestive heart failure (CHF). The Company is preparing to launch its CHF Phase 1 clinical trials in early 2013. The worldwide CHF patient population is estimated to be four times larger than that of AMI.

About NeoStem, Inc.

NeoStem, Inc. ("we," "NeoStem" or the "Company") continues to develop and build on its core capabilities in cell therapy to capitalize on the paradigm shift that we see occurring in medicine. In particular, we anticipate that cell therapy will have a large role in the fight against chronic disease and in lessening the economic burden that these diseases pose to modern society. Our January 2011 acquisition of Progenitor Cell Therapy, LLC ("PCT") provides NeoStem with a foundation in both manufacturing and regulatory affairs expertise. We believe this expertise, coupled with our existing research capabilities and collaborations, will allow us to achieve our mission of becoming a premier cell therapy company. Our PCT subsidiary's manufacturing base is one of the few current Good Manufacturing Practices ("cGMP") facilities available for contracting in the burgeoning cell therapy industry. Amorcyte, LLC ("Amorcyte"), which we acquired in October 2011, is developing a cell therapy for the treatment of cardiovascular disease. Amorcyte's lead compound, AMR-001, represents NeoStem's most clinically advanced therapeutic and Amorcyte is enrolling patients for a Phase 2 trial to investigate AMR-001's efficacy in preserving heart function after a heart attack. We also expect to begin a Phase 1 clinical trial in 2013 to investigate AMR-001's utility in arresting the progression of congestive heart failure and the associated comorbidities of that disease. Athelos Corporation ("Athelos"), which is approximately 80%-owned by our subsidiary, PCT, is engaged in collaboration with Becton-Dickinson that is exploring the earlier stage clinical development of a T-cell therapy for autoimmune conditions. In addition, our pre-clinical assets include our VSELTM Technology platform as well as our MSC (mesenchymal stem cells) product candidate for regenerative medicine.

For more information on NeoStem, please visit http://www.neostem.com.

Forward-Looking Statements for NeoStem, Inc.

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements reflect management's current expectations, as of the date of this press release, and involve certain risks and uncertainties. Forward-looking statements include statements herein with respect to the successful execution of the Company's business strategy, including with respect to the Company's or its partners' successful development of AMR-001 and other cell therapeutics, the size of the market for such products, its competitive position in such markets, the Company's ability to successfully penetrate such markets and the market for its CDMO business, and the efficacy of protection from its patent portfolio, as well as the future of the cell therapeutics industry in general, including the rate at which such industry may grow. Forward-looking statements also include statements with respect to satisfying all conditions to closing the disposition of Erye, including receipt of all necessary regulatory approvals in the PRC. The Company's actual results could differ materially from those anticipated in these forward-looking statements as a result of various factors, including but not limited to (i) the Company's ability to manage its business despite operating losses and cash outflows, (ii) its ability to obtain sufficient capital or strategic business arrangement to fund its operations, including the clinical trials for AMR-001, (iii) successful results of the Company's clinical trials of AMR-001 and other cellular therapeutic products that may be pursued, (iv) demand for and market acceptance of AMR-001 or other cell therapies if clinical trials are successful and the Company is permitted to market such products, (v) establishment of a large global market for cellular-based products, (vi) the impact of competitive products and pricing, (vii) the impact of future scientific and medical developments, (viii) the Company's ability to obtain appropriate governmental licenses and approvals and, in general, future actions of regulatory bodies, including the FDA and foreign counterparts, (ix) reimbursement and rebate policies of government agencies and private payers, (x) the Company's ability to protect its intellectual property; (xi) the company's ability to successfully divest its interest in Erye, and (xii) matters described under the "Risk Factors" in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 20, 2012 and in the Company's other periodic filings with the Securities and Exchange Commission, all of which are available on its website. The Company does not undertake to update its forward-looking statements. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

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NeoStem Reports Data Safety Monitoring Board Recommends Continuation of PreSERVE AMI Phase 2 Trial

Utilizing neuroscience, gene therapy, and optogenetics, a pair of researchers from Cornell University have created a bionic prosthetic eye that can restore almost-normal vision to animals blinded by destroyed retinas.

We have discussed bionic eyes at length, but for the most part these have been dumb prosthetics chips that wire themselves into the ganglion cells behind the retina, which are the interface between the retina and optic nerve. These chips receive optical stimuli (via a CMOS sensor, for example), which they transmit as electrical signals to the ganglion cells. These prosthetic eyes can produce a low-resolution grayscale field that the brain can then interpret which is probably better than being completely blind but they dont actually restore sight.

The Cornell prosthetic eye however, developed by Sheila Nirenberg and Chethan Pandarinath, is a much closer analog to a real eye. Its construction and implementation is rather complex, so bear with me.

First, gene therapy is used to deliver special proteins to the patients damaged retina (i.e. caused by degenerative diseases, such as macular degeneration or diabetic retinopathy). By using optogenetics, these proteins have been modified so that theyre sensitive to light theyre not quite rods and cones, but theyre along the same lines.

The next step is the clever/unique bit. For years now, Nirenberg has been working on decoding the signals sent by the retina to the brain. A year ago, she cracked this code. At the time, she had only cracked the code used by the mouse retina, but now shes cracked the monkey code too and a monkeys retina is very similar to ours.

Thats not the breakthrough here, though: Nirenberg and Pandarinath have now taken the mouse retina code and developed a working prosthetic, completely restoring a mouses vision.

The prosthetic contains a camera pointed forward, a Texas Instruments OMAP 3530 SoC (system-on-a-chip), and a tiny DLP pico projector. The SoC converts the cameras output into encoded data that the mouses brain can understand, and then the projector is used to beam that data to the optogenetic proteins that were earlier placed in the retina using gene therapy. The optogenetic proteins then transmit the encoded signal to the brain, via the ganglion cells and optic nerve. Voila: restored (grayscale) vision.

In the image above you can see just how effective Nirenberg and Pandarinaths prosthetic eye is. The top row is what a normal mouse eye would see (just before it gets eaten, seemingly), and the second row shows the images produced by the prosthetic eye. The bottom right corner shows the image your eye would see if it had only received the optogenetic gene therapy, and none of the fancy camera/neural-encoding tricks.

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Scientists reverse engineer animal brains to create bionic prosthetic eyes

Public release date: 15-Aug-2012 [ | E-mail | Share ]

Contact: Proffesor Dr. Gunther Meinlschmidt gunther.meinlschmidt@rub.de 49-234-507-73173 Ruhr-University Bochum

Acute stress alters the methylation of the DNA and thus the activity of certain genes. This is reported by researchers at the Ruhr-Universitt Bochum together with colleagues from Basel, Trier and London for the first time in the journal Translational Psychiatry. "The results provide evidence how stress could be related to a higher risk of mental or physical illness", says Prof. Dr. Gunther Meinlschmidt from the Clinic of Psychosomatic Medicine and Psychotherapy at the LWL University Hospital of the RUB. The team looked at gene segments which are relevant to biological stress regulation.

Epigenetics - the "second code" - regulates gene activity

Our genetic material, the DNA, provides the construction manual for the proteins that our bodies need. Which proteins a cell produces depends on the cell type and the environment. So-termed epigenetic information determines which genes are read, acting quasi as a biological switch. An example of such a switch is provided by methyl (CH3) groups that attach to specific sections of the DNA and can remain there for a long time - even when the cell divides. Previous studies have shown that stressful experiences and psychological trauma in early life are associated with long-term altered DNA methylation. Whether the DNA methylation also changes after acute psychosocial stress, was, however, previously unknown.

Two genes tested

To clarify this issue, the research group examined two genes in particular: the gene for the oxytocin receptor, i.e. the docking site for the neurotransmitter oxytocin, which has become known as the "trust hormone" or "anti-stress hormone"; and the gene for the nerve growth factor Brain-Derived Neurotrophic Factor (BDNF), which is mainly responsible for the development and cross-linking of brain cells. The researchers tested 76 people who had to participate in a fictitious job interview and solve arithmetic problems under observation - a proven means for inducing acute stress in an experiment. For the analysis of the DNA methylation, they took blood samples from the subjects before the test as well as ten and ninety minutes afterwards.

DNA methylation changes under acute psychosocial stress

Stress had no effect on the methylation of the BDNF gene. In a section of the oxytocin receptor gene, however, methylation already increased within the first ten minutes of the stressful situation. This suggests that the cells formed less oxytocin receptors. Ninety minutes after the stress test, the methylation dropped below the original level before the test. This suggests that the receptor production was excessively stimulated.

Possible link between stress and disease

Originally posted here:
Acute stress alters control of gene activity

ScienceDaily (Aug. 15, 2012) Acute stress alters the methylation of the DNA and thus the activity of certain genes. This is reported by researchers at the Ruhr-Universitt Bochum together with colleagues from Basel, Trier and London for the first time in the journal Translational Psychiatry. "The results provide evidence how stress could be related to a higher risk of mental or physical illness," says Prof. Dr. Gunther Meinlschmidt from the Clinic of Psychosomatic Medicine and Psychotherapy at the LWL University Hospital of the RUB. The team looked at gene segments which are relevant to biological stress regulation.

Epigenetics -- the "second code" -- regulates gene activity

Our genetic material, the DNA, provides the construction manual for the proteins that our bodies need. Which proteins a cell produces depends on the cell type and the environment. So-termed epigenetic information determines which genes are read, acting quasi as a biological switch. An example of such a switch is provided by methyl (CH3) groups that attach to specific sections of the DNA and can remain there for a long time -- even when the cell divides. Previous studies have shown that stressful experiences and psychological trauma in early life are associated with long-term altered DNA methylation. Whether the DNA methylation also changes after acute psychosocial stress, was, however, previously unknown.

Two genes tested

To clarify this issue, the research group examined two genes in particular: the gene for the oxytocin receptor, i.e. the docking site for the neurotransmitter oxytocin, which has become known as the "trust hormone" or "anti-stress hormone"; and the gene for the nerve growth factor Brain-Derived Neurotrophic Factor (BDNF), which is mainly responsible for the development and cross-linking of brain cells. The researchers tested 76 people who had to participate in a fictitious job interview and solve arithmetic problems under observation -- a proven means for inducing acute stress in an experiment. For the analysis of the DNA methylation, they took blood samples from the subjects before the test as well as ten and ninety minutes afterwards.

DNA methylation changes under acute psychosocial stress

Stress had no effect on the methylation of the BDNF gene. In a section of the oxytocin receptor gene, however, methylation already increased within the first ten minutes of the stressful situation. This suggests that the cells formed less oxytocin receptors. Ninety minutes after the stress test, the methylation dropped below the original level before the test. This suggests that the receptor production was excessively stimulated.

Possible link between stress and disease

Stress increases the risk of physical or mental illness. The stress-related costs in Germany alone amount to many billions of Euros every year. In recent years, there have been indications that epigenetic processes are involved in the development of various chronic diseases such as cancer or depression. "Epigenetic changes may well be an important link between stress and chronic diseases" says Prof. Meinlschmidt, Head of the Research Department of Psychobiology, Psychosomatics and Psychotherapy at the LWL University Hospital. "We hope to identify more complex epigenetic stress patterns in future and thus to be able to determine the associated risk of disease. This could provide information on new approaches to treatment and prevention." The work originated within the framework of an interdisciplinary research consortium with the University of Trier, the University of Basel and King's College London. The German Research Foundation and the Swiss National Science Foundation supported the study.

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Acute stress alters control of gene activity: Researchers examine DNA methylation

By Rick Nauert PhD Senior News Editor Reviewed by John M. Grohol, Psy.D. on August 13, 2012

In a new mouse study, University of California, Davis, researchers have found that a defective gene is responsible for brain changes that lead to the disrupted social behavior that accompanies autism.

Investigators believe the discovery could lead to the development of medications to treat the condition.

Prior research had determined that the gene is defective in children with autism, but its effect on neurons in the brain was not known.

The new studies in mice show that abnormal action of just this one gene disrupted energy use in neurons. The harmful changes were coupled with antisocial and prolonged repetitive behavior traits found in autism.

The research is published in the scientific journal PLoS ONE.

A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism how one gene defect may trigger this type of neurological behavior, said study senior author Cecilia Giulivi, Ph.D.

Once you understand the mechanism, that opens the way for developing drugs to treat the condition, she said.

The defective gene appears to disrupt neurons use of energy, Giulivi said, the critical process that relies on the cells molecular energy factories called mitochondria.

In the research, a gene called pten was modififed in the mice so that neurons lacked the normal amount of ptens protein. The scientists detected malfunctioning mitochondria in the mice as early as 4 to 6 weeks after birth.

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Gene Related to Autism Behavior ID’d in Mice Study

STURGEON BAY, Wis. - Stored inside a nondescript building and greenhouse in Door County is the equivalent of much of the world's potato blueprints.

Wisconsin is home to many things, but it's safe to say that few people know the globe's largest collection of wild and cultivated potato species are here.

Most folks traveling past the Peninsular Agriculture Research Station just outside Sturgeon Bay have no idea the potato chips or French fries they gobbled at lunch were most likely developed through the efforts of the U.S. Potato Genebank. Potato germ plasm is sent from Sturgeon Bay to researchers throughout the world who are trying to figure out how to make potatoes more frost- and pest-resistant, easier to digest and even various colors.

"Part of our business is to find things, characterize them as unusual, determine if there's interest, publish and see if anyone wants to run with it," said John Bamberg, director of the gene bank.

The gene bank is a repository of thousands of seeds and cultivars collected throughout the U.S. and world over more than six decades. The oldest potato seeds at the facility, which was established by Wisconsin potato farmers in 1948, date to the early 1950s.

The Sturgeon Bay site, part of the National Plant Germplasm System preserving the genetic diversity of plants, is the only gene bank based in Wisconsin. Gene banks are scattered across the country, including facilities for rice in Arkansas, soybeans and maize in Illinois, wheat in Idaho and tomatoes in California.

The gene banks are used to acquire, preserve and evaluate plant varieties and then distribute them free to researchers. The potato facility houses about 5,000 seed populations and 1,000 clonal varieties. U.S. scientists and breeders outnumber international researchers seeking germ plasm 3 to 2. Plus horticulturists from companies such as Frito-Lay work with potato germ plasm from the gene bank.

Scientists like Shelley Jansky need access to genetic diversity to develop varieties that are resistant to pests and extreme weather. She's working on solving the problem of verticillium wilt, a common fungus in the soil. To solve the problem, potato farmers must inject chemicals in their fields before planting.

Through the potato gene bank, Jansky has found a wild species of potato from South America that's mostly immune to verticillium wilt.

"It's a tremendous resource that's right at my fingertips. I call them and say, 'Can you send me this, this and this?' and they send me seeds in the mail," said Jansky, a U.S. Department of Agriculture research scientist and associate professor of horticulture at the University of Wisconsin, Madison.

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Potato gene bank stores world's varieties