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Leading stem cell scientists to focus on diabetes, eye diseases at Cedars-Sinai symposium

Public release date: 17-Sep-2012 [ | E-mail | Share ]

Contact: Nicole White nicole.white@cshs.org 310-423-5215 Cedars-Sinai Medical Center

LOS ANGELES Sept. 17, 2012 Leading scientists and clinicians from across the nation will discuss the latest findings on potential stem cell treatments for diabetes and eye diseases at the second Cedars-Sinai Regenerative Medicine Scientific Symposium.

WHO: Stem cell scientists, clinicians and industry leaders.

The symposium is being hosted by the Cedars-Sinai Regenerative Medicine Institute, led by Clive Svendsen, PhD. The institute brings together basic scientists with specialist clinicians, physician scientists and translational scientists across multiple medical specialties to convert fundamental stem cell studies to therapeutic regenerative medicine.

FEATURED RESEARCH: The symposium's morning session will feature an overview of the current state of stem cells and diabetes, including efforts to start the first clinical trials with stem cells for the treatment of diabetes. Other research to be presented includes an update on regenerative medicine approaches to treating macular degeneration, a progressive deterioration of the eye that causes gradual loss of vision. This will include an update from Gad Heilweil , MD, on a key, stem-cell clinical trial on macular degeneration at the University of California Los Angeles.

WHEN: Sept. 21, 2012 8:30 a.m. to 6 p.m. Thomson's lecture begins at 8:40 a.m.

WHERE: Harvey Morse Auditorium Cedars-Sinai Medical Center 8700 Beverly Boulevard Los Angeles, CA 90048

How to register: http://www.cedars-sinai.edu/RMI

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Mechanism that leads to diabetes, blindness, identified

ScienceDaily (Sep. 16, 2012) The rare disorder Wolfram syndrome is caused by mutations in a single gene, but its effects on the body are far reaching. The disease leads to diabetes, hearing and vision loss, nerve cell damage that causes motor difficulties, and early death.

Now, researchers at Washington University School of Medicine in St. Louis, the Joslin Diabetes Center in Boston and the Novartis Institutes for BioMedical Research report that they have identified a mechanism related to mutations in the WFS1 gene that affects insulin-secreting beta cells. The finding will aid in the understanding of Wolfram syndrome and also may be important in the treatment of milder forms of diabetes and other disorders.

The study is published online in the journal Nature Cell Biology.

Insulin-secreting beta cells in the pancreas (above) cannot make enough cyclic AMP in patients with Wolfram syndrome. As a result, the pancreas produces and secretes less insulin, and the cells eventually die.

"We found something we didn't expect," says researcher Fumihiko Urano, MD, PhD, associate professor of medicine in Washington University's Division of Endocrinology, Metabolism and Lipid Research. "The study showed that the WFS1 gene is crucial to producing a key molecule involved in controlling the metabolic activities of individual cells." That molecule is called cyclic AMP (cyclic adenosine monophosphate).

In insulin-secreting beta cells in the pancreas, for example, cyclic AMP rises in response to high blood sugar, causing those cells to produce and secrete insulin.

"I would compare cyclic AMP to money," Urano says. "You can't just take something you make to the store and use it to buy food. First, you have to convert it into money. Then, you use the money to buy food. In the body, external signals stimulate a cell to make cyclic AMP, and then the cyclic AMP, like money, can 'buy' insulin or whatever else may be needed."

The reason patients with Wolfram syndrome experience so many problems, he says, is because mutations in the WFS1 gene interfere with cyclic AMP production in beta cells in the pancreas.

"In patients with Wolfram syndrome, there is no available WFS1 protein, and that protein is key in cyclic AMP production," he explains. "Then, because levels of cyclic AMP are low in insulin-secreting beta cells, those cells produce and secrete less insulin. And in nerve cells, less cyclic AMP can lead to nerve cell dysfunction and death."

By finding that cyclic AMP production is affected by mutations in the WFS1 gene, researchers now have a potential target for understanding and treating Wolfram syndrome.

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Mechanism that leads to diabetes, blindness, identified

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'Maternal gene' identified in mice

The findings, published in the Proceedings of the National Academy of Sciences, suggest the single gene could be responsible for motivating mothers to protect, feed and raise their young, the scientists said.

Earlier research has established that nerve cells react to oestrogen, the female sex hormone, and contain high levels of oestrogen receptor alpha, a chemical linked to maternal care and sexual behaviour.

In the new study, scientists artificially lowered the levels of the chemical in the medial preoptic area of female mice, to examine how they functioned without it.

They found that the mice spent less time caring for their pups but that their levels of aggression remained unchanged.

Dr Ana Ribiero, who led the study, said: "The main finding of this paper is manipulation of a specific gene in a specific group of neurons (nerve cells) can drastically alter the expression of a complete, biologically crucial behaviour."

The effects were "remarkably specific" to maternal care because even related behaviours, such as aggression, remained unchanged, she added.

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'Maternal gene' identified in mice

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Dawn of the GM baby: Technique that gives children three parents may only be a year away

Germline therapy - the alteration of genes in eggs or sperm - could be made legal by Parliament next year Critics say it's wrong to tamper with the sanctity of life and consequences for future generations are uncertain

By Fiona Macrae

PUBLISHED: 18:17 EST, 16 September 2012 | UPDATED: 01:46 EST, 17 September 2012

The creation of genetically-modified babies could win Parliaments backing next year.

A law change would allow for children to be designed to be free of horrific diseases that can kill within hours of birth.

The children would effectively have two mothers and one father.

Green light ahead: A change in the law could soon permit the creation of genetically modified babies free from congenital diseases. (File picture)

Supporters say the genetic engineering of eggs and embryos will help couples who have suffered the trauma of multiple miscarriages and the deaths of their newborns because of genetic diseases.

But critics say it is wrong to tamper with the sanctity of life, especially when the consequences for future generations are uncertain.

Germline therapy, or the alteration of genes in eggs or sperm, is banned in most countries.

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Dawn of the GM baby: Technique that gives children three parents may only be a year away

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Drug combination against NRAS-mutant melanoma discovered

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

Contact: Hilary Graham hngraham@mdanderson.org 713-794-4383 University of Texas M. D. Anderson Cancer Center

HOUSTON A new study published online in Nature Medicine, led by scientists at The University of Texas MD Anderson Cancer Center, describes the discovery of a novel drug combination aimed at a subset of melanoma patients who currently have no effective therapeutic options.

Melanoma patients have different responses to therapy, depending on what genes are mutated in their tumors. About half of melanomas have a mutation in the BRAF gene; while a quarter have a mutation in the NRAS gene.

New BRAF inhibitor drugs are effective against BRAF-mutant melanoma, but no comparable therapies are currently available against NRAS-mutant melanoma. For the first time, this study provides new hope for patients with NRAS-mutant melanoma that an effective targeted treatment might be developed in the coming years.

By analyzing a sophisticated, genetically engineered mouse model of NRAS-mutant melanoma with a novel systems biology approach, scientists discovered that combining two different classes of drugs shrinks these tumors.

The researchers, led by Lynda Chin, M.D., chair of the Department of Genomic Medicine and scientific director of the Institute for Applied Cancer Science, at MD Anderson together with colleagues from the Dana-Farber Cancer Institute at Harvard Medical School and from Boston University discovered that the two drugs, which inhibit proteins Mek and Cdk4, complement one another by targeting unique cancer features.

