Two neurospheres forming connections

Two neurospheres, compact masses of neuron precursor cells, derived from human embryonic stem cells, as captured by a fluorescent microscope. Differentiated neurons, whose nuclei are shown in red, have begun to extend neuronal processes (green) toward one another, forming connections.

The image was taken in the lab of Fred H. Gage at the Salk Institute for Biological Studies.

GoogleNews.com, May 6, 2010, by Clive Cookson  –  Regenerative medicine has immense potential for renewing failing or damaged tissues throughout the body, from the skin on the surface to organs deep inside. But the most exciting prospect is for regeneration of the brain and nervous system, both because the unmet medical need is so great and because the science is so challenging.

There are two complementary approaches to neural regeneration. The more traditional one is cell therapy – putting new neurons – nerve cells – or their progenitor cells into the brain or nervous system.

The first transplants of foetal neurons into Parkinson’s disease patients took place in the 1980s – with mixed results – and today several companies are on the brink of clinical trials of therapies based on stem cells.

They include: ReNeuron of the UK, which is about to test neural stem cells in stroke patients; and Geron, from California, which plans to treat acute spinal injury with nerve cells derived from human embryonic stem cells.

The other possibility is to stimulate the latent power of some human neurons to regenerate themselves. Scientists have long known that neuro­genesis takes place in more primitive organisms, including some fish and amphibians, but one of the dogmas of 20th century neuroscience – that adult humans do not make new brain cells – was only overturned in the late 1990s.

The discovery then of adult neurogenesis at the Salk Institute in California has inspired a great wave of research, as scientists and biotechnology companies look for ways to increase the low natural level of brain cell generation, without risking the cancer that might accompany unnatural neural growth.

“Very little is known still about human neurogenesis, because it is difficult to look at the growth of neurons in the living human brain,” says Mike Modo of the Institute of Psychiatry in London. “But in postmortems of stroke victims, there is clear evidence of neurogenesis after the stroke.”

Sygnis Pharma, a German biotechnology company, wants to achieve this effect with a protein called “granulocyte colony stimulating factor” or G-CSF, produced naturally in the brain after a stroke – apparently acting both to reduce cell death in the acute phase and to stimulate subsequent regeneration of blood vessels and neurons.

After successful animal tests, Sygnis is undertaking a clinical trial to assess the efficacy of its G-CSF treatment – which the company calls AX200. About 350 stroke patients are taking part in the double-blinded trial; half will receive an infusion of AX200 and the other half a placebo saline solution.

Results are expected in the middle of next year.

A Swedish company, Neuro­Nova, is following a similar approach with two neuro-stimulating proteins – both in early clinical trials. One is a formulation of “platelet-derived growth factor” (PDGF) to treat Parkinson’s disease; the other contains “vascular endothelial growth factor” (VEGF) for amyotrophic lateral sclerosis (known in the US as Lou Gehrig’s disease), the most common form of motor neuron disease.

A third neurogenesis company, BrainCells of San Diego, is taking a different tack. It is pursuing the discovery made in 2003 by one of its founders, René Hen of Columbia University, that antidepressant drugs achieve some of their effects by stimulating the growth of neurons in the hippocampus, a brain area involved in learning and memory.

In contrast to Sygnis and Neuro­Nova, whose early work is focusing on proteins that might help people with serious or acute brain disease, BrainCells is concentrating initially on “small molecule” chemicals that people can take as pills or capsules, with a screening programme that has looked at hundreds of potential drugs to find the ones that best trigger the proliferation of new neurons in cell cultures.

Two of its drugs are already giving promising results in clinical trials with patients suffering from severe depression and anxiety, who do not respond to existing antidepressants.

In terms of results, there may not be much practical difference between the two approaches to brain repair – transplanting neurons and stimulating the brain’s intrinsic growth potential – because animal experiments suggest that cell transplants are particularly good at stimulating neurogenesis. This is because the very presence of newly transplanted cells seems to help the brain repair itself, by activating its own “endogenous” stem cells and growth factors.

Mr Modo says that in cases of serious brain injury or disease, a third component may be necessary for effective treatment. Shrinkage and neuronal death often leave a hole in the brain, which transplanted and regenerated cells cannot fill on their own.

A potential solution then is to add a scaffold, made from biocompatible materials and laden with neurostimulating factors, which can guide and support the cells as they grow.

Neural regeneration may be a young field, with much still to prove, but it is one of the fastest growing and most exciting in the whole of bioscience.

By Duke University Medical Center
May 6, 2010

(HealthNewsDigest.com) – A class of drugs commonly used for asthma, inflammation, and skin injury also may hold promise for tissue-repairing regenerative medicine, according to Duke University Medical Center researchers.

In studies on cells from mice, the drugs, a kind of steroid hormone called glucocorticoids, appear to be promoting and protecting stem cell populations that perform tissue repair.

“We found that these common compounds could help to produce populations of (nerve-repairing) neuronal stem cells, and may even have a protective effect on the new stem cells, which could assist in tissue repair processes,” said senior author Wei Chen, PhD, assistant professor in the Duke Department of Medicine. “Next we would like to study how these drugs work in specific conditions, starting with spinal cord injury repair and neural regeneration in the setting of Parkinson’s disease.”

The research was published online in the Proceedings of the National Academy of Sciences the week of May 3.

Chen said the findings are exciting because millions of people have taken the glucocorticoid drugs, and the drugs are well known to be safe. He foresees new roles for these drugs to help grow new blood vessel networks after heart attack, to improve wound healing in people with diabetes, and to stimulate hair growth.

“This work is an excellent example of basic science research having the potential to positively impact patients in unexpected ways,” said H. Kim Lyerly, MD, George Barth Geller Professor of Research in Cancer and director of the Duke Comprehensive Cancer Center. “This discovery may pave the way to better therapies for conditions from spinal cord injury to neuron degeneration. In addition, it allows us to look at cancer risk and potential cancer therapies in new ways that may benefit patients and their families.”

The Duke researchers were searching for a medication that activates a cell-signaling pathway called “Hedgehog” that is critical to stem cell growth. They found that these glucocorticoid drugs — especially fluticasone, halcinonide, clobetasol, and fluocinonide — stimulated a receptor called “Smoothened,” which in turn helped to stimulate stem cell growth and protect neuronal cells.

Chen said Smoothened works by activating the Hedgehog pathway, which in turn regulates stem cells, and is important in embryo growth and mature tissue integrity and repair. Although genetic mutations of Smoothened are linked with skin cancer, these drugs that activate the pathway have a proven safety record over more than two decades. Researchers and clinicians have not found any evidence of cancer association with glucocorticoid drugs, Chen said.

The PNAS paper is a proof of principle that the glucocorticoids used in asthma might work for asthmatic tissue remodeling in lung injury models, Chen said. “Asthma drugs like fluticasone provide a chemical means to treat inflammation,” Chen said. “No one thought that fluticasone could help asthmatic patients because it might be doing something to protect new cells.”

“Using medicinal chemistry, we hope to be able to create effective and safe compounds that will be new tools for the science of regenerative medicine,” Chen said.

Other authors included Larry Barak of the Duke Department of Cell Biology, and Jiangbo Wang, Jiuyi Lu, Michael Bond, Minyong Chen, and Xiurong Ren of the Duke Department of Medicine.

The study was funded by NIH grants, the V Foundation, the American Cancer Society, and funds from Alice and Fred Stanback.

The New York Times, April/May 2010, by Tara Parker-Pope  –  After we hit 40, many of us begin to worry about our aging brains. Will we spend our middle years searching for car keys and forgetting names?

The new book “The Secret Life of the Grown-Up Brain: The Surprising Talents of the Middle-Aged Mind,” by Barbara Strauch, has the answers, and the news is surprisingly upbeat. Sure, brains can get forgetful as they get old, but they can also get better with age, reports Ms. Strauch, who is also the health editor at The New York Times. Ms. Strauch, who previously tackled teenage brains in her book “The Primal Teen,” spoke with me this week about aging brains and the people who have them. Here’s our conversation:

Barbara Strauch

Q.

After exploring the teenage brain, why did you decide to write a book about grown-ups?

A.

Well, I have a middle-aged brain, for one thing. When I would go give talks about “The Primal Teen,” I’d be driven to the airport or back by a middle-aged person, and they’d turn to me and say: “You should do something about my brain. My brain is suddenly horrible. I can’t remember names.” That’s why I started looking into it. I had my own middle-aged issues like going into an elevator and seeing somebody and thinking, “Who are you?”

Q.

So what’s the bad news about the middle-aged brain?

A.

Obviously, there are issues with short-term memory. There are declines in processing speed and in neurotransmitters, the chemicals in our brain. But as it turns out, modern middle age is from 40 to 65. During this long time in the middle, if we’re relatively healthy our brains may have a few issues, but on balance they’re better than ever during that period.

Q.

Do teenage brains and middle-aged brains have much in common?

A.

The thing the middle-aged brain shares with the teenage brain is that it’s still developing. It’s not some static blob that is going inexorably downhill. Scientists found that when they watched the brains of teenagers, the brains were expanding and growing and cutting back and shaping themselves, even when the kids are 25 years old. I think for many years scientists just left it at that. They thought that from 25 on, we just get “stupider.” But that’s not true. They’ve found that during this period, the new modern middle age, we’re better at all sorts of things than we were at 20.

Q.

So what kinds of things does a middle-aged brain do better than a younger brain?

A.

Inductive reasoning and problem solving — the logical use of your brain and actually getting to solutions. We get the gist of an argument better. We’re better at sizing up a situation and reaching a creative solution. They found social expertise peaks in middle age. That’s basically sorting out the world: are you a good guy or a bad guy? Harvard has studied how people make financial judgments. It peaks, and we get the best at it in middle age.

Q.

Doesn’t that make sense, since our young adult lives are often marked by bad decisions?

A.

I think most of us think that while we make bad decisions in our 20s, we also have the idea that we were the sharpest we ever were when we were in college or graduate school. People think if I tried to go to engineering school or medical school now, I couldn’t do it. Because of these memory problems that happen in middle age, we tend to think of our brains as, on the whole, worse than in our 20s. But on the whole, they’re better.

Q.

So what’s happening in middle age that leads to these improvements?

A.

What we have by middle age is all sorts of connections and pathways that have been built up in our brain that help us. They know from studies that humans and animals do better if they have a little information about a situation before they encounter it. By middle age we’ve seen a lot. We’ve been there, done that. Our brains are primed to navigate the world better because they’ve been navigating the world better for longer.

There also are some other physical changes that they can see. We used to think we lost 30 percent of our brain cells as we age. But that’s not true. We keep them. That’s probably the most encouraging finding about the physical nature of our brain cells.

Q.

Is there anything you can do to keep your brain healthy and improve the deficits, like memory problems?

A.

There’s a lot of hype in this field in terms of brain improvement. I did set out to find out what actually works and what we know. What we do with our bodies has a huge impact on our brains. Our brains are more like our hearts in that everything you do for your heart is thought to be equally as good or better for your brain. Exercise is the best studied thing you can do to your brain. It increases brain volume, produces new baby brain cells in grownup brains. Even when our muscles contract, it produces growth chemicals. Using your body can help your brain.

Q.

What about activities like learning to play an instrument or learning a foreign language?

A.

The studies on this are slim. We’ve all been told to do crossword puzzles. Learning a foreign language, walking a different way to work, all that is an effort to make the brain work hard. And it’s true we need to make our brains work hard. One of the most intriguing findings is that if you talk to people who disagree with you, that helps your brain wake up and refine your arguments and shake up the cognitive egg, which is what you want to do.

Q.

Do social connections and relationships make a difference in how the brain ages?

A.

There is a whole bunch of science about being social and how cognitive function seems to be better if you are social. There is a fascinating study in Miami where they studied people who lived in apartments. Those who had balconies where they could see their neighbors actually aged better cognitively than others. There are a whole bunch of studies like that. People who volunteer and help kids seem to age better and help their brains. We forget how difficult it is to meet, greet and deal with another human being. It’s hard on our brains and good for them.

Q.

What was the most surprising thing you learned about the middle-aged brain?

A.

The hope I saw from real scientists was surprising. A lot of the myths we think of in terms of middle age, myths that I grew up with, turn out to be based on almost nothing. Things like the midlife crisis or the empty nest syndrome. We’re brought up to think we’ll enter middle age and it will be kind of gloomy. But as scientists look at real people, they find out the contrary. One study of men found that well-being peaked at age 65. Over and over they find that middle age, instead of being a time of depression and decline, is actually a time of being more optimistic overall.

http://ngm.nationalgeographic.com/2007/11/memory/brain-interactive

Go to the link above, for interactive brain information

GoogleNews.com, 5/6/2010

CHICAGO — If you think only U.S. biotech companies will be interested in coming to Rochester, Pine Island and other southeast Minnesota locations, you might be surprised by the locations some companies at the Biotechnology Industry Organization conference this week are coming from when they approach local representatives at the Minnesota pavilion.

Rochester Mayor Ardell Brede spoke at BIO Tuesday with a representative of a European company that wants to treat heart disease with stem cells.

Whether by design or happenstance, Rochester appears headed for a transformation that will make it a mecca for” regenerative medicine” — the science of producing replacement tissue and organs.

In biotech’s future, “we will continue to see progress in stems cells and regenerative medicine,” G. Steven Burrill told thousands of audience members who attended his BIO “supersession” keynote in Chicago Tuesday.

Mayo Clinic CEO Dr. John Noseworthy told the Post-Bulletin editorial board last week that Mayo has made regenerative medicine one of its top priorities. That makes Brede’s conversation with a European biotech especially compelling.

His contact expressed concern about the size of Rochester’s airport. But Brede pointed out that if the biotech brings its own 747, Rochester can handle it.

“I pointed out the many flights we have,” Brede said. He noted that the King of Jordan flew into the airport and that Fed-Ex has multiple daily fights.

He described how IBM used to struggle to attract employees to Rochester but then it found that it was even more difficult to get them to transfer away than it was to attract them in the first place. He noted that Rochester has a highly skilled workforce, with many people following a spouse to Mayo but wishing for a more-diversified work environment.

“We talked a great deal about the diversity of the community, the closeness of the Twin Cities,” Brede said. The Belgium company is interested in first an office and later a manufacturing facility in the Rochester area.

No deals were signed and no promises made. But connecting with companies that have an interest is the point of attending the conference for local representatives.

“So who knows?” Brede said. “It’s a possibility.”

Mayo Clinic spokeswoman Kathy Anderson said the clinic’s Office of Intellectual Properties had perhaps 50 or more requests Tuesday alone from companies interested in licensing Mayo technologies that are ready for commercialization.

BIO, she said, is “really great networking for us.”

Separately, John Wade, president of the Rochester Area Chamber of Commerce, said he, too, had good experiences at BIO Tuesday.

“We were focusing some effort on Brazil and Australia, and met with some folks from Korea as well. You explain a little bit about what Minnesota has to offer. I found the people from Brazil, Australia and Korea particularly interested in partners who want to collaborate, with a strong U.S. partner,” Wade said.

Again, no deals were made. But it’s this kind of development work that can later lead to deals, or even business collaborations without a direct company presence. But it’s not just about coaxing a company to come to southeast Minnesota for the science. The company also has to be convinced its workforce would want to live in the area.

“If we can also sell a great community, people will respond to that,” Wade said.

American Society of Hypertension (ASH) 25th Annual Scientific Meeting and Exposition

Drs Suzanne Oparil and Louis Aronne

 

Medscape.com, by Lisa Nainggolan, May 6, 2010 (New York, New York) — New data on an investigational weight-loss therapy, a combination of phentermine and controlled-release topiramate, have unusually been presented at the American Society of Hypertension (ASH) 2010 Scientific Meeting. The highest dose of the drug combination induced a “substantial” weight loss of 10% after one year and resulted in significant drops in systolic blood pressure, reported Dr Suzanne Oparil (University of Alabama at Birmingham).

Obesity expert Dr Louis Aronne (Weill Cornell Medical Center, New York), who worked with Oparil on the studies, told heartwire that the “clever thing is in the combination.” Oparil concurred: “They [phentermine and topiramate] work together.” However, they stressed the importance of this particular formulation, which uses a controlled-release form of topiramate, an anticonvulsant drug, and “very, very” low doses of phentermine, an appetite suppressant, and strongly advised against anyone trying to use currently available forms of these drugs together. “Don’t try this at home,” Oparil cautioned.

Asked by heartwire why a pooled analysis of trials on an obesity drug had been presented as a late breaker at a hypertension meeting, ASH president Dr Henry Black said: “We’re about more than just blood pressure; we’re about cardiovascular risk.”

Product to Be Discussed by an FDA Advisory Committee This Summer

The combination product, which if approved will be known as Qnexa (Vivus), is to be discussed by an FDA advisory committee this summer, Aronne told heartwire . It will be appropriate for patients with a body-mass index (BMI) of 27 to 30 and comorbidities or those with a BMI of >30, he said, and therefore will potentially fill “a big gap between diet/physical activity and surgery. This is a breakthrough; drugs that we know are effective but using more appropriate doses.

Don’t try this at home.

“The trend now is to use less invasive surgeries and combination therapies, and these things are beginning to meet in the middle, and that’s where the greatest need is,” Aronne added. “If your BMI is very high, then surgery might be the thing to do; if your BMI is a little bit above normal, then diet and exercise is the best thing, but what do you do for the millions, a third of the population, who fit in the middle and have all the risk and are appearing in the doctor’s office with all these complications?”

ASH president-elect Dr George Bakris (University of Chicago Pritzker School of Medicine, IL) agrees. He told heartwire that Qnexa could “definitely” fill the gap left by Sanofi-Aventis’s rimonabant, which was never approved in the US and was removed from the market in Europe and elsewhere because of psychiatric side effects. “I like it. It’s been packaged with careful thought about the correct doses, of how to use them. There is a very meaningful drop in body weight and, unlike what I predicted knowing the drugs individually, blood pressure went down.”

Bakris says the latter is important because the product “is not revving the system very much, the weight loss is overcoming any potential [BP] increase you would see [from phentermine].” He also emphasized the warnings of Oparil and Aronne, stressing how important it is that people do not try to re-create this cocktail of drugs themselves: “You could easily blow out your heart or your brain if you use those high doses; they will rev the catecholamine system and raise your pressure dramatically.”

Oparil reported the findings of a pooled analysis of three Qnexa studies in a press conference and presented them at the late-breaking clinical-trial session.

She explained that the product harnesses the effects of the two different but complementary mechanisms specific to each component, phentermine and topiramate, “which allows for lower doses of each agent, which should be safer.” Phentermine was part of the controversial fen-phen combination used for weight loss, use of which was abandoned when fenfluramine was associated with abnormal valvular regurgitation.

Phentermine, as an appetite suppressant, works immediately, and then the sustained-release form of topiramate is longer lasting, inducing a sense of satiety, Oparil said.

The three trials included in her analysis were EQUATE, which compared full-dose Qnexa (15 mg of phentermine/92 mg of topiramate sustained release [SR]) and mid-dose Qnexa (7.5 mg/46 mg) with placebo and the respective single agent phentermine and topiramate components for 28 weeks in obese adults (BMI >27); EQUIP, which compared full-dose and low-dose (3.75 mg/23 mg) Qnexa with placebo for 56 weeks, again in obese individuals (BMI>35); and CONQUER, which compared full-dose and mid-dose Qnexa with placebo for 56 weeks in “all-comers,” including the obese and overweight adults (BMI 27–45) who had to have two or more weight-related comorbidities.

After 28 weeks, the primary end point–least-squares (LS) mean percentage weight loss of the intention-to-treat last-observation-carried-forward (ITT-LOCF) population–was significantly greater for all the doses of Qnexa: reductions were 9.9% with the full dose (n=1581), 8.0% with the mid dose (n=591), 5.1% (n=234) with the low dose, and 1.9% (n=1579) with placebo (p<0.0001 for all doses of Qnexa vs placebo).

The 56-week data, from CONQUER and EQUIP, showed that the weight loss was maintained out past a year: 1479 patients taking the full dose had a mean weight loss of 10.4%; 488 taking the mid dose lost, on average, 8.2% of body weight, and 234 on the lowest dose lost 4.7%, all of which were significant losses compared with the 1.5% mean loss in the 1477 placebo patients (p<0.0001).

Adverse reactions were “characteristic” of those that would be expected from these two agents, said Oparil, including altered taste, constipation, dizziness, dry mouth, and headache.

And discontinuations due to side effects were higher with Qnexa, peaking at 17.5% of patients on the highest dose and around 11.5% of those on the mid and low doses, compared with 8.5% on placebo.

Topiramate Contributes to BP Reduction, as Does Weight Loss

Overall in the three trials, significantly greater reductions in mean blood pressure were seen with the mid and high doses of Qnexa, compared with placebo, averaging a decrease of 6.5/2.8 mm Hg with the higher dose and 6.8/3.1 with the mid-dose, compared with a drop of 3.1/1.3 mm Hg with placebo.

And among a prespecified subgroup of patients with hypertension enrolled in the all-comers CONQUER trial, the only doses of Qnexa tested, mid and high, also led to statistically significant reductions in BP, of 9.1/5.8 mm Hg with the high dose and 6.9/5.2 mm Hg for the mid dose compared with 4.9/3.9 mm Hg with placebo. This illustrates “that the BP reduction in the hypertensive subjects was comparable with the study group as a whole,” said Oparil.

In addition, 10.5% and 6.6% of the hypertensive patients in CONQUER taking the high and mid doses of Qnexa, respectively, were able to reduce the number of antihypertensive medications they were on over the year of the study, compared with a net increase of 3.4% in such medications seen in the placebo group.

Oparil explained that topiramate itself has some intrinsic antihypertensive efficacy and that the weight loss incurred among those taking the active drug combination also contributes to the reduction in blood pressure that is seen.

“If you can get people to lose weight you get a lot of benefits–improvement in every cardiometabolic risk factor,” Aronne commented.

Oparil agreed, adding that if patients can lose even a little bit of weight, it may motivate them to exercise and diet more aggressively to get to where they should be: “It takes away the hopelessness.” Such weight loss might also enable adjustment of doses of antihypertensive medications or even eventually allow doctors “to take away an antihypertensive medication people didn’t like,” she concluded.

Oparil and Aronne are consultants to Vivus.

GoogleNews.com, May 6, 2010   –   A combination of antiviral drugs may be needed to combat the drug resistance that rapidly develops in potentially deadly hepatitis C infections, a new study using sophisticated computer and mathematical modeling has shown.

 Using probabilistic and viral dynamic models, researchers at the University of Illinois at Chicago, Oakland University and Los Alamos National Laboratory predict why rapid resistance emerges in hepatitis C virus and show that a combination of drugs that can fight three or more mutated strains may be needed to eradicate the virus from the body. They compared their model with data from a clinical trial of the new direct-acting antiviral medication telaprevir.

The findings are published in Science Translational Medicine.

Hepatitis C is a progressive liver disease that can lead to cirrhosis and liver cancer. Current standard treatment is a combination of the antiviral drugs interferon and ribavirin for a period of 24 to 48 weeks — a regimen that is long and expensive, carries side effects, and is successful only in about half of patients.

Intensive effort has focused on developing direct antiviral drugs. But the virus is genetically diverse, and so may be particularly prone to develop resistance, said Harel Dahari, research assistant professor of hepatology in the UIC College of Medicine and one of the paper’s co-authors.

One way to combat resistance would be to administer multiple drugs, each with a different mechanism of inhibiting the virus.

“We found that rapid emergence of resistance to these types of drugs is due to a population of viruses already present, allowing the resistant virus to become the dominant strain,” said Dahari.

The researchers suggest that a combination of new antiviral drugs will be needed to fight all of the resistant virus strains and achieve better cure rates for the disease.

“We are moving to a new era where we can treat these patients with direct-acting agents against the virus, in which we specifically target the life-cycle of the virus,” Dahari said.

To replace the standard treatment, four or more different types of direct drugs may be needed, Dahari said. However, some patients may need fewer drugs. It depends on the level of the virus in their blood, among other factors.

It is frustrating for patients to go through a long, difficult treatment and know that they might not be cured, said Dr. Scott Cotler, associate professor of medicine at UIC and a hepatologist who treats patients at the University of Illinois Medical Center’s Walter Payton Liver Center.

“Patients are looking forward to a day when they don’t have to take interferon and ribavirin,” said Cotler. “But as we are learning with this study, if we are going to need four different direct drugs, it is going to be awhile before we get there. Now at least we know where the goal line is.”

Dahari suggests that future treatment that includes the standard treatment and direct antivirals, such as telaprevir or boceprevir, will be tailored to each patient and that using direct antivirals may also shorten the duration of treatment.

Provided by University of Illinois at Chicago

PRESS RELEASE

May 6, 2010

PALO ALTO, Calif., May 6, 2010 (GlobeNewswire via COMTEX) — StemCells, Inc. /quotes/comstock/15*!stem/quotes/nls/stem (STEM 1.16, 0.00, 0.00%) announced today that Martin McGlynn, President and CEO, and Stewart Craig, Ph.D., Senior Vice President, Development and Operations, will each present at the Fifth Annual World Stem Cells and Regenerative Medicine Congress to be held May 11 — 13 in London, UK. The World Stem Cells and Regenerative Medicine Congress brings together business leaders, academic researchers, regulators, policy-makers, advocates, and legal and industry experts from around the world to network, collaborate and discuss the challenges and commercial opportunities for stem cell applications. StemCells’ invitation to participate in multiple speaking sessions at this conference reflects the Company’s leading position and broad reach in the stem cell field, including a wide range of stem cell technology platforms for both therapeutic and non-therapeutic use.

Mr. McGlynn’s presentation, entitled “Case Study: Working with the FDA for Regulatory Approval,” is scheduled for May 11th at 10:05 a.m. local time. Mr. McGlynn will also participate in a panel discussion entitled “Constructing a ‘Regulatory Roadmap’ to Bring Cell Therapy to the Clinic,” scheduled for 10:30 a.m. local time the same day. As the first company to receive FDA authorization for a clinical trial using purified human neural stem cells, StemCells has significant experience with advancing novel stem cell treatments into the clinic. Its two successful IND filings to date have led to the completion in January 2009 of a Phase I clinical trial in neuronal ceroid lipofuscinosis (NCL, also often referred to as Batten disease) and initiation in November 2009 of a Phase I clinical trial in Pelizaeus-Merzbacher Disease (PMD), both fatal neurodegenerative disorders in children. The Company has also recently submitted a protocol to the FDA for initiation of a second NCL trial.

Dr. Craig’s presentation, entitled “Platform Solutions for Stem Cell-based Drug Discovery Applications”, is scheduled for May 11th at 5:30 p.m. local time. StemCells has in-house expertise and infrastructure for providing cell-based assays for drug discovery and development, including an automated cell culture platform for the production of stem and progenitor cells for drug screening applications. The Company is currently leveraging its broad technology platform, including embryonic stem cells, induced pluripotent stem cells and tissue-derived (adult) stem cells, and its leading position in the neural stem cell field to develop neural stem cell-based assays to facilitate drug discovery for diseases of the central nervous system.

StemCells will also exhibit its stem cell technologies and research products at the conference, including its SC Proven(R) specialty cell culture products, which enable leading edge stem cell research.

About StemCells, Inc.

StemCells, Inc. is engaged in the research, development, and commercialization of stem cell therapeutics and enabling technologies for use in stem cell-based research and drug discovery. In its cellular medicine programs, StemCells is targeting diseases of the central nervous system and liver. StemCells’ lead product candidate, HuCNS-SC cells (purified human neural stem cells), is in clinical development for the treatment of two fatal neurodegenerative disorders that primarily affect young children. StemCells also markets specialty cell culture products under the SC Proven brand, and is developing stem cell-based assay platforms for use in pharmaceutical research, drug discovery and development. The Company has exclusive rights to approximately 55 issued or allowed U.S. patents and over 200 granted or allowed non-U.S. patents. Further information about StemCells is available at www.stemcellsinc.com.

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

Apart from statements of historical fact, the text of this press release constitutes forward-looking statements within the meaning of the U.S. securities laws, and is subject to the safe harbors created therein. These statements include, but are not limited to, statements regarding the clinical development of its HuCNS-SC cells; the Company’s ability to commercialize drug discovery and drug development tools; and the future business operations of the Company. These forward-looking statements speak only as of the date of this news release. The Company does not undertake to update any of these forward-looking statements to reflect events or circumstances that occur after the date hereof. Such statements reflect management’s current views and are based on certain assumptions that may or may not ultimately prove valid. The Company’s actual results may vary materially from those contemplated in such forward-looking statements due to risks and uncertainties to which the Company is subject, including those described under the heading “Risk Factors” in the Company’s Annual Report on Form 10-K for the year ended December 31, 2009 and in its subsequent reports on Form 10-Q and Form 8-K.

The results do not mean eating broccoli will stop cancer

GoogleNews.com, May 6, 2010  –  “Broccoli could stop breast cancer spreading,” according to the Daily Mail. The newspaper says that sulforaphane, a chemical found in the “green superfood”, targets the cells that fuel the growth of tumours.

This valuable laboratory research has found that sulforaphane, a natural compound found in broccoli, appears to have anti-cancer properties. In human breast cancer cells in a laboratory and in mice injected with cancer cells, treating cells with sulforaphane was found to prevent the growth of breast cancer stem cells and thus halt the tumour’s progression.

These findings will undoubtedly lead to further testing of the anti-cancer properties of sulphoraphane and its potential to target the cancer stem cell population. Current chemotherapy and radiotherapy regimes are reportedly incapable of doing this. However, this research is in the very early stages, and there are no immediate implications for breast cancer treatment or prevention. Most importantly, it cannot be assumed that eating broccoli has the same effect as applying the sulforaphane compound directly to cancer cells under controlled conditions in the laboratory. A lot more research is needed to ascertain this.

Where did the story come from?

Yanyan Li and colleagues from the University of Michigan and The Ohio State University carried out this research. The study was funded by the University of Michigan Cancer Center Research Grant, and the University of Michigan Cancer Center Core Grant. The study was published in the peer-reviewed medical journal Clinical Cancer Research.

This research has generally been well represented by the Daily Mail. However, people should not be confused into thinking that these laboratory findings mean that eating broccoli is likely to stop cancer in its tracks.

What kind of research was this?

This was a laboratory study, which has aimed to examine how cancer stem cells in breast cancer are affected by sulforaphane, a natural chemical found in broccoli and broccoli sprouts. The potential for the compounds in broccoli and other cruciferous vegetables to prevent cancer has been frequently studied. Sulforaphane is believed to ‘block’ the conversion of procarcinogen chemicals into carcinogens, enhance their breakdown in the body, and also ‘suppress’ the growth of cancerous cells. Several cancers, including breast cancer, are believed to be initiated by the growth of a group of cancer stem cells that continuously renew and change into different cell types. These cancer stem cells are believed to be involved in the cancer relapse and resistance to treatment.

This particular research involved applying sulforaphane to breast cancer cells in a laboratory, and looking at the chemical’s effect on cell growth. This is valuable research, but it must be interpreted in this context. Applying the compound directly to the cells outside of the body and injecting the compound into mouse models cannot be assumed to be comparable to eating broccoli. This early, speculative research has no immediate implications for cancer treatment or prevention.

What did the research involve?

The researchers obtained and cultured two different breast cancer cell lines called MCF7 and SUM159, of which the latter is negative for the presence of oestrogen and progesterone receptors. They treated both cell lines with increasing concentrations of sulforaphane. They used various different laboratory methods to assess the number of living cancer cells found after 48 hours of incubation with protein and sulforaphane, and looked at the activity of an enzyme called aldehyde dehydrogenase, which is believed to ‘enrich’ cancer stem cells. They also carried out a process called a ‘mammosphere formation assay’ which promotes the growth of breast cancer stem cells. They looked at how this was affected by seven days incubation with sulforaphane.

In a separate part of the experiment, the researchers then injected SUM159 cancer cells into the mammary glands of immuno-deficient female mice. After two weeks of tumour growