Archive for March, 2012

ScienceDaily (Mar. 6, 2012) Northwestern University scientists have developed a powerful analytical method that they have used to direct stem cell differentiation. Out of millions of possibilities, they rapidly identified the chemical and physical structures that can cue stem cells to become osteocytes, cells found in mature bone.

Researchers can use the method, called nanocombinatorics, to build enormous libraries of physical structures varying in size from a few nanometers to many micrometers for addressing problems within and outside biology.

Those in the fields of chemistry, materials engineering and nanotechnology could use this invaluable tool to assess which chemical and physical structures -- including size, shape and composition -- work best for a desired process or function.

Nanocombinatorics holds promise for screening catalysts for energy conversion, understanding properties conferred by nanostructures, identifying active molecules for drug discovery or even optimizing materials for tissue regeneration, among other applications.

Details of the method and proof of concept is published in the Proceedings of the National Academy of Sciences.

"With further development, researchers might be able to use this approach to prepare cells of any lineage on command," said Chad A. Mirkin, who led the work. "Insight into such a process is important for understanding cancer development and for developing novel cancer treatment methodologies."

Mirkin is the George B. Rathmann Professor of Chemistry in the Weinberg College of Arts and Sciences and professor of medicine, chemical and biological engineering, biomedical engineering and materials science and engineering. He also is the director of Northwestern's International Institute for Nanotechnology (IIN).

The new analytical method utilizes a technique invented at Northwestern called polymer pen lithography, where basically a rubber stamp having as many as 11 million sharp pyramids is mounted on a transparent glass backing and precisely controlled by an atomic force microscope to generate desired patterns on a surface. Each pyramid -- a polymeric pen -- is coated with molecules for a particular purpose.

In this work, the researchers used molecules that bind proteins found in the natural cell environment, such as fibronectin, which could then be attached onto a substrate in various patterns. (Fibronectin is a protein that mediates cell adhesion.) The team rapidly prepared millions of textured features over a large area, which they call a library. The library consisted of approximately 10,000 fibronectin patterns having as many as 25 million features ranging in size from a couple hundred nanometers to several micrometers.

To make these surfaces, they intentionally tilt the stamp and its array of pens as the stamp is brought down onto the substrate, each pen delivering a spot of molecules that could then bind fibronectin. The tilt results in different amounts of pressure on the polymeric pens, which dictates the feature size of each spot. Because the pressure varies across a broad range, so does the feature size.

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Influencing stem cell fate: New screening method helps scientists identify key information rapidly

GAYVILLE When it came to helping his brother, Jason Selchert was willing to do a lot more than give the shirt off his back. In January, he became a bone marrow donor for his sibling, Jeff Selchert.

Jason, 39, superintendent of the Gayville-Volin School, said he had plenty of time to prepare for the procedure.

A little over two years ago, my brother, who is four years older than I am, was diagnosed with leukemia, he stated. When he was diagnosed, they determined that probably at some point in his illness, he was going to have to undergo a bone marrow transplant. Luckily enough, he has five siblings, and we were all tested. Two of the five were a match. I was one of the two.

Since the chance that a sibling will be a match is about one in four, the fact that two were a match was fortuitous, Jason said.

Jason and his oldest brother were both perfect matches, according to the blood and DNA testing.

However, Jason was selected as the best candidate.

After undergoing treatment following the initial diagnosis, Jeffs leukemia went into remission. But a few days prior to last Thanksgiving, the cancer had returned.

It was pretty well advanced, and they determined that the only way to treat it was going to be a transplant, Jason said. I had known for more than two years that it was maybe going to be an option. Its a pretty lengthy psychological process you go through to make sure that you are mentally stable enough to go through it, and understand what is going to happen and what could be the end result for me and my brother.

Jason donated his bone marrow stem cells Jan. 30. A successful transplant to his brother occurred the next day.

The worst part of the process was the time leading up to the donation, according to Jason. During the four previous days, he was given medication that caused his body to overproduce bone marrow stem cells. The process made Jason ache and feel nauseated, similar to the flu.

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Selchert Undergoes Transplant For Brother

alan bernstein From Wednesday's Globe and Mail Published Wednesday, Mar. 07, 2012 2:00AM EST

Most Canadians are unaware that two of their own a lanky physics whiz from Alberta and a rumpled Shakespeare-quoting MD from Toronto made a discovery 50 years ago that transformed the understanding of human biology and opened new doors to the treatment of cancer and other diseases.

Toiling away in labs atop Torontos old Princess Margaret Hospital, James Edgar Till and Ernest Armstrong (Bun) McCulloch proved that a single rare cell could produce the red blood cells, white blood cells and platelets needed to make blood, while simultaneously reproducing itself. Dr. Till and Dr. McCulloch originally called the cell a colony-forming unit. Today, its better known as a stem cell.

A great new book, Dreams and Due Diligence, by Joe Sornberger, tells the story. Still, that so few of us know let alone celebrate the fact that the stem cell is a Canadian discovery is baffling. Canada founded the entire field of stem-cell science. We have done much of the heavy lifting for decades: discovering neural stem cells, skin stem cells and cancer stem cells. If hockey is Canadas game, stem-cell science is Canadas science. Not knowing about Dr. Till and Dr. McCulloch is not knowing about Maurice Richard and Wayne Gretzky.

The way it happened didnt help. Their original paper was published in an obscure journal, Radiation Research, in 1961. Public interest went viral only after American James Thomson isolated human embryonic stem cells in 1998, which simultaneously raised hopes that stem cells could be used to repair any damaged cell in the body and ethical concerns that doing so would encourage the destruction of human embryos.

In 2002, the Canadian Institutes of Health Research developed guidelines for all stem-cell research carried out in Canada with its funds. These guidelines have become the gold standard for other countries, including the United States.

Whats even more remarkable is that Canada does such groundbreaking research on a dime. The all in investment in stem-cell research in Canada public, private and charitable funding is about $75-million. This support is provided by Canadians through taxes, donations to health charities and the generosity of community leaders individuals such as Robert and Cheryl McEwen of Toronto and the late Harley Hotchkiss of Calgary. But we still seriously lag behind California, which, with roughly the same population as Canada, has committed $3-billion over 10 years for stem-cell research.

How much further Canadas star scientists can go, however, is in doubt. According to the Stem Cell Network, there are 40 to 50 early-phase clinical trials using transplanted cells ready to roll out over the next four years. All are currently unfunded.

Prime Minister Stephen Harper has said his government will continue to make the key investments in science and technology but bemoaned Canadas less-than-optimal results for those investments. Stem-cell research has already proved itself a sound investment: Dr. Till and Dr. McCullochs work formed the basis of the bone marrow transplantation program at Princess Margaret Hospital that alone has saved thousands of lives. But it will take more than government funding: Private industry and private citizens also need to support life-saving research.

Canadians have good reason to be proud of our countrys contributions to health research and medicine. Two stand out as landmarks: the discovery of insulin in the 1920s and the discovery of stem cells in the 1960s. On Wednesday, at a dinner that brings together many of the countrys leading figures in business, the arts, entertainment, sports and science, the Canadian Stem Cell Foundation will be launched. The event will look back at that great discovery 50 years ago and look forward to ensure that Canadians continue to contribute to stem-cell research and its application to human disease.

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If Canada's game is hockey, its science is stem cells

Washington, Mar 7 (ANI): Researchers have offered a potential insight into a known anti-cancer gene, which may also open the door to new therapeutic options that may aid weight loss and longevity in humans.

Mice with an extra dose of a known anti-cancer gene lose weight even as their appetites grow. Not only that, but according to the report, the animals also live longer, and that isn't just because they aren't getting cancer, either.

One of the animals' youthful secrets is hyperactive brown fat, which burns energy instead of storing it.

The findings add to evidence that tumour suppressors aren't designed only to protect us against cancer, the researchers say. They also point to new treatment strategies aimed to boost brown fat and fight aging.

"Tumor suppressors are actually genes that have been used by evolution to protect us from all kinds of abnormalities," said Manuel Serrano of the Spanish National Cancer Research Center.

In this case, the researchers studied a tumour suppressor commonly lost in human cancers. Mice with an extra copy of the gene known as Pten didn't get cancer, but that's not the half of it.

Those mice were also leaner, even as they ate more than controls, Serrano said. That suggested that the animals were experiencing some sort of metabolic imbalance-and a beneficial one at that.

Cancer protection aside, the animals lived longer than usual. They were also less prone to insulin resistance and had less fat in their livers.

Those benefits seem to trace back to the fact that those Pten mice were burning more calories thanks to overactive brown fat.

Studies in isolated brown fat cells confirmed that a boost in Pten increases the activity of those cells. Pten also made it easier for brown fat to form.

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Gene tweak shows promise to keep you cancer free and slim

One of the world's leading researchers into spinal cord injuries says China could hold the key to a cure that he has been searching for since he met late actor Christopher Reeve in the 1990s.

US-based Doctor Wise Young first used the word "cure" in relation to his work after a conversation with Reeve, the Superman hero who became a quadriplegic in an equestrian accident in 1995.

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Reeve contacted him looking for help and the two became close friends. The actor died of heart failure in 2004 at the age of 52, having devoted his life to raising awareness about spinal cord injuries and stem-cell research.

But it was a star of a different sort, Chinese gymnast Sang Lan, who set Young on the path he believes has brought a cure closer than ever, thanks to ground-breaking clinical trials of stem-cell therapy he is conducting in China.

"Everybody assumed that I'm doing this in China because I wanted to escape George W. Bush, but that's not the case at all," Young told AFP, recalling the former US president's 2001 decision to effectively stop federal funding of embryonic stem cell research.

"I started the clinical trials in 2005 here in Hong Kong . . . mainly because of a promise that I made to a young woman. Her name is Sang Lan."

Sang crushed her spine during a routine warm-up exercise at the Goodwill Games in New York in 1998. She met Young as she underwent treatment and rehabilitation in the US over the next 12 months.

"Her parents came to me and asked whether or not there would ever be a cure for her, and I said we're working very hard on it," said Young, who was by then one of the leading US experts on spinal cord injuries.

"When she went back to China after doing her rehabilitation in New York she cried and asked how would therapies go from the United States to China.

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Young aims for spinal injury 'cure'

by Stephen Coates

HONG KONG, March 7, 2012 (AFP) - One of the world's leading researchers into spinal cord injuries says China could hold the key to a cure that he has been searching for since he met late actor Christopher Reeve in the 1990s.

US-based Doctor Wise Young first used the word "cure" in relation to his work after a conversation with Reeve, the "Superman" hero who became quadriplegic in an equestrian accident in 1995.

Reeve contacted him looking for help and the two became close friends. The actor died of heart failure in 2004 at the age of 52, having devoted his life to raising awareness about spinal cord injuries and stem-cell research.

But it was a star of a different sort, Chinese gymnast Sang Lan, who set Young on the path he believes has brought a cure closer than ever, thanks to ground-breaking clinical trials of stem-cell therapy he is conducting in China.

"Everybody assumed that I'm doing this in China because I wanted to escape George W. Bush, but that's not the case at all," Young told AFP in an interview, recalling the former US president's 2001 decision to effectively stop Federal funding of embryonic stem cell research.

"I started the clinical trials in 2005 here in Hong Kong ... mainly because of a promise that I made to a young woman. Her name is Sang Lan."

Sang crushed her spine during a routine warm-up exercise at the Goodwill Games in New York in 1998. She met Young as she underwent treatment and rehabilitation in the United States over the next 12 months.

"Her parents came to me and asked whether or not there would ever be a cure for her, and I said we're working very hard on it," recalled Young, who was by then one of the leading US experts on spinal cord injuries.

"When she went back to China after doing her rehabilitation in New York she cried and asked how would therapies go from the United States to China.

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Doctor looks to China for spinal injury 'cure'

Newswise (PHILADELPHIA) Researchers at the Rothman Institute at Jefferson have shown that patients who receive surgery less than 24 hours after a traumatic cervical spine injury suffer less neural tissue destruction and improved clinical outcomes. The results of their study, the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) are available in PLoS One.

This practice-changing study is the first to show that the timing of surgery after traumatic spinal cord injury (SCI) matters, says Alexander Vaccaro, MD, PhD, professor of Orthopaedics and Neurosurgery at Jefferson Medical College of Thomas Jefferson University and attending surgeon at Thomas Jefferson University Hospital, the largest spinal cord injury center in the country.

The multicenter study recruited 313 patients; 182 of whom underwent surgery less than 24 hours after traumatic cervical SCI and 131 of whom underwent surgery at or after 24 hours post-SCI.

For both groups, the degree of neurologic improvement was measured by change in American Spinal Injury Associations (ASIAs) ASIA Impairment Scale (AIS). A two-grade improvement in AIS scores post-surgery was associated with improved neurologic outcomes. Baseline neurological assessments were performed within 24 hours of injury on all subjects.

A total of 222 patients were followed to six months post-surgery.

In the early surgery group (surgery performed less than 24 hours post-injury), 42.7 percent showed no improvement, 36.6 percent had a one grade improvement, 16.8 percent had a two-grade improvement and 3.1 percent had a three grade improvement. Comparatively, in the late surgery group (surgery performed at 24 hours or more post-injury), 50 percent showed no improvement, 40.7 percent had a one grade improvement and 8.8 percent had a two grade improvement.

What this tells us is that the odds of a significant (at least two grade) improvement in neurologic status is 2.8 times higher when surgery is performed within 24 hours post-injury. This can be the difference between walking and not for the rest of ones life, says Vaccaro.

Complications occurred in 24.2 percent of early surgery patients versus 30.5 percent of late surgery patients.

Previous research has been inconclusive on the issue, with the common thought among most surgeons that you can wait up to five days post-injury and have the same outcomes. We should not practice that way anymore armed with this new information, says Vaccaro.

Research was performed in collaboration with the University of Toronto; University of Virginia; University of Maryland, Baltimore; University of British Columbia; and the University of Kansas.

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Decompression Surgery Performed Less than 24 Hours After Traumatic Cervical Spinal Cord Injury Leads to Improved ...

Public release date: 6-Mar-2012 [ | E-mail | Share ]

Contact: Lee-Ann Landis leeann.landis@jefferson.edu 215-955-2240 Thomas Jefferson University

(PHILADELPHIA) Researchers at the Rothman Institute at Jefferson have shown that patients who receive surgery less than 24 hours after a traumatic cervical spine injury suffer less neural tissue destruction and improved clinical outcomes. The results of their study, the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) are available in PLoS One.

"This practice-changing study is the first to show that the timing of surgery after traumatic spinal cord injury (SCI) matters," says Alexander Vaccaro, MD, PhD, professor of Orthopaedics and Neurosurgery at Jefferson Medical College of Thomas Jefferson University and attending surgeon at Thomas Jefferson University Hospital, the largest spinal cord injury center in the country.

The multicenter study recruited 313 patients; 182 of whom underwent surgery less than 24 hours after traumatic cervical SCI and 131 of whom underwent surgery at or after 24 hours post-SCI.

For both groups, the degree of neurologic improvement was measured by change in American Spinal Injury Association's (ASIA's) ASIA Impairment Scale (AIS). A two-grade improvement in AIS scores post-surgery was associated with improved neurologic outcomes. Baseline neurological assessments were performed within 24 hours of injury on all subjects.

A total of 222 patients were followed to six months post-surgery.

In the early surgery group (surgery performed less than 24 hours post-injury), 42.7 percent showed no improvement, 36.6 percent had a one grade improvement, 16.8 percent had a two-grade improvement and 3.1 percent had a three grade improvement. Comparatively, in the late surgery group (surgery performed at 24 hours or more post-injury), 50 percent showed no improvement, 40.7 percent had a one grade improvement and 8.8 percent had a two grade improvement.

"What this tells us is that the odds of a significant (at least two grade) improvement in neurologic status is 2.8 times higher when surgery is performed within 24 hours post-injury. This can be the difference between walking and not for the rest of one's life," says Vaccaro.

Complications occurred in 24.2 percent of early surgery patients versus 30.5 percent of late surgery patients.

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Surgery less than 24 hours after traumatic cervical spinal cord injury leads to improved outcomes

WASHINGTON, DC--(Marketwire -03/05/12)- The Alliance for Regenerative Medicine issued the following statement today: "An article about stem cell treatments taking place in Texas published by Nature last week is extremely troubling. The article suggests that patients are being administered stem cell treatments that have not been systematically demonstrated to be safe and effective therapies through the established FDA regulatory process.

"Cell therapy treatments, including those using adult stem cells, hold the promise of providing patients with treatments and cures for numerous diseases and disabilities. However, FDA regulation is key to ensuring that the treatments available to patients are safe and effective.

"The Alliance for Regenerative Medicine (ARM), a non-profit organization whose mission is to promote increased funding and development of regenerative medicine products, believes cell therapy and regenerative medicine products, including autologous cell therapy products, must go through the rigorous safety testing that is part of the FDA regulatory process before they can be marketed to the public. These regulations are designed to promote safe collection, manufacture, storage, and use of human cells, and cellular and tissue based products. ARM members comply with these rules because they know that FDA oversight helps to prevent patients from exposure to potentially unsafe products.

"We urge all companies developing stem cell treatments to follow FDA rules governing research and product development. ARM remains committed to working with all stakeholders to ensure that safe and effective products reach patients as soon as possible."

About The Alliance for Regenerative Medicine (ARM) The Alliance for Regenerative Medicine (ARM) is a Washington, DC-based non-profit organization that promotes legislative, regulatory, reimbursement, and financing initiatives necessary to facilitate access to life-giving advances in regenerative medicine. ARM also works to increase public understanding of the field and its potential to transform human healthcare, and provides services to support the growth of its member companies and organizations. To learn more about ARM or to become a member, visit http://www.alliancerm.org.

Continued here:
The Alliance for Regenerative Medicine Statement on Use of Cell Therapies Not Approved by the Federal Drug ...

Released: 3/5/2012 12:00 PM EST Embargo expired: 3/6/2012 2:30 PM EST Source: Laurantis Pharma

Newswise (Ventura, CA, March 6, 2012) Lymphedema Awareness Day was established to support the needs of patients with lymphedema and to raise awareness for the need to develop new treatment options. Today, researchers have presented investigational pre-clinical data on the first potential pharmacologic agent used in combination with surgery for the treatment of breast cancer associated lymphedema at the Gordon Research Conference for Molecular Mechanisms in Lymphatic Function & Disease.

Currently there is no advanced pharmacologically-based therapeutic for lymphedema, said Stanley G. Rockson, MD, Director, Center for Lymphatic and Venous Disorders, Stanford University School of Medicine, and Principal Investigator of the upcoming first in human trial for Lymfactin. Although the research Is still early, the preliminary data show a remarkable improvement in the ability to successfully conduct lymph node transplant surgery with the benefit of Lymfactin.

Lymphedema occurs in about 20 percent of the three million patients with breast cancer.The condition occurs from trauma to the lymph nodes, and blockages in the lymphatic system as a result of breast cancer treatment. The symptoms include painful swelling and inflammation of the limbs.

Turku, Finland-based Laurantis Pharma Oy is developing Lymfactin, a vascular endothelial growth factor C (VEGF-C) in an adenoviral vector, for the treatment of secondary lymphedema associated with breast cancer. The therapy with Lymfactin involves a surgical operation where a lymph node flap is harvested from the patients lower abdominal wall and injected with Lymfactin, which leads to the transient presence of the adenovirus containing the VEGF-C gene. The lymph node is then transferred to the axillary region.

This new treatment is very promising, said Wendy Chaite, Founder, Lymphatic Research Foundation, a national organization devoted to advancing lymphatic research and to finding improved treatments and cures for lymphedema and lymphatic diseases. Lymphedema is one of those seldom discussed but far too common conditions that biotech and pharmaceutical companies have yet to explore. Although this research is at an early stage, the lack of any advanced treatments makes this research all the more important for those who suffer from this condition.

Professor Kari Alitalo of the University of Helsinki who made the discovery that the growth factor VEGF-C regulates the growth and development of the lymphatic system in humans and other mammals, presented the findings. From this discovery and in association with his co-workers Dr. Tuomas Tammela and Dr. Anne Saaristo, they identified that if VEGF-C is injected into tissues in mice and subsequently in pigs, growth of new lymphatic vessels and the restoration of the lymphatic architecture is catalyzed. Previous studies have shown that transferring lymph nodes from the inguinal region to the axillary region in patients with secondary lymphedema following their treatment for breast cancer was found to offer a slight improvement in their condition. Removal of old scar tissue from the axilla is considered an important step of this procedure.

The team in Finland then went a step further and showed that by combining VEGF-C injections with lymph node transfer in animal models using mice and then pigs, the response seen was even better than lymph node transfer alone. The results in mice indicated that lymphedema treated with lymph node transfer alone resulted in about 20% improvement. However, when combined with the administration of VEGF-C, the overall response was increased to around 80%.

In collaboration with Dr Rockson, Dr Anne Saaristo, MD and Prof. Kari Alitalo, Laurantis researchers are developing a treatment to potentially enable much higher transfer success. The Company plans to start a phase I/II study in patients with breast cancer associated lymphedema in early 2013. Lymfactin is an investigational therapy and has not been approved by the U.S. Food and Drug Administration.

Target Indication: Breast Cancer Associated Lymphedema The impairment of lymphatic drainage caused by dysfunction of the lymphatic vasculature leads to an accumulation of proteins and associated fluid, and finally to lymphedema-a chronic progressive swelling of the affected tissues. Lymphedema can either be hereditary - in which case it is diagnosed as primary lymphedema - or it can occur as a consequence of a disease, trauma, surgery, or radiotherapy and-thereby diagnosed as secondary lymphedema.

Original post:
On Lymphedema Awareness Day, Researchers Present Pre-Clinical Data Offering Cautious Hope for Breast Cancer Patients ...

Research Explores the Role of the SRY Gene in the Male Fight-Or-Flight Response.

The pulse quickens, the heart pounds and adrenalin courses through the veins, but in stressful situations is our reaction controlled by our genes, and does it differ between the sexes?

Australian scientists, writing in BioEssays, believe the SRY gene, which directs male development, may promote aggression and other traditionally male behavioural traits resulting in the fight-or-flight reaction to stress.

Research has shown how the body reacts to stress by activating the adrenal glands which secrete catecholamine hormones into the bloodstream and trigger the aggressive fight-or-flight response. However, the majority of studies into this process have focused on men and have not considered different responses between the sexes.

Historically males and females have been under different selection pressures which are reflected by biochemical and behavioural differences between the sexes, said Dr Joohyung Lee, from the Prince Henrys Institute in Melbourne. The aggressive fight-or-flight reaction is more dominant in men, while women predominantly adopt a less aggressive tend-and-befriend response.

Dr Lee and co-author Professor Vincent Harley, propose that the Y-chromosome gene SRY reveals a genetic underpinning for this difference due to its role in controlling a group of neurotransmitters known as catecholamines. Professor Harleys earlier research had shown that SRY is a sex-determining gene which directs the prenatal development of the testes, which in turn secrete hormones which masculinise the developing body.

If the SRY gene is absent the testes do not form and the foetus develops as a female. People long thought that SRYs only function was to form the testes said Professor Harley. Then we found SRY protein in the human brain and with UCLA researchers led by Professor Eric Vilain, showed that the protein controls movement in males via dopamine.

Besides the testes, SRY protein is present in a number of vital organs in the male body, including the heart, lungs and brain, indicating it has a role beyond early sex determination, said Dr Lee. This suggests SRY exerts male-specific effects in tissues outside the testis, such as regulating cardiovascular function and neural activity, both of which play a vital role in our response to stress.

The authors propose that SRY may prime organs in the male body to respond to stress through increased release of catecholamine and blood flow to organs, as well as promoting aggression and increased movement which drive fight-or-flight in males. In females oestrogen and the activation of internal opiates, which the body uses to control pain, may prevent aggressive responses.

The role of SRY regulation of catecholamines also suggests the gene may have a role in male-biased disorders such as Parkinsons disease.

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Men Respond More Aggressively Than Women to Stress, and it’s All Down to a Single Gene

Public release date: 6-Mar-2012 [ | E-mail | Share ]

Contact: Dr. Hilary Glover hilary.glover@biomedcentral.com 44-203-192-2370 BioMed Central

Spinal muscular atrophy (SMA) is an incurable, and progressive, disease caused by an inheritable defect in the gene SMN1. Depending on the severity of the mutation it can result in the loss of spinal cord motor neurons, muscle wasting (atrophy) and even death of an affected child. A new study published in Biomed Central's open access journal BMC Medicine shows that Fasudil, a ROCK inhibitor, can improve both the size of muscle fibers and their connection to motor neurons. Fasudil also increased the lifespan and improved the movement of SMA mice.

SMA affects 1 in 6,000 births and is the leading cause of death in young children. In its less severe form the muscle wasting of SMA traps bright young children within their bodies. Researchers from the Ottawa Hospital Research Institute and the University of Ottawa realized that SMA caused problems in regulation of the ROCK intracellular signaling pathway and that inhibiting this pathway could increase the lifespan of SMA mice.

By targeting the ROCK pathway in spinal cord and muscles, Fasudil bypasses the genetic defect SMN1. Dr Kothary, who led the team, explained, "Fasudil increased the lifespan of SMA mice from 30 to 300 days, allowing them to survive well into adulthood. Although it had no apparent effect on the damaged neurons themselves, Fasudil increased muscle size and the endplate junction between muscles and their motor neurons. Consequently, the mice were also better coordinated, better groomed, and could move about more freely than untreated SMA mice."

Melissa Bowerman from the Ottawa Hospital Research Institute continued, "Finding a cure for SMA is still a long way off, however we hope that treatment with drugs like Fasudil, which goes some way towards restoring normal developmental, or HDAC inhibitors, which alter how genes are regulated, along with nutrition and physiotherapy will provide a package of therapy to improve the quality and length of life of SMA children."

###

Notes to Editors

1. Fasudil improves survival and promotes skeletal muscle development in a mouse model of spinal muscular atrophy Melissa Bowerman, Lyndsay M Murray, Justin G Boyer, Carrie L Anderson and Rashmi Kothary BMC Medicine (in press)

Please name the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central's open access policy.

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Fasudil bypasses genetic cause of spinal birth defect

ScienceDaily (Mar. 6, 2012) Scientists from the Ottawa Hospital Research Institute (OHRI) and the University of Ottawa (uOttawa) have discovered that a drug called fasudil can extend the average lifespan of mice with Spinal muscular atrophy (SMA) from 30.5 days to more than 300 days.

The study is published March 6 in BioMed Central's open access journal BMC Medicine, by Dr. Rashmi Kothary, his graduate student Melissa Bowerman and others.

SMA is the leading inherited cause of death in infants and toddlers, affecting approximately 25,000 people in Canada and the United States. Scientists have known for many years that this disease is caused by inherited mutations in a gene called survival motor neuron 1 (SMN1). Most early attempts at developing treatments for SMA focused on replacing this gene, however, Dr. Kothary's group has focused on understanding and targeting the physiological defects present in certain nerve cells with SMA. These cells have a weakened internal scaffold, which hinders their ability to connect with muscle cells and contributes to the severe muscle weakness associated with SMA.

Two years ago, Dr. Kothary and his team showed that a laboratory compound called Y-27632, which targets an enzyme that is involved in maintaining the cellular scaffold, could greatly increase lifespan in a certain mouse model of SMA. In this new study, they tested a compound called fasudil, which is similar to Y-27632, but has the advantage that it has already been approved for human clinical trials for other conditions, meaning that it could possibly be re-targeted to use in clinical trials for SMA more quickly than a completely new drug.

The Kothary group found that fasudil-treated SMA mice survived for an average of more than 300 days, compared to just 30.5 days for untreated SMA mice. However, the average lifespan of fasudil-treated SMA mice was still only about half as long as that of normal mice. Fasudil-treated SMA mice also had larger muscle fibres than the untreated SMA mice, and they behaved more normally with respect to grooming and other regular activities. However, they did not perform any better in strength and balance tests and they still had low numbers of motor neurons, which is typical for SMA.

"Our study is important because it expands a new area of research into SMA, which could lead to the development of new treatments," said Melissa Bowerman. "Of course, this research is still at the early stages and although we found that fasudil could significantly increase lifespan in a mouse model of SMA, this drug couldn't correct all the problems in these mice, and it had serious side effects when used at higher doses."

"A number of groups are working to develop fasudil-like compounds with fewer side effects, and we're very excited to see how these perform in our models, and hopefully in human SMA clinical trials some day," said Dr. Kothary "However, we continue to believe that SMA is a disease that will best be addressed using multiple strategies together, including nutrition and possibly drug, cell and gene therapies."

"Dr. Kothary's group has been a pioneer in SMA research, both in characterizing the impact of SMA on tissues and organs, and in discovering a novel therapeutic pathway involving enzymes that target the cell scaffold," said Dr. Alex MacKenzie, an expert in SMA at CHEO Research Institute and the University of Ottawa, who was not involved in the study. "It has to be said that this approach was not intuitively obvious and Dr. Kothary and his team are to be commended for their creativity in its discovery. It represents an important addition to the armamentarium of experimental SMA treatments."

Although fasudil has been approved by the U.S. Food and Drug Administration for use in certain adult human clinical trials, it is still considered experimental, and has not been approved for the treatment of any human condition in the United States or Canada. Individuals who are interested in experimental therapies should discuss this with their health care professional.

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New approach for treating genetic muscle wasting disease shows promise in mice

ScienceDaily (Mar. 6, 2012) A new research discovery by a team of Stanford and European scientists offers hope that people with atherosclerotic disease may one day be able to avoid limb amputation related to ischemia. A new research report appearing online in the FASEB Journal suggests that the delivery of genes for two molecules naturally produced by the body, called "PDGF-BB" and "VEGF" may successfully cause the body to grow new blood vessels that can save ischemic limbs.

"We hope that our findings will ultimately develop into a safe and effective therapy for the many patients, suffering from blocked arteries in the limbs, who are currently not adequately treated by surgery or drugs," said Helen M. Blau, Ph.D., a senior researcher involved in the work and Associate Editor of the FASEB Journal from the Baxter Laboratory for Stem Cell Biology at the Institute for Regenerative Medicine and Stem Cell Biology at Stanford. "This could help avoid the devastating consequences of limb amputations for both patients and their families."

To make this discovery, Blau and colleagues, including Andrea Banfi (now at Basel University), introduced the genes for PDGF-BB and VEGF into the muscles of mice, either independently or together. When high doses of VEGF alone were produced, they caused the growth of vascular tumors. When the two factors were produced in unbalanced amounts, tumor growth also occurred. When VEGF and PDGF were delivered in a fixed ratio relative to one another, however, no tumors occurred, and blood flow was restored to ischemic muscle tissue and damage repaired without any toxic effects. To achieve a "balanced" delivery of PDGF-BB and VEGF, scientists placed both genes in a single gene therapy delivery mechanism, called a "vector."

Although the report shows the feasibility of growing robust and safe new blood vessels that restore blood flow to diseased tissues, Blau points out that "there are multiple challenges to correcting peripheral vasculature disease by using proangiogenic gene therapy strategies. Two important challenges are what to deliver and how to get it to where it can have beneficial effects. Clinical success will require both delivering a gene therapy construct that encodes for effective angiogenic factors and ensuring that the sites of delivery are where the construct can have the greatest clinical benefit."

"This ingenious work, based on the latest techniques of molecular biology, tells us that it is possible to reinvigorate parts of our body that can't get enough blood to keep them going," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "The next question is whether this approach will work in humans and exactly how to deliver the new treatment to places that need it the most."

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The above story is reprinted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Gene therapy approach to grow blood vessels in ischemic limbs

19-02-2012 22:16 SNP Stem Cell Activator Program : Functional wrinkle cosmetic product Registered for the first time in the nation and third in the world in ICID and contains a new natural material called stem cell activator. SNP ACSYS LINE : SNP ACSYS LINE is the foundation exclusive for oily and troubled skin. It makes oily and troubled skin texture, which is shiny and sticky, neat and clean by adjusting excessively secreted serum. snpcos.en.ecplaza.net

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Stem Cell Activator Program by SD Biotechnologies - Video

CAMBRIDGE, UK--(BUSINESS WIRE)--

Lab21 Limited, the global specialist in personalized medicine and clinical diagnostics, today announces the launch of a new Clinical Genomics Center located within the Greenville Hospital System (GHS) Memorial Medical Campus in Greenville, South Carolina.

The center will be physically located within the GHS Institute for Translational Oncology Research (ITOR) as part of an on-going collaboration to facilitate the introduction of complex biomarker analysis into routine cancer patient management. This represents a long-standing commitment from the local oncology community and Lab21 to introduce state-of-the-art next-generation sequencing (NGS) technology as part of its growing translational medicine clinical services portfolio in the US.

Bringing this leading-edge technology to the cancer clinic represents a significant breakthrough and the culmination of a seven-year journey, said Dr. Joe Stephenson, medical director for ITOR. This genomics center is another major step towards fulfilling our vision to provide personalized cancer care better enabling us to offer the right drug, at the right time, to the right patient.

The establishment of this center was facilitated through a strategic relationship with Life Technologies who are providing their new Ion Torrent Personal Genome Machine as the key launch platform technology. Michael Bolick, President of Lab21 Inc., explained we conducted extensive due diligence on the underpinning technology for the center and are confident that our engagement with Life Technologies will enable us to offer a comprehensive and cost-effective NGS service to the oncology community.

Lab21s CEO, Graham Mullis, said: This is a major step forward for Lab21 in North America and we are delighted to be working with Dr. Joe Stephenson and the team at ITOR in this fast changing market of personalized medicine. The establishment of this center underlines our commitment to our personalized medicine strategy and to introduce state-of-the-art molecular services and products into North America. It also reinforces our relationship with ITOR and the potential to use this technology for clinical trial applications with a view to identifying new biomarkers which can subsequently build our proprietary companion diagnostic portfolio. Importantly, it marks our intention to utilize this NGS technology in other therapeutic areas in addition to oncology. Lab21 is a company with an established business in infectious diseases, particularly virology, and we are already negotiating new contracts to exploit this expertise using NGS technology.

END

About Lab21

Lab21 is a global leader in personalized healthcare. It provides diagnostic products and services and supports blood bank screening, medical diagnostics and drug discovery. Lab21 customers include international healthcare providers, pharmaceutical and diagnostic companies. The Products division of Lab21 manufactures immunodiagnostic kits and reagents that are distributed internationally and is focused on infectious diseases for the blood-banking and clinical markets. Our clinical services operations have a growing test portfolio providing companion diagnostics and high technology molecular assays. Lab21's corporate offices are based in Cambridge, UK and Greenville, South Carolina, with a GMP manufacturing site in Cambridge and other manufacturing facilities in Newmarket, Camberley, Manchester and Bridport. Website: http://www.lab21.com

About GHS

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Lab21 and ITOR launch Clinical Genomics Center in USA

By Ian Lucas MP - 6th March 2012

Ahead of tomorrow's Spinal Research parliamentary reception, Ian Lucas MP urges parliamentarians to learn more about the concerns of those afflicted with spinal cord injuries.

I first saw the devastating effects that spinal cord injuries can have on someone in my former life when working as a personal injury lawyer. I saw also how the right specialist treatment, promptly delivered, can in many cases help a patient walk again.

The reasons for the injuries varied from client to client and included road traffic accidents, sporting accidents and accidents in the workplace. At the very least the injury posed uncertainty and difficult challenges for the affected person and their families. At worst, it turned worlds upside down.

I helped form the all-party parliamentary group on spinal cord injury, which I chair, to promote greater awareness of the impact of spinal cord injuries and the importance of correct, prompt treatment. The group works closely with spinal injuries patients, medical specialists and related groups in particular, the Spinal Injuries Association. The aims of the group are to look into issues faced by people with spinal injuries, particularly focusing on developments in treatments, as well as social care and wider issues.

The group has concentrated on the importance of specialised NHS spinal units. Initial handling of a spinal cord injury at the acute stage is critical to the chances of recovery, as is timing. Patients with trauma to the spinal cord who have decompression surgery within 24 hours of the injury have a much higher chance of improved neurological recovery than those who had to wait longer. Put simply, this means that less damage will occur to the brain and nervous system if patients receive this treatment.

The specialist centres which provide such treatment need to be protected, and the debate into this and related issues will only intensify as the governments proposed reorganisation of the NHS continues to be contested.

Similarly, people with spinal cord injuries are very concerned about some aspects of the Welfare Reform Bill. Understandably, there have been calls from patients and medical specialists for reassurance and safeguards to help those most vulnerable.

Spinal Research does invaluable work. The UK-based charity funds medical research on a global scale, to develop reliable treatment for paralysis caused by a spinal injury. I am delighted to be hosting the Spinal Research Parliamentary Reception on Wednesday 7 March.

This is an opportunity for parliamentary colleagues to learn more about spinal injuries and their impact on their constituents. The event will provide a forum to discuss the current issues affecting those with spinal cord injuries, including developments in the treatment. This needs to be firmly on the political agenda. Please come along!

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Putting spinal cord injury on the political agenda

HOLLISTON, Mass., March 6, 2012 (GLOBE NEWSWIRE) -- Harvard Bioscience, Inc. (Nasdaq:HBIO - News), a global developer, manufacturer, and marketer of a broad range of tools to advance life science research and regenerative medicine is deeply saddened to learn of the passing of Mr. Christopher Lyles. Mr. Lyles was a recent recipient of a tracheal transplant regenerated in a Harvard Bioscience InBreath Bioreactor. Currently, we do not know the cause of Mr. Lyle's death. Our thoughts are with his family at this time. His family has released the following statement:

"We, the family of Christopher Lyles, sorrowfully inform you that Christopher passed away this morning, March 5, 2012. Christopher was a recipient and strong advocate of stem cell therapy. We do not want his journey to be in vain. We hope his bravery will pave the way for further research and development and acceptance of stem cell based therapies in the United States. We would like to thank everyone for their thoughts and prayers throughout Christopher's trailblazing journey."

About Harvard Bioscience

Harvard Bioscience ("HBIO") is a global developer, manufacturer and marketer of a broad range of specialized products, primarily apparatus and scientific instruments, used to advance life science research and regenerative medicine. We sell our products to thousands of researchers in over 100 countries primarily through our 850 page catalog (and various other specialty catalogs), our website, through distributors, including GE Healthcare, Thermo Fisher Scientific and VWR, and via our field sales organization. HBIO has sales and manufacturing operations in the United States, the United Kingdom, Sweden, Germany and Spain with additional facilities in France and Canada. For more information, please visit http://www.harvardbioscience.com.

The Harvard Bioscience, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=6426

Forward-looking Statements

The statements made in this press release that are not statements of historical fact are forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. You can identify these forward-looking statements by our use of such words as "will," "guidance," "objectives," "optimistic," "potential," "future," "expect," "plans," "estimates," "continue," "drive," "strategy," "crucial," "potential," "potentially," "growth," "long-term," "projects," "projected," "produce," "intends," "believes," "goals," "sees," "seek," "develop," "possible," "new," "enabling," "emerging," "opportunity," "pursue" and similar expressions that do not relate to historical matters. Forward-looking statements in this press release may include, but are not limited to, statements or inferences about the HBIO's or management's beliefs or expectations, the field of regenerative medicine, opportunities or potential opportunities in the field of regenerative medicine, HBIO's business strategy, the positioning of HBIO for growth, the market demand and opportunity for HBIO's current products or products it is developing or intends to develop, and HBIO's plans, objectives and intentions that are not historical facts.

These statements involve known and unknown risks, uncertainties and other factors that may cause HBIO's actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Factors that may cause HBIO's actual results, performance or achievements to differ materially from those in the forward-looking statements include, but are not limited to, HBIO's failure to successfully expand its product offerings, introduce new products or commercialize new technologies, including in the field of regenerative medicine, decreased demand for the HBIO's products, including products in the field of regenerative medicine, due to changes in our customers' needs, our ability to obtain regulatory approvals, including FDA approval, for our products, including any products in the field of regenerative medicine, the current size or anticipated size of the regenerative medicine market, the existence and size of opportunities in the regenerative medicine market, our financial position, plus risk factors set forth under the heading "Item 1A. Risk Factors" in HBIO's Annual Report on Form 10-K for the fiscal year ended December 31, 2010 or described in HBIO's other public filings. HBIO's results may also be affected by factors of which HBIO is not currently aware. HBIO may not update these forward-looking statements, even though its situation may change in the future, unless it has obligations under the federal securities laws to update and disclose material developments related to previously disclosed information.

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Harvard Bioscience Comments on the Passing of Christopher Lyles

Public release date: 6-Mar-2012 [ | E-mail | Share ]

Contact: Elisabeth (Lisa) Lyons elyons@cell.com 617-386-2121 Cell Press

In a perfect world, we could eat to our heart's content without sacrificing our health and good looks, and now it appears that maybe we can. Mice with an extra dose of a known anti-cancer gene lose weight even as their appetites grow. Not only that, but according to the report in the March issue of the Cell Press journal Cell Metabolism, the animals also live longer, and that isn't just because they aren't getting cancer, either.

One of the animals' youthful secrets is hyperactive brown fat, which burns energy instead of storing it. The findings add to evidence that tumor suppressors aren't designed only to protect us against cancer, the researchers say. They also point to new treatment strategies aimed to boost brown fat and fight aging.

"Tumor suppressors are actually genes that have been used by evolution to protect us from all kinds of abnormalities," said Manuel Serrano of the Spanish National Cancer Research Center.

In this case, the researchers studied a tumor suppressor commonly lost in human cancers. Mice with an extra copy of the gene known as Pten didn't get cancer, but that's not the half of it. Those mice were also leaner, even as they ate more than controls, Serrano said. That suggested that the animals were experiencing some sort of metabolic imbalanceand a beneficial one at that.

Cancer protection aside, the animals lived longer than usual. They were also less prone to insulin resistance and had less fat in their livers. Those benefits seem to trace back to the fact that those Pten mice were burning more calories thanks to overactive brown fat. Studies in isolated brown fat cells confirmed that a boost in Pten increases the activity of those cells. Pten also made it easier for brown fat to form.

"This tumor suppressor protects against metabolic damage associated with aging by turning on brown fat," Serrano says.

A small compound inhibitor that mimics the effects of Pten also came with those varied benefits. That's encouraging news for the prospect of finding a drug that might do for us what the extra Pten gene did for the mice.

After all, Serrano said, humans were built for a time when 30 would have been considered old age. "We're well protected against cancer and cardiovascular disease" early in life. As it has become commonplace to live to the age of 80, we could all use a little help.

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With extra gene, mice are footloose and cancer free

Public release date: 6-Mar-2012 [ | E-mail | Share ]

Contact: Juan J. Gmez juanj.gomez@cnio.es Centro Nacional de Investigaciones Oncologicas (CNIO)

This result, obtained after five years' research, is published in leading journal Cell Metabolism. The authors, led by Manuel Serrano (CNIO), believe it will open the door to new therapeutic options not only against cancer, but against obesity and even the ageing process.

The team has also demonstrated that a synthetic compound developed in-house produces the same anti-obesity benefits in animals as the study gene.

Their findings add new weight to a hypothesis that is gaining currency among researchers in the field; namely that cancer and ageing, and now obesity too, are all manifestations of the same global process that unfolds in the body as its tissues accumulate more damage than natural repair mechanisms are able to cope with.

Prominent among these natural repair mechanisms are a small set of genes noted primarily for their protective effect against cancer. In recent years, some of these genes have also been shown to promote longevity again by researchers from the CNIO and to play a significant role in other high-incidence conditions like diabetes and cardiovascular diseases.

The Serrano team set out to test whether the Pten gene, one of the four most potent anti-cancer genes, could be linked to other beneficial effects, particularly longevity.

And it turns out the answer is yes. The CNIO researchers created transgenic mice with double the standard levels of the Pten protein. The animals, as anticipated, proved far more resistant to cancer than their non-transgenic fellows. But they also lived an average of 12% longer.

This effect is independent of cancer resistance. It is not that the mice die of cancer later than otherwise, but that those that never develop cancer also live longer and exhibit fewer ageing-related symptoms. As the researchers put it, "Pten has a direct impact on length of life."

A "real surprise"

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CNIO scientists discover in studies with mice that an anti-cancer gene also fights obesity

London, March 6 (ANI): A gene involved in fat taste may explain why some people like fatty foods and others prefer low-fat diets, a new study suggests.

About five years ago, animal studies first revealed the presence of entirely novel types of oral fat sensors or receptors on the tongue.

Prior to this time, it was believed that fats were perceived only by flavour and texture cues. With this new information, "everything that we thought we knew about fat perception got turned on its head," said Beverly Tepper, a professor in the Department of Food Science at Rutgers School of Environmental and Biological Sciences.

Tepper has been studying consumer preferences for high-fat versus low-fat foods, and has been intrigued by the questions: "Why are some people more sensitive and others less sensitive to fat?" "Is this a personal trait?" "And do genes contribute to these differences?"

Those new discoveries suggest that fats are perceived on the tongue as a "taste" sensation by binding to specialized receptors on taste buds.

More specifically, Tepper explained, "fats are broken down in the mouth to fatty acids, and it's the fatty acids that bind to these receptors."

One oral fat receptor that has attracted a great deal of recent attention is CD36, a carrier protein that helps fatty acids traverse cell membranes in many tissues of the body.

But how is CD36 related to consumer fat preferences and the possible genetic differences that Tepper and colleagues are so keen on understanding?

The answer lies in a new study by Tepper, in conjunction with her former student Kathleen Keller, who received her Ph.D. in 2002 from Rutgers' graduate program in nutritional sciences.

Keller, now an assistant professor of nutritional sciences at The Pennsylvania State University and lead author on the article, studied an overweight population of African-American adults and found those who had a specific change or variation in the CD36 gene perceived the creaminess and fattiness of salad dressings quite well, but they were less able to differentiate the high-fat from the low-fat versions.

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Gene linked to preference of high-fat foods

05-03-2012 18:07 Dead Doctors Don't Lie Program 02 March 2012 Monologue Dr. Wallach starts the show discussing genetic diseases. Contending that most diseases that have been deemed "genetic" such as Lou Gehrigs disease, Alzheirmer's, Type 2 diabetes and arthritis. Asserting these are due to nutritional deficiencies either in the child or in the mother during conception. Pearls of Wisdom Doug Winfrey and Dr. Wallach discuss two news articles concerning anti-depressant drugs. A study conducted by a Harvard psychologist an Irving Kirsch who has researched the "placebo effects" for over 30 years. Using data he obtained through the Freedom of Information Act has concluded that anti-depressant drug clinical trials showed no proof of efficacy. Finding that several trials showed no efficacy and a small amount showed some efficacy. Only these trials were submitted to the FDA and were ultimately approved for the market. Irving Kirsch has concluded those showing some efficacy were due to the placebo effect. Calls * Bruce has questions regarding joint pain. * JP asks questions concerning hypertension, high cholesterol and ED (erectile dysfunction). * Ray has frequent urination and sinusitis. * Greg has two questions the first concerns his father who has neuropathies in his legs and gout. Second he has questions regarding a friend's mother who has kidney cancer. Call Dr. Wallach's live radio program weekdays from noon until 1pm pacific time at 831-685-1080 or toll free at 831-685-2552. to add comment ...

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3/5 Dead Doctors Don't Lie Program - Genetic Diseases - Video

05-03-2012 18:36 Dead Doctors Don't Lie Program 02 March 2012 Monologue Dr. Wallach starts the show discussing genetic diseases. Contending that most diseases that have been deemed "genetic" such as Lou Gehrigs disease, Alzheirmer's, Type 2 diabetes and arthritis. Asserting these are due to nutritional deficiencies either in the child or in the mother during conception. Pearls of Wisdom Doug Winfrey and Dr. Wallach discuss two news articles concerning anti-depressant drugs. A study conducted by a Harvard psychologist an Irving Kirsch who has researched the "placebo effects" for over 30 years. Using data he obtained through the Freedom of Information Act has concluded that anti-depressant drug clinical trials showed no proof of efficacy. Finding that several trials showed no efficacy and a small amount showed some efficacy. Only these trials were submitted to the FDA and were ultimately approved for the market. Irving Kirsch has concluded those showing some efficacy were due to the placebo effect. Calls * Bruce has questions regarding joint pain. * JP asks questions concerning hypertension, high cholesterol and ED (erectile dysfunction). * Ray has frequent urination and sinusitis. * Greg has two questions the first concerns his father who has neuropathies in his legs and gout. Second he has questions regarding a friend's mother who has kidney cancer. Call Dr. Wallach's live radio program weekdays from noon until 1pm pacific time at 831-685-1080 or toll free at 831-685-2552. to add comment ...

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4/5 Dead Doctors Don't Lie Program - Genetic Diseases - Video

CAMBRIDGE, Mass.--(BUSINESS WIRE)--

Foundation Medicine, Inc., a molecular information company that brings comprehensive cancer genomic analysis to routine clinical care, today announced a collaboration with Array BioPharma (NASDAQ: ARRY - News). Foundation Medicine will use its genomic sequencing and analytic capabilities to assess potentially relevant molecular alterations to assist Array in targeting patients that are most likely to respond to treatment.

Foundation Medicine has established a remarkable portfolio of collaborations around the discovery and clinical development of targeted cancer therapeutics, said Michael J. Pellini, M.D., president and chief executive officer of Foundation Medicine. The molecular information generated by our platform is designed to help biopharma companies like Array expedite the development of targeted drug candidates that impact the genomic pathways driving a specific cancer.

Array has a portfolio of targeted cancer agents in early stages of clinical development. Through this collaboration with Foundation Medicine, Array intends to determine the genetic profile of tumors of patients who are treated with certain of its anticancer agents. The goal of this work is to understand how to identify patients who may respond to a given targeted therapy to ensure that each patient gets the optimal drug to treat their individual disease.

Foundation Medicines industry and academic partnerships complement the companys core cancer diagnostics capability, a comprehensive cancer genomic test that provides physicians with genomic information that may help match patients with treatments or clinical trials specific for the genomic profile of their tumor.

About Foundation Medicines Comprehensive Cancer Genomic Test

Foundation Medicines comprehensive cancer genomic test uses next-generation sequencing to analyze routine clinical specimens (i.e., small amounts of formalin fixed, paraffin embedded tumor tissue) for molecular alterations in approximately 200 cancer-related genes. The test is optimized for clinical-grade analysis of tumor tissues, overcoming multiple complexities (such as purity, ploidy, and clonality) inherent to tumor genomes. Test results are reported through a secure, interactive website linking genomic data to a structured knowledge base of relevant, publicly available scientific and medical information. The company also aims to provide information on relevant clinical trials to enable a more rapid recruitment of patients into trials for targeted therapies. Foundation Medicines test can serve as a helpful decision-support tool for physicians to recommend cancer treatment approaches tailored to each patients molecular subtype.

About Foundation Medicine

Foundation Medicine is dedicated to improving cancer care through the development of comprehensive cancer diagnostics that will help physicians inform treatment decisions based on an individual patients molecular cancer subtype. Foundation Medicines first laboratory developed test, based on a next-generation sequencing platform, is designed to accommodate a broad landscape of cancer genome information and a growing repertoire of targeted treatments and clinical research opportunities. Foundation Medicines test will assist physicians to make prompt and informed determinations about the best cancer treatments and clinical trial options for each patient, taking into account each patients unique cancer-associated alterations alongside publicly available scientific and medical information. The companys founding advisors are world leaders in genome technology, cancer biology and medical oncology; they, alongside clinicians, biotech and molecular diagnostics industry leaders, are working to harness emerging technologies to develop unparalleled tests that will identify and interpret an ever-growing set of actionable genomic alterations, truly enabling personalized cancer medicine. For more information, please visit the companys website at http://www.foundationmedicine.com.

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Foundation Medicine Announces Collaboration with Array BioPharma

Eight mutations occurred in the common bacteria Staphylococcus aureus as it turned from an innocuous resident inside one persons nose into a fatal blood infection, an Oxford University study has found.

The study, which sequenced the complete DNA of the bacteria at regular time intervals, was able to identify for the first time the genetic changes that accompanied the transition to a dangerous infection.

Understanding the biological causes of serious bacterial infections could help guide screening in hospitals, and could inform efforts to develop vaccines against such infections. The study is published in the journal PNAS and was carried out in partnership with Oxford University Hospitals NHS Trust through the National Institute of Health Research (NIHR) Oxford Biomedical Research Centre.

"We have observed a significant genetic change in the bacteria corresponding with the development of a fatal blood infection," said Dr Bernadette Young of the Nuffield Department of Clinical Medicine at Oxford University, one of the lead researchers.

"It is one case study we simply dont know how much these results will be mirrored in others. But it could be a step towards identifying genetic changes that may be important in driving infection generally."

S. aureus is common, with one in four people carrying it inside the nose without any symptoms. Occasionally S. aureus can cause serious invasive infections, such as blood poisoning. Blood poisoning can develop as a complication of a skin infection, or via medical equipment that goes inside the body such as a feeding tube or catheter. But sometimes it appears to occur spontaneously, and it is thought that this can happen when nasal bacteria change in some way to allow invasive disease.

The Oxford researchers set out to understand more about the carriage of S. aureus inside the nose. They enrolled over 1,100 adults at GP practices in Oxfordshire and carried out nasal swabs. 360 people were found to carry S. aureus, who were then monitored with regular nasal swabs.

However, one elderly participant became ill a number of months into the study. The participant developed a serious condition requiring treatment, but soon after became unwell with blood poisoning and later passed away.

Complete DNA sequencing of the bacteria from the patients blood showed just a handful of changes from the bacteria in nose swabs before the patient became ill. It was the same bug causing infection that had been carried in the nose. But the few DNA changes may have been significant.

Eight new mutations were detected in the bacterial DNA from the patients blood. Four of the mutations cut genes short and are likely to have impaired the functions of bacterial proteins. One of these was in a protein that regulates stress response and virulence in S. aureus and could conceivably be connected to a biological change leading to infection.

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Genetic changes tracked as bacteria become a fatal infection