"The lack of a drug like the BRAF inhibitor that works against NRAS means that there is still no effective treatment option for NRAS-mutant patients to fall back on," said Chin. "Developing an effective combination using existing drugs or drugs already in clinical development is a path to address this unmet need for this population of melanoma patients."

A roadmap for effective drug combinations

Researchers must first know what an effective treatment actually looks like before they can identify and develop effective drug combinations. To accomplish this, Chin and her colleagues generated an inducible NRAS (iNRAS) mouse model. In the model, activating mutant NRAS caused melanomas to form, while turning it off caused the melanomas to shrink exactly what an effective drug therapy should do.

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Drug combination against NRAS-mutant melanoma discovered

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Cleveland Clinic study shows vitamin E may decrease cancer risk in Cowden syndrome patients

Public release date: 17-Sep-2012 [ | E-mail | Share ]

Contact: Stephanie Jansky janskys@ccf.org 216-636-5869 Cleveland Clinic

Saturday, September 15, 2012, Cleveland: Cleveland Clinic researchers have discovered that vitamin E may prevent cancer in patients with an under-recognized genetic disorder.

Several genetic mutations are known to be present in Cowden Syndrome (CS) a disease that predisposes individuals to several types of cancers, including breast and thyroid cancers. One type of mutation in the succinate dehydrogenase (SDH) genes may be responsible for cancer development, according to research by Charis Eng, M.D., Ph.D., Hardis Chair and Director of the Genomic Medicine Institute and Director of its Center for Personalized Genetic Healthcare at Lerner Research Institute, published today in Clinical Cancer Research.

Dr. Eng discovered that mutations in SDH genes, responsible for energy production, result in an accumulation of reactive oxygen species (ROS). These changes damage the cells and make them resistant to apoptosis our bodies' natural method of weeding out cancerous cells.

However, when vitamin E was applied to the mutant cells, ROS accumulation decreased, as well as the accompanying cellular damage.

"These findings support the notion that vitamin E may be useful as an anti-cancer therapeutic adjunct or preventive agent, especially for CS patients harboring SDH mutations, and its protective properties should be further explored," said Dr. Eng.

CS predisposes individuals to several types of cancers an 85 percent lifetime risk of breast cancer, a 35 percent risk for epithelial thyroid cancer, and increased risk of other cancers as well. Approximately one in 200,000 people are affected by CS.

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Dr. Eng's research was supported by the Breast Cancer Research Foundation and National Institutes of Health National Cancer Institute (NIH/NCI) grant P01CA124570-04S1.

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Cleveland Clinic study shows vitamin E may decrease cancer risk in Cowden syndrome patients

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How genetic testing is swelling the ranks of the 'worried well'

By Jacqueline Savard. First published in The Conversation.

17 September 2012

Jacqueline Savard explores the growing prevalence of genetic testing and what impact they have on over-diagnosis.

Genetic testing and screening is increasingly becoming a presence in our lives. Daily news reports discuss new associations between genes and common conditions. And these associations are used to calculate risks for individuals who have the genes for the conditions, but don't display any symptoms.

In essence, these people become the "worried well", a group of people not yet ill, but at risk of developing diseases.

Genetic tests and over-diagnosis

Once restricted to the domain of the clinic, genetic testing is now available to most people, either through their doctor or via the internet. There are a variety of tests in the market, some of which can provide risk estimates associated with complex common diseases such as diabetes, obesity, Alzheimer's disease and cancer.

A major concern with such tests is that they're the beginning of a path toward over-diagnosis, where the potential to develop a disease or being at risk for the disease is strong enough to constitute a label of sickness.

Over-diagnosing includes, but is not limited to, widening disease definitions, early detections of abnormalities that may or may not cause symptoms or death and the use of increasingly sensitive technologies that detect "abnormalities," the causes and consequences of which are unknown at this time.

Genetic testing and screening could be seen as the ultimate test (the most fundamental part of one's body and life is used to classify a person as ill or potentially ill), so what are the implications of using this technology to assist in diagnosing and classifying people?

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How genetic testing is swelling the ranks of the 'worried well'

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Genetic Testing and Mobile Health Technology Combine to Provide Significant Improvements in Patient Results

SAN DIEGO--(BUSINESS WIRE)--

Pathway Genomics Corporation, a San Diego-based clinical laboratory that offers its genetic tests internationally, has partnered with innovative La Jolla-based medical practiceMD Revolution. Founded byDr. Samir DamaniandDr. Sunil Bhoyrul, MD Revolution is the first clinical practice to systematically incorporate genomic and mobile health technologies into chronic disease management and prevention. Dr. Damani,a board-certified cardiologistwho currently serves as the practices primary physician, has fully integrated Pathway Genomics premier nutrigenetic test,Pathway Fit, into his practice, and has experienced exceptionally positive results in patient outcomes.

We have enrolled over 50 patients into one of our programs. Among patients that have completed the program, we found dramatic clinical and statistically significant improvements in at least one of four key health parameters including weight loss, visceral fat reduction, increases in metabolism and allowable daily caloric intake, said Dr. Damani. Other parameters have included improved blood pressure control and marked improvements in cardiorespiratory fitness as measured by sub-maximal VO2 (oxygen consumption) testing.

Through its patent pending processes, MD Revolution is defining how genomic and mobile health technologies can be leveraged for superior clinical outcomes for adults of any age who have a range of health goals, from simply optimizing their health to treating chronic conditions such as diabetes.

One of Dr. Damanis patients, Mitch Thrower, can attest to the benefits of Pathway Fit and the positive impact that MD Revolutions program had on his life. As a seasoned triathlete and former owner and chairman ofTriathletemagazine, Thrower realizes the importance of understanding how ones body responds to food and exercise.

Going through the MD Revolution process, we tested for basic metabolic rate and we tracked my diet everything I ate for a couple of weeks. I was going to bed at least 1,500 calories deficient every night and was eating the wrong foods, said Thrower. Thats where Pathway Fit was helpful, in terms of determining what kinds of foods are best over what timeframe. After he started MD Revolutions program, Thrower was able to successfullymanage his weight, and he improved his overall health and wellness. Ive never felt healthier, he explained.

While Throwers background is somewhat unique, the successful outcome he experienced is one that is very familiar to Dr. Damani. Nutrigenomics provides valuable insight into how we process nutrients, respond to exercise, maladaptive eating behaviors, and our propensity for vitamin deficiencies. It enables a more tailored approach to diet and exercise, said Dr. Damani. Patients no longer have to be pushed from one fad diet to another. While the field of genomics and its implications on disease and health is evolving, we cannot ignore the tools available today that enable better prevention and treatment of chronic disease.

About Pathway Genomics

Pathway Genomics owns and operates an on-sitegenetic testinglaboratory that is accredited by the College of American Pathologists (CAP), accredited in accordance with the U.S. Health and Human Services Clinical Laboratory Improvement Amendments (CLIA) of 1988, and licensed by the state of California. Using only a saliva sample, the company incorporates customized and scientifically validated technologies to generate personalized reports, which address a variety of medical issues, including an individuals carrier status for recessive genetic conditions, food metabolism and exercise response, prescription drug response, and propensity to develop certain diseases such as heart disease, type 2 diabetes and cancer. For more information about Pathway Genomics, visitwww.pathway.com.

About MD Revolution

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Genetic Testing and Mobile Health Technology Combine to Provide Significant Improvements in Patient Results

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Recombinant Executive Jason Oliveira to Present CHIME College Live Session on Healthcare Performance Management

NEWTON, MA--(Marketwire - Sep 17, 2012) - Jason Oliveira, Managing Director, Health Systems Consulting with Recombinant, a provider of data warehousing and clinical intelligence solutions for healthcare performance management, personalized medicine and translational research, will deliver an online lecture on healthcare performance metrics as part of The College of Healthcare Information Management Executives (CHIME) College LIVE executive education program. The session begins at 12 noon ET on Wednesday, September 19. Registration is limited to CHIME members, but Recombinant has made the content available for download at http://www.recomdata.com/resources_library_presentations.html?=CHIME_PerfMgmt.pdf.

Oliveira has been a strategic advisor to healthcare organizations pursuing their business intelligence planning, technology evaluation, architecture design, and implementation program management efforts for more than 25 years. "Independent of the perceived value of these performance measurement systems as drivers of desirable change, the reality is that they are here; they affect the bottom line; and they are now an operational reality, and burden, to provider organizations," said Oliveira. "My lecture will examine the drivers, requirements, operational impact, and next-generation IT architecture responses for more efficient healthcare performance measurement."

College LIVE is a compelling alternative to traditional, classroom-style education and provides a unique forum for CHIME members to collaborate, interact, and learn. College LIVE presentations focus on healthcare, IT, and executive issues of particular interest to healthcare CIOs.

Performance Measurement Remains a Vexing Problem The convergence of healthcare information technology (HIT), electronic medical records/electronic health records (EMR/EHR), informatics, and data warehousing is helping to surmount the significant data barriers in achieving insight into health system processes, but HIT is not yet making performance measurement easier.Virtually all health care organizations, including providers, payers, pharmaceutical companies, and research organizations suffer from a glut of unstructured and unformatted content, including dictated and transcribed physician notes and scanned documents. Health information is dispersed among multiple operational information systems. Many provider organizations still rely on paper-based legal medical records.

HIT solutions such as physician order entry, clinical documentation, and e-prescribing have improved health care operations and quality, but still require time-consuming performance data capture, measurement, and reporting.Often performance measurement data collection occurs as an additional task for doctors and nurses to conduct, rather than being a by-product of patient care delivery.

While there is promise for facilitating traditional measure sets, as well as new possibilities afforded by HIT, health care organizations are currently still struggling to capture, organize, and utilize performance data.

Solution Pathway The road to pragmatic healthcare performance management begins by determining short- and long-term requirements and identifying gaps with an organization's current methods.The roadmap for optimal movement from the current to the future state will likely include such initiatives as:

In addition, support must be established to empower the accomplishment of these initiatives, primarily through:

These interventions collectively will enable effective performance measurement and ease the burden, cost, and inefficiencies for participating organizations.

About CHIME The College of Healthcare Information Management Executives (CHIME) is an executive organization dedicated to serving chief information officers and other senior healthcare IT leaders. With more than 1,400 CIO members and over 87 healthcare IT vendors and professional services firms, CHIME provides a highly interactive, trusted environment enabling senior professional and industry leaders to collaborate; exchange best practices; address professional development needs; and advocate the effective use of information management to improve the health and healthcare in the communities they serve. For more information, please visit http://www.cio-chime.org.

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Recombinant Executive Jason Oliveira to Present CHIME College Live Session on Healthcare Performance Management

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Cytomedix Shares Now Trading on OTCQX

GAITHERSBURG, Md., Sept. 17, 2012 /PRNewswire/ -- Cytomedix, Inc. (CMXI), a fully integrated regenerative medicine company commercializing and developing innovative platelet and adult stem cell technologies, today announced that its common shares are now trading on the highest OTC marketplace, OTCQX, under the ticker symbol "CMXI."

Cytomedix upgraded from OTCQB today to trade on the OTC market's prestigious marketplace, OTCQX. Investors can find current financial disclosure and real-time Level 2 quotes for the Company's common shares at http://www.otcmarkets.com.

"We believe investors will appreciate the quality-controlled admission process, the transparent trading and easy access to company information that are hallmarks of the OTCQX," said Martin P. Rosendale, Chief Executive Officer of Cytomedix.

C. K. Cooper & Company will serve as Cytomedix's Designated Advisor for Disclosure ("DAD") on OTCQX, and will be responsible for providing guidance on OTCQX requirements.

About Cytomedix, Inc. Cytomedix, Inc. is a fully integrated regenerative medicine company commercializing and developing innovative platelet and adult stem cell separation products that enhance the body's natural healing processes. The Company's advanced autologous technologies offer clinicians a new treatment paradigm for wound and tissue repair. The Company's patient-derived PRP systems are marketed by Cytomedix in the U.S. and distributed internationally. The Company's commercial products include the AutoloGel System, cleared by the FDA for wound care and the Angel Whole Blood Separation System. The Company is developing novel regenerative therapies using the proprietary ALDH Bright Cell ("ALDHbr") technology to isolate a unique, biologically active population of a patient's own stem cells. A Phase 2 trial evaluating the use of ALDHbr for the treatment of ischemic stroke is underway. For additional information please visit http://www.cytomedix.com.

About OTC Markets Group Inc. OTC Markets Group Inc. (OTCM) operates Open, Transparent and Connected financial marketplaces for investors to easily trade almost 10,000 equity and debt securities through the broker of their choice. Our OTC Link ATS directly links a diverse network of broker-dealers that provide liquidity and execution services for a wide spectrum of securities. We organize these securities into tiered marketplaces to inform investors of opportunities and risks including OTCQX - The Intelligent Marketplace for the Best OTC Companies; OTCQB - The Venture Marketplace; and OTC Pink - The Open Marketplace. Our data-driven platform enables efficient trading through any broker at the best possible price and empowers a broad range of companies to improve the quality and availability of information for their investors. To learn more about how we create smarter financial marketplaces, visit http://www.otcmarkets.com.

OTC Link ATS is operated by OTC Link LLC, member FINRA/SIPC and SEC registered ATS.

About Cytomedix, Inc.Cytomedix, Inc. is a fully integrated regenerative medicine company commercializing and developing innovative platelet and adult stem cell separation products that enhance the body's natural healing processes. The Company's advanced autologous technologies offer clinicians a new treatment paradigm for wound and tissue repair. The Company's patient-derived PRP systems are marketed by Cytomedix in the U.S. and distributed internationally. Our commercial products include the AutoloGel System, cleared by the FDA for wound care and the Angel Whole Blood Separation System. The Company is developing novel regenerative therapies using our proprietary ALDH Bright Cell ("ALDHbr") technology to isolate a unique, biologically active population of a patient's own stem cells. A Phase 2 trial evaluating the use of ALDHbr for the treatment of ischemic stroke is underway. For additional information please visit http://www.cytomedix.com.

Safe Harbor Statement Statements contained in this press release not relating to historical facts are forward-looking statements that are intended to fall within the safe harbor rule for such statements under the Private Securities Litigation Reform Act of 1995. The information contained in the forward-looking statements is inherently uncertain, and Cytomedix' actual results may differ materially due to a number of factors, many of which are beyond Cytomedix' ability to predict or control, including among many others, risks and uncertainties related to the Company's reimbursement related efforts, the Company's ability to capitalize on the benefits of the above-referenced CMS determination, the Company's ability to successfully and favorably conclude the negotiations and related discussions with the above-referenced global pharmaceutical company, the Company's ability to successfully integrate the Aldagen acquisition, to successfully manage contemplated clinical trials, to manage and address the capital needs, human resource, management, compliance and other challenges of a larger, more complex and integrated business enterprise, viability and effectiveness of the Company's sales approach and overall marketing strategies, commercial success or acceptance by the medical community, competitive responses, the Company's ability to raise additional capital and to continue as a going concern, and Cytomedix's ability to execute on its strategy to market the AutoloGel System as contemplated. To the extent that any statements made here are not historical, these statements are essentially forward-looking. The Company uses words and phrases such as "believes", "forecasted," "projects," "is expected," "remain confident," "will" and/or similar expressions to identify forward-looking statements in this press release. Undue reliance should not be placed on forward-looking information. These forward-looking statements are subject to known and unknown risks and uncertainties that could cause actual events to differ from the forward-looking statements. More information about some of these risks and uncertainties may be found in the reports filed with the Securities and Exchange Commission by Cytomedix, Inc. Cytomedix operates in a highly competitive and rapidly changing business and regulatory environment, thus new or unforeseen risks may arise. Accordingly, investors should not place any reliance on forward-looking statements as a prediction of actual results. Except as is expressly required by the federal securities laws, Cytomedix undertakes no obligation to update or revise any forward-looking statements, whether as a result of new information, changed circumstances or future events or for any other reason. Additional risks that could affect our future operating results are more fully described in our U.S. Securities and Exchange Commission filings, including our Annual Report on Form 10-K for the year ended December 31, 2011 and other subsequent filings. These filings are available at http://www.sec.gov.

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Regenerative Medicine Gets A Boost With Quick Printing Of 3D Microstructures

September 16, 2012

Image Caption: NanoEngineering Professor Shaochen Chen has demonstrated the capability of printing three-dimensional blood vessels in mere seconds out of soft, biocompatible hydrogels. Being able to print blood vessels is essential to achieving the promise of regenerative medicine because it is how the body distributes oxygen and nutrients. Image Credit: Biomedical Nanotechnology Laboratory, Chen Research Group, UC San Diego Jacobs School of Engineering.

April Flowers for redOrbit.com Your Universe Online

Nanoengineers at the University of California, San Diego have created a new technology that has far-reaching implications for regenerative medicine. The results of the project have been reported in Advanced Materials.

The team has been able to fabricate, in seconds, microscale three-dimensional (3D) structures out of soft biocompatible hydrogels. This could lead to better systems for growing and studying cells, including stem cells, in the laboratory. In the long-term, the goal is to be able to print biological tissues for regenerative medicine. For example, repairing the damage caused by a heart attack by replacing it with tissue from a printer.

Professor Shaochen Chen developed this new biofabrication technology, called dynamic optical projection stereolithography (DOPsL). Current fabrication techniques, such as photolithography and micro-contact printing, are limited to generating simple geometries or 2D patterns. Stereolithography is best known for its ability to print large objects such as tools and car parts.

The difference between earlier stereolithography and DOPsL, Chen says, is in the micro- and nanoscale resolution required to print tissues that mimic natures fine-grained details, including blood vessels, which are essential for distributing nutrients and oxygen throughout the body. Without the ability to print vasculature, an engineered liver or kidney, for example, is useless in regenerative medicine. With DOPsL, Chens team was able to achieve more complex geometries common in nature such as flowers, spirals and hemispheres. Other current 3D fabrication techniques, such as two-photon photopolymerization, can take hours to fabricate a 3D part.

The system uses a computer projection system and precisely controlled micromirrors to shine light on a selected area of a solution containing photo-sensitive biopolymers and cells. This begins the solidification process, which forms one layer of solid structure at a time, but in a continuous fashion. The Obama administration in March launched a $1 billion investment in advanced manufacturing technologies, including creating the National Additive Manufacturing Innovation Institute with $30 million in federal funding to focus on 3D printing. The term additive manufacturing refers to the way 3D structures are built layering very thin materials.

The development of this new technology is part of a grant that Chen received from the National Institutes of Health (NIH). Chens research group focuses on fabrication of nanostructured biomaterials and nanophotonics for biomedical engineering.

Source: April Flowers for redOrbit.com - Your Universe Online

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Gene breakthrough could boost rice yields

Published on 24 August 2012 Hits: 682 Written by AFP

PARIS: Scientists on Wednesday said that they had developed a strain of rice that grows well in soils lacking the nutrient phosphorus, a feat that could boost crop yields for some farmers by as much as a fifth.

The announcement ends a quest to pinpoint a mystery gene that helps the roots of baby rice plants tease phosphorus from the soil, enabling them to notch up strong, early growth.

The gene has now been transferred to modern varieties of rice using classic methods of cross-breeding, not genetic engineering, said Sigrid Heuer at the International Rice Research Institute (IRRI) in Los Baos town, Laguna province.

Next week, national rice breeders from Bangladesh, India, and Thailand will be briefed on the exciting find, which should benefit small farmers most of all, Heuer said in a phone interview from Manila.

I would expect to see [an improvement in yield of about] 20 percent, but it depends so much on the type of the soil and how severe the stress is, Heuer said.

But realistically, we are talking conservatively of an average of 10 to 20 percent, and locally a little more if the [phosphorus] stress is severe, she added.

The breakthrough seeks to address one of the biggest problems facing rice growers from the southeastern United States to South America, Southeast Asia and China.

Many soil types bond tightly to phosphorus, surrendering only a tiny amount of the precious mineral to plant roots.

To get around this, farmers look to phosphorus fertilizers, which are spread on the field.

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Gene breakthrough could boost rice yields

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Prop. 37: Another example of the perils of the initiative process

Love it or hate it, the one thing you can say for sure about California's ballot initiative process is that it's the absolute worst way to craft policy dealing with complex scientific issues.

That doesn't stop advocates on one side or another from constantly trying, with the result that the public's understanding of the underlying facts plummets faster than you can say, well, "Proposition 37."

Proposition 37 is on November's ballot. The measure would require some, but not all, food sold in California and produced via genetic engineering to be labeled as such. (There are exemptions for milk, restaurant food and other products.)

Genetic engineering, or genetic modification, which involves manipulating DNA or transferring it from one species to another, is increasingly common in agriculture and food processing, and wouldn't be banned or even regulated by the measure. Genetic engineering has pluses and minuses. It can increase crop yields and pest resistance. But it can also affect the environment in negative ways pollen or seeds from genetically engineered crops can be spread by wind, birds or insects to territory where they're unwanted, for example.

Once you've said that, you've said pretty much everything that's known to be relevant to Proposition 37. The rest is baloney, of the non-genetically engineered variety.

So what does this mean for you? It means that between now and election day your airwaves are likely to be filled with steaming piles of fatuous nonsense about genetically engineered foods (which will be depicted as horrifically perilous or absolutely safe), about trial lawyers, about struggling mom-and-pop grocery stores, about the evils of multinational agribusinesses and federal regulators. You'll be presented with learned scientific and economic studies on both sides, and they'll almost certainly be misleading, incomplete or irrelevant, though they'll sound pretty danged convincing.

This will all come to you courtesy of war chests that are already in the neighborhood of $30 million, total.

Great initiative system we have here in the Golden State. As a procedure for producing rational law, it could only be designed by a mad scientist working with rogue DNA.

Let's start with the Yes on 37 campaign. It describes its bottom line as your right to know what's in your food; so what's wrong with mandating explicit labeling? That's fair as far as it goes, but it doesn't go very far. The danger in enacting rules like this is that while they sound perfectly reasonable, they distract from the need for thoughtful and effective regulation and for action at the Legislature, not the ballot box.

"All consumers should have a right to know how their food is produced," observes Gregory Jaffe, head of the biotechnology project at the Center for Science in the Public Interest, which is no crony of the food industry. "But that includes not merely genetic engineering, but irradiated foods and those produced from cloning."

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Prop. 37: Another example of the perils of the initiative process

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An "Obesity Gene" May Decrease Diabetes Risk

A mutated gene that increases the chances of obesity could also lower the risk of diabetes, despite the proven link between the two conditions, a study has shown.

Researchers at the Oxford BioBank in the UK measured insulin resistance, which is associated with obesity. They found that the subjects who had a mutation in the phosphate and tensin homologue (PTEN) gene had a low level of insulin resistance but were more likely to be obese.

A high level of insulin resistance is associated with pre-diabetes, which almost inevitably leads to diabetes.

The link between diabetes and obesity has long been accepted, and this is the first study to show that there isnt a connection in all cases. In an article accompanying the studys publication in the New England Journal of Medicine, Ulf Smith, MD, of the University of Gothenburg in Sweden, said the research had both expected and unexpected results.

The findings may have implications for treatment of type 2 diabetes, since physicians may be unaware that trying to reduce the action of the PTEN gene could make the illness worse.

Free Diabetic Recipe Book Get your free meal guide and recipe booklet today, packed with more than 60 recipes to help you or your loved ones better manage diabetes symptoms. Click here to get yours!

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An "Obesity Gene" May Decrease Diabetes Risk

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Rudolph E. Tanzi, Ph.D. Joins Genomind's Scientific Advisory Board

WASHINGTON, Sept. 13, 2012 (GLOBE NEWSWIRE) -- Genomind, LLC, a neuropsychiatric personalized medicine company, recently announced the addition of a new member to its leading Scientific Advisory Board.

Rudolph E. Tanzi, Ph.D., is the director of the Genetics and Aging Research Unit at the MassGeneral Institute for Neurodegenerative Disease in Boston. He is also a professor of neurology and holder of the Joseph P. and Rose F. Kennedy Endowed Chair in Neurology and Mental Retardation at Harvard University.

Dr. Tanzi is an internationally respected researcher focusing on the molecular and genetic factors of neurological diseases, with significant interest in Alzheimer's disease. For the last 30 years, he has been dedicated to gene research on neurodegenerative disease and co-discovered the three genes that cause early-onset familial Alzheimer's.

Dr. Tanzi is also responsible for co-discovering genes that trigger Huntington's disease, Wilson's disease, Autism, and other neurological disorders. He is the head of the Alzheimer's Genome Project, a research project of the Cure Alzheimer's Fund, which identified four new related genes - a finding that was named one of the Top Ten Medical Breakthroughs of 2008 by Time magazine. He is the co-author of the book Decoding Darkness: The Search for the Genetic Causes of Alzheimer's Disease, and has co-authored more than 340 articles, making him one of the top ten most cited researchers on Alzheimer's. Dr. Tanzi has been honored with a significant number of awards for his work, which include the Metropolitan Life Foundation Award and The Potamkin Prize.

Dr. Tanzi received his BS from the University of Rochester with a double major in microbiology and history and his Ph.D. in neurobiology from Harvard University.

"It is an honor to welcome Dr. Tanzi to our Scientific Advisory Board," said Genomind Co-founder and Chief Scientific Officer Dr. Jay Lombard. "He is recognized by his peers as the preeminent expert internationally on the genetic basis of Alzheimer's disease pathogenesis. He has dedicated his career to investigating the molecular and genetic causes of Alzheimer's disease, and his discovery of all three genes causing early-onset familial AD is groundbreaking for patients. His discoveries give us hope that there will be more sophisticated ways to develop preventive strategies when diagnosing and treating Alzheimer's disease."

"I am looking forward to working with the Genomind Scientific Advisory Board and the impressive team already in place," said Dr. Tanzi. "Genomind's philosophy of improving patient lives through neurological research aligns perfectly with my research and beliefs, and I hope my past and future findings will help them bring the findings of recent scientific research into real-world use."

Dr. Tanzi joins a distinguished group of thought leaders on the Scientific Advisory Board, all known for their work at the forefront of psychiatric and neurologic research. Board members include Scott T. Aaronson, MD; P. Murali Doraiswamy, MD; Maurizio Fava, MD; Allan I. Levey, MD, PhD; Anil Malhotra, MD; Roy H. Perlis, MD, MSc; and Stephen M. Stahl, MD, PhD.

About Genomind

Genomind is a personalized medicine company comprised of innovative researchers and expert leaders in psychiatry and neurology. Genomind is committed to discovery of the underlying causes of neuropsychiatric disorders and supports the development of personalized medicine that improves patients' lives. Genomind was founded by Ronald I. Dozoretz, MD, a psychiatrist who has devoted his career to improving mental health. Jay Lombard, DO, a neurologist and co-founder of Genomind, is a critically acclaimed author and nationally recognized thought leader in neuropsychiatry practice and research. Learn more at http://www.genomind.com.

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Rudolph E. Tanzi, Ph.D. Joins Genomind's Scientific Advisory Board

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Genetics to determine cancer treatments

The war on cancer is poised to enter a new phase that promises more precise treatments, fewer side effects and, most of all, more survivors.

And none too soon. Although death rates from many cancers have slowly but steadily declined over the decades, experts agree that current treatments are mostly too blunt, too scattershot and too dangerous for the patients they are intended to save.

Today, treating cancer often means an all-out chemical assault on tumors. Doctors bombard patients' bodies with drugs that aim to destroy cancer cells. But like shelling an entire city to wipe out a few rebels, the strategy leaves civilian casualties in its wake: Standard cancer treatments destroy healthy cells alongside diseased ones, taking a toll on a patient's body and strength.

Now, however, the battle tactics are shifting. Researchers have learned how to gather intelligence on a cancer's traits, turn off the tumor's defenses and precisely target only the cells that are causing disease.

"We have the confluence of all these advances coming together at once," says Dr. Ronald DePinho, president of the University of Texas MD Anderson Cancer Center in Houston. "I'm not saying we can cure cancer within 10 years. But we've been handed a complete toolbox. Within this decade, there's no question that we're going to accelerate the decline in mortality due to cancer."

DePinho says the recent revolution in genetics has reignited the world of cancer research. Scientists can sequence all the genes in a cancer cell faster than ever before, compare the cancer genes with those in the rest of the body and even turn genes on and off.

Using these technologies, researchers have discovered that similar-looking cancers can have very different genetic makeups. Understanding the world of mutations can help doctors predict how quickly cancer will grow and which drugs will kill it.

"Oncology as a discipline has always divided itself around body sites," says geneticist Elaine Mardis of Washington University School of Medicine in St. Louis. "There are people who focus on lung cancer and people who focus on breast cancer and people who focus on pancreatic cancer." But the field has realized that cancers are defined as much by their genetic mutations as by location, she says.

When new cancer drugs are in clinical trials, it's already standard practice to see whether the patients who respond have any telltale genetic markers. And in some, cases, such genetic signatures have been found.

Last year, the Food and Drug Administration approved vemurafenib, a melanoma drug that works only in patients with a particular mutation in a gene called BRAF. The drug has no effect in patients without the mutation, so a genetic test is required before a doctor can prescribe it.

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Genetics to determine cancer treatments

Recommendation and review posted by Bethany Smith

Rudolph E. Tanzi, Ph.D. Joins Genomind's Scientific Advisory Board

WASHINGTON, Sept. 13, 2012 (GLOBE NEWSWIRE) -- Genomind, LLC, a neuropsychiatric personalized medicine company, recently announced the addition of a new member to its leading Scientific Advisory Board.

Rudolph E. Tanzi, Ph.D., is the director of the Genetics and Aging Research Unit at the MassGeneral Institute for Neurodegenerative Disease in Boston. He is also a professor of neurology and holder of the Joseph P. and Rose F. Kennedy Endowed Chair in Neurology and Mental Retardation at Harvard University.

Dr. Tanzi is an internationally respected researcher focusing on the molecular and genetic factors of neurological diseases, with significant interest in Alzheimer's disease. For the last 30 years, he has been dedicated to gene research on neurodegenerative disease and co-discovered the three genes that cause early-onset familial Alzheimer's.

Dr. Tanzi is also responsible for co-discovering genes that trigger Huntington's disease, Wilson's disease, Autism, and other neurological disorders. He is the head of the Alzheimer's Genome Project, a research project of the Cure Alzheimer's Fund, which identified four new related genes - a finding that was named one of the Top Ten Medical Breakthroughs of 2008 by Time magazine. He is the co-author of the book Decoding Darkness: The Search for the Genetic Causes of Alzheimer's Disease, and has co-authored more than 340 articles, making him one of the top ten most cited researchers on Alzheimer's. Dr. Tanzi has been honored with a significant number of awards for his work, which include the Metropolitan Life Foundation Award and The Potamkin Prize.

Dr. Tanzi received his BS from the University of Rochester with a double major in microbiology and history and his Ph.D. in neurobiology from Harvard University.

"It is an honor to welcome Dr. Tanzi to our Scientific Advisory Board," said Genomind Co-founder and Chief Scientific Officer Dr. Jay Lombard. "He is recognized by his peers as the preeminent expert internationally on the genetic basis of Alzheimer's disease pathogenesis. He has dedicated his career to investigating the molecular and genetic causes of Alzheimer's disease, and his discovery of all three genes causing early-onset familial AD is groundbreaking for patients. His discoveries give us hope that there will be more sophisticated ways to develop preventive strategies when diagnosing and treating Alzheimer's disease."

"I am looking forward to working with the Genomind Scientific Advisory Board and the impressive team already in place," said Dr. Tanzi. "Genomind's philosophy of improving patient lives through neurological research aligns perfectly with my research and beliefs, and I hope my past and future findings will help them bring the findings of recent scientific research into real-world use."

Dr. Tanzi joins a distinguished group of thought leaders on the Scientific Advisory Board, all known for their work at the forefront of psychiatric and neurologic research. Board members include Scott T. Aaronson, MD; P. Murali Doraiswamy, MD; Maurizio Fava, MD; Allan I. Levey, MD, PhD; Anil Malhotra, MD; Roy H. Perlis, MD, MSc; and Stephen M. Stahl, MD, PhD.

About Genomind

Genomind is a personalized medicine company comprised of innovative researchers and expert leaders in psychiatry and neurology. Genomind is committed to discovery of the underlying causes of neuropsychiatric disorders and supports the development of personalized medicine that improves patients' lives. Genomind was founded by Ronald I. Dozoretz, MD, a psychiatrist who has devoted his career to improving mental health. Jay Lombard, DO, a neurologist and co-founder of Genomind, is a critically acclaimed author and nationally recognized thought leader in neuropsychiatry practice and research. Learn more at http://www.genomind.com.

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Rudolph E. Tanzi, Ph.D. Joins Genomind's Scientific Advisory Board

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Neural stem cells regenerate axons

SAN DIEGO In a study at the University of California, San Diego and VA San Diego Healthcare, researchers were able to regenerate an astonishing degree of axonal growth at the site of severe spinal cord injury in rats. Their research revealed that early stage neurons have the ability to survive and extend axons to form new, functional neuronal relays across an injury site in the adult central nervous system (CNS).

The study also proved that at least some types of adult CNS axons can overcome a normally inhibitory growth environment to grow over long distances. Importantly, stem cells across species exhibit these properties. The work will be published in the journal Cell on Friday (Sept. 14).

The scientists embedded neural stem cells in a matrix of fibrin (a protein key to blood clotting that is already used in human neuron procedures), mixed with growth factors to form a gel. The gel was then applied to the injury site in rats with completely severed spinal cords.

Using this method, after six weeks, the number of axons emerging from the injury site exceeded by 200-fold what had ever been seen before, said Mark Tuszynski, M.D., Ph.D., professor in the UC San Diego Department of Neurosciences and director of the UC San Diego Center for Neural Repair, who headed the study. The axons also grew 10 times the length of axons in any previous study and, importantly, the regeneration of these axons resulted in significant functional improvement.

In addition, adult cells above the injury site regenerated into the neural stem cells, establishing a new relay circuit that could be measured electrically. By stimulating the spinal cord four segments above the injury and recording this electrical stimulation three segments below, we detected new relays across the transaction site, said Tuszynski.

To confirm that the mechanism underlying recovery was due to formation of new relays, when rats recovered, their spinal cords were re-transected above the implant. The rats lost motor function confirming formation of new relays across the injury.

The grafting procedure resulted in significant functional improvement: On a 21-point walking scale, without treatment, the rats score was only 1.5; following the stem cell therapy, it rose to 7 a score reflecting the animals ability to move all joints of affected legs.

Results were then replicated using two human stem cell lines, one already in human trials for ALS. We obtained the exact results using human cells as we had in the rat cells, said Tuszynski.

The study made use of green fluorescent proteins (GFP), a technique that had never before been used to track neural stem cell growth. By tagging the cells with GFP, we were able to observe the stem cells grow, become neurons and grow axons, showing us the full ability of these cells to grow and make connections with the host neurons, said first author Paul Lu, assistant research scientist at UC San Diegos Center for Neural Repair. This is very exciting, because the technology didnt exist before.

According to the researchers, the study makes clear that early-stage neurons can overcome inhibitors present in the adult nervous system that normally work to maintain the elaborate central nervous system and to keep cells in the adult CNS from growing aberrantly.

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Neural stem cells regenerate axons

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Neural stem cells regenerate axons in severe spinal cord injury; functional recovery in rats

ScienceDaily (Sep. 13, 2012) In a study at the University of California, San Diego and VA San Diego Healthcare, researchers were able to regenerate "an astonishing degree" of axonal growth at the site of severe spinal cord injury in rats. Their research revealed that early stage neurons have the ability to survive and extend axons to form new, functional neuronal relays across an injury site in the adult central nervous system (CNS).

The study also proved that at least some types of adult CNS axons can overcome a normally inhibitory growth environment to grow over long distances. Importantly, stem cells across species exhibit these properties. The work will be published in the journal Cell on Sept. 14.

The scientists embedded neural stem cells in a matrix of fibrin (a protein key to blood clotting that is already used in human neuron procedures), mixed with growth factors to form a gel. The gel was then applied to the injury site in rats with completely severed spinal cords.

"Using this method, after six weeks, the number of axons emerging from the injury site exceeded by 200-fold what had ever been seen before," said Mark Tuszynski, MD, PhD, professor in the UC San Diego Department of Neurosciences and director of the UCSD Center for Neural Repair, who headed the study. "The axons also grew 10 times the length of axons in any previous study and, importantly, the regeneration of these axons resulted in significant functional improvement."

In addition, adult cells above the injury site regenerated into the neural stem cells, establishing a new relay circuit that could be measured electrically. "By stimulating the spinal cord four segments above the injury and recording this electrical stimulation three segments below, we detected new relays across the transaction site," said Tuszynski.

To confirm that the mechanism underlying recovery was due to formation of new relays, when rats recovered, their spinal cords were re-transected above the implant. The rats lost motor function -- confirming formation of new relays across the injury.

The grafting procedure resulted in significant functional improvement: On a 21-point walking scale, without treatment, the rats score was only 1.5; following the stem cell therapy, it rose to 7 -- a score reflecting the animals' ability to move all joints of affected legs.

Results were then replicated using two human stem cell lines, one already in human trials for ALS. "We obtained the exact results using human cells as we had in the rat cells," said Tuszynski.

The study made use of green fluorescent proteins (GFP), a technique that had never before been used to track neural stem cell growth. "By tagging the cells with GFP, we were able to observe the stem cells grow, become neurons and grow axons, showing us the full ability of these cells to grow and make connections with the host neurons," said first author Paul Lu, PhD, assistant research scientist at UCSD's Center for Neural Repair. "This is very exciting, because the technology didn't exist before."

According to the researchers, the study makes clear that early-stage neurons can overcome inhibitors present in the adult nervous system that normally work to maintain the elaborate central nervous system and to keep cells in the adult CNS from growing aberrantly.

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Neural stem cells regenerate axons in severe spinal cord injury; functional recovery in rats

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Neural stem cells regenerate axons in severe spinal cord injury

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

Contact: Debra Kain ddkain@ucsd.edu 619-543-6163 University of California - San Diego

In a study at the University of California, San Diego and VA San Diego Healthcare, researchers were able to regenerate "an astonishing degree" of axonal growth at the site of severe spinal cord injury in rats. Their research revealed that early stage neurons have the ability to survive and extend axons to form new, functional neuronal relays across an injury site in the adult central nervous system (CNS).

The study also proved that at least some types of adult CNS axons can overcome a normally inhibitory growth environment to grow over long distances. Importantly, stem cells across species exhibit these properties. The work will be published in the journal Cell on September 14.

The scientists embedded neural stem cells in a matrix of fibrin (a protein key to blood clotting that is already used in human neuron procedures), mixed with growth factors to form a gel. The gel was then applied to the injury site in rats with completely severed spinal cords.

"Using this method, after six weeks, the number of axons emerging from the injury site exceeded by 200-fold what had ever been seen before," said Mark Tuszynski, MD, PhD, professor in the UC San Diego Department of Neurosciences and director of the UCSD Center for Neural Repair, who headed the study. "The axons also grew 10 times the length of axons in any previous study and, importantly, the regeneration of these axons resulted in significant functional improvement."

In addition, adult cells above the injury site regenerated into the neural stem cells, establishing a new relay circuit that could be measured electrically. "By stimulating the spinal cord four segments above the injury and recording this electrical stimulation three segments below, we detected new relays across the transaction site," said Tuszynski.

To confirm that the mechanism underlying recovery was due to formation of new relays, when rats recovered, their spinal cords were re-transected above the implant. The rats lost motor function confirming formation of new relays across the injury.

The grafting procedure resulted in significant functional improvement: On a 21-point walking scale, without treatment, the rats score was only 1.5; following the stem cell therapy, it rose to 7 a score reflecting the animals' ability to move all joints of affected legs.

Results were then replicated using two human stem cell lines, one already in human trials for ALS. "We obtained the exact results using human cells as we had in the rat cells," said Tuszynski.

Read more from the original source:
Neural stem cells regenerate axons in severe spinal cord injury

Recommendation and review posted by sam

Riverdale nonprofit applauds September’s recognition of Spinal Cord Injury Awareness Month in the state.

The spinal cord rehabilitation group Push to Walk, based in this borough, has seen its campaign to raise awareness augmented with September's recognition of Spinal Cord Injury Awareness Month in the state.

Governor Christie signed a proclamation marking the campaign on Aug. 17.

Push to Walk President Cynthia Templeton had been advocating that the state recognize spinal cord injury awareness for 18 months, and she was pleased to see it come to a reality.

In a letter-writing campaign, Templeton was able to gain support from organizations including the Kessler Institute of Rehabilitation, the Christopher and Dana Reeve Foundation, Dr. Wise Young, and Disability Rights New Jersey.

"It's just exciting to be able to spread awareness and to tell people that it is Spinal Cord Injury Awareness Month," said Stephanie Lajam, the communication and special event coordinator for Push to Walk.

Throughout the month, Push to Walk will be sending out information to various organizations to help bring awareness to this medical condition.

At the end of September the group will host its fifth annual golf outing, where it is pleased to have Dr. Young as its honorary chairman this year.

Dr. Young is the founding director of the W.M. Keck Center of Collaborative Neuroscience.

Lajam explained that Dr. Young will be introducing clinical trials for people with spinal cord injuries and paralysis in the United States.

"We were lucky enough to work with him toward this, and it's the best tie-in for us at this time with having September proclaimed Spinal Cord Injury Awareness Month in the State of New Jersey," she said.

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Riverdale nonprofit applauds September's recognition of Spinal Cord Injury Awareness Month in the state.

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Research Study of Triple Negative Breast Cancer Highlights Ability of NextBio Clinical to Identify Biomarkers

SANTA CLARA, Calif.--(BUSINESS WIRE)--

The ability of NextBio Clinical to rapidly identify biomarkers and possible disease targets in an aggressive form of breast cancer was highlighted this week in a poster presentation at the American Society of Clinical Oncologys 2012 Breast Cancer Symposium. NextBio Clinical was used to investigate a cohort of published patient data, curated by NextBio, for key differences between Triple Positive Breast Cancer (TPBC) and Triple Negative Breast Cancer (TNBC), a form of the disease that offers a worse prognosis for those diagnosed. Results of the study quickly identified several key differences in gene expression and methylation status between the two breast cancer types, as well as a novel biomarker and potential alternate way of treating TNBC.

This study clearly demonstrates the power of curated public data and the ability of NextBios sophisticated computational engine to employ big data technology for rapid discovery in translational research studies, said Anita Umesh, Ph.D., NextBio scientist and lead author of the study. Our work involved stratification of a patient population and comparison of the biomarkers between the two patient sub-groups, an otherwise complex task that was easily accomplished in a short amount of time by the NextBio platform. A similar process can be applied by all NextBio users in their translational research projects to enable unique insights.

The researchers first stratified the NextBio-curated TCGA roster of breast cancer patients into two distinct groups: those with Triple Positive Breast Cancer (TPBC) versus those with Triple Negative Breast Cancer (TNBC). A comparison of the two cohorts in NextBio Clinical identified a biomarker Anterior Gradient 3 or AGR3, which was reduced in the TNBC group but up-regulated in the TPBC group. The researchers also found significant differences in the methylation status of the AGR3 gene between TPBC and TNBC, with significantly higher percentage of hypo-methylation in the former, suggesting that methylation was a regulatory mechanism for the gene.

These findings, along with the fact that reduction of AGR3 was associated with severe mutations of TP53, suggest that the AGR3 gene should be further evaluated to identify alternate ways of treating TNBC, said Dr. Umesh. Triple Negative Breast Cancer patients have a much worse prognosis than those that are triple positive. The ability to rapidly identify novel biomarkers and potential targets for drug discovery offers the opportunity to improve future outcomes for this hard-to-treat form of breast cancer.

About NextBio

NextBio provides a state of the art scientific platform to aggregate and interpret large quantities of molecular and other life sciences data for research and clinical applications. NextBios platform integrates data from multiple repositories and diverse technologies by means of a unique correlation engine, which pre-computes billions of significant connections between disparate public and proprietary clinical and experimental data. This feature enables interpretation of an individuals molecular data. It also provides translational researchers the ability to look across the clinical and molecular data of entire populations for clinical trial stratification and selection, hypotheses generation, and biomarker discovery. NextBio Clinical, which recently passed an independent HIPAA audit, is designed for seamless integration with existing clinical and research systems. Backed by highly scalable, Big Data technology, it is capable of analyzing petabytes of data. NextBios platform is delivered as a SaaS (Software as a Service) solution resulting in quick deployment and rapid return on investment.

Today, NextBio is used by researchers and clinicians in over 50 top commercial and academic institutions including the University of Southern California, Sanford-Burnham Medical Research Institute, Celgene, Eli Lilly, Genzyme, Johnson & Johnson, Merck, Regeneron, Scripps Research Institute, Stanford University, University of California at Berkeley, Takeda and many others. To learn more about NextBio, please visit our website at http://www.nextbio.com.

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Research Study of Triple Negative Breast Cancer Highlights Ability of NextBio Clinical to Identify Biomarkers

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Single gene mutation found to cause insulin sensitivity

Oxford researchers have discovered the first single gene responsible for insulin sensitivity in humans. Since the opposite condition of insulin resistance is a significant marker of type 2 diabetes, the discovery could potentially lead to new pathways for diabetes drugs and future treatments.

The scientists decided to look at the gene PTEN based on previous studies, which examined common variants across the human genome that might lead to an increased risk for diabetes.

Theyve shown a link between the cell cycle and a risk for type 2 diabetes, which has started to suggest there might be a genetic overlap in terms of your predisposition for getting diabetes and cancer, study author Dr. Anna Gloyn, of the Oxford Center for Diabetes, Endocrinology and Metabolism at Oxford, told FoxNews.com,

Mutations in just one PTEN gene have been associated with an increased risk of cancers such as breast, womb and thyroid cancer. To go along with this established link, mouse models have shown that PTEN also plays a role in the pathways important for metabolism.

This gene was a good candidate to pick because you could hypothesize that if there was a defect in this gene, it could impact not only cell growth, which would lead to cancer, but it could also affect their metabolic outcome, Gloyn said.

The scientists, interested in learning more about the genes dual role, recruited people in the U.K. with a condition known as Cowden syndrome, which is caused by a faulty mutation in the PTEN gene. People with Cowden syndrome have a higher risk for cancer and often develop polyps on their skin, mouth and bowels.

Cowden syndrome is rare; only one out of every 200,000 people have the condition. An estimated 300 people have the condition in the U.K., which made it difficult for the researchers to study. However, they were able to assemble 15 people with the condition, matching each participant with a healthy counterpart who served as their control test subject.

Both the participants and the control subjects were given glucose drinks to see how well their bodies could cope. Those with Cowden syndrome showed increased insulin sensitivity.

With very low amounts of this [insulin] hormone, they could clear the glucose from their system, Gloyn said. the cells in our pancreas are responsible for secreting insulin which helps to clear glucose from our blood. The people who have these mutations respond very quickly to lower levels of glucose.

For those suffering from type 2 diabetes, the opposite is true. The bodys insulin is less effective at clearing glucose essentially sugar from the blood. Because it is more difficult for their bodies to metabolize glucose, people who suffer from diabetes are typically overweight or obese. Drugs used to combat diabetes typically strive to boost insulin sensitivity.

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Single gene mutation found to cause insulin sensitivity

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Lung cancer tumours in smokers have 10-times more genetic mutations

Lung cancer image; Credit: Shutterstock

Smokers who have lung cancer suffer 10-times more genetic mutations in tumours than non-smokers with the disease, a new study shows.

The findings of the research, from the Washington University School of Medicine in St. Louis, USA, have just been published in the journal Cell.

Senior author Richard K. Wilson, PhD, who is director of The Genome Institute at Washington University, says, "None of us were surprised that the genomes of smokers had more mutations than the genomes of never-smokers with lung cancer. But it was surprising to see 10-fold more mutations. It does reinforce the old message - don't smoke."

The study identified around 3,700 mutations in 17 patients suffering from non-small cell lung cancer, which is the most common type. All but five of them were smokers.

In each non-smoker, the researchers discovered at least one mutated gene that is able to be treated with drugs currently available for other diseases or through clinical trials. In all patients, they found 54 mutated genes linked with existing drugs.

First author Ramaswamy Govindan, MD, an oncologist who treats patients at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University, says, "Whether these drugs will actually work in patients with these DNA alterations still needs to be studied.

"But papers like this open up the landscape to understand what's happening. Now we need to drill deeper and do studies to understand how these mutations cause and promote cancer, and how they can be targeted for therapy."

There are two types of lung cancer - small cell and non-small cell. Around 85% of all cases are non-small cell and they are split into three more classifications. This current study examined two of them - adenocarcinoma - that was linked to 16 patients and large-cell carcinoma that one patient had.

Ramaswamy Govindan, who is national co-chair of the lung cancer group, and Richard K Wilson also took part in a bigger genomic study of 178 patients with the third type, squamous cell carcinoma, which was recently detailed in the journal Nature and was part of The Cancer Genome Atlas project that aims to describe the genetics of common cancers.

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Lung cancer tumours in smokers have 10-times more genetic mutations

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How to Differentiate Your Pharmaceutical Product in the Personalized Medicine Segment

FARMINGTON, Conn., Sept. 13, 2012 /PRNewswire-iReach/ -- Global Information Inc. is pleased to announce a limited time offer on personalized medicine, next generation sequencing (NGS) and epigenetics research from Takeda Pacific, a bio/pharmaceutical and life sciences industry analyst firm based in California.

(Photo: http://photos.prnewswire.com/prnh/20120913/CG74123)

Personalized Medicine: Companies, Trends and World Market

The Personalized Medicine market includes significant core medical product areas that will continue to have a powerful impact on current and future healthcare delivery. The science driving personalized medicine includes pharmacogenetics, pharmacogenproteomics and pharmacometabalomix. Personalized medicine uses a targeted drug that depends on the patient information identified by a companion diagnostic (genetic biomarker test).

This report examines key market segments such as targeted drugs and key personalized medicine diagnostics, including companion diagnostic IVDs, LDTs, diagnostic services and related tools or technologies. Important technologies examined include: microarray, next-generation sequencing, polymerase chain reaction (PCR), bioinformatics, nanotechnology and other platforms. The report highlights new personalized diagnostics and also covers key biomarkers, commercial diagnostics and therapeutics that drive personalized medicine.

Save up to 20% by purchasing this report before October 15, 2012.

For a detailed executive summary, sample charts, and table of contents, or to request free sample pages from the full report, please visit http://www.giiresearch.com/report/tak238167-personalized-medicine-companies-trends-world.html

Epigenetics: Technologies, Drugs, Diagnostics, and World Market

Many people already know about DNA, genes and the human genome. The DNA code defines the structure of who we are, our potential health and our characteristics that we pass on to our children. Epigenetics refers to the second code of life and links environmental impacts to a person's health. Epigenetic mechanisms signal how and when genes are activated or silenced.

This research study discusses the market for life science tools and technologies that support epigenetics R&D. The report discusses important technologies, equipment and consumables including microarray, next-generation sequencing, PCR and other platforms. Topics such as microRNA and human stem cells are lightly covered.

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How to Differentiate Your Pharmaceutical Product in the Personalized Medicine Segment

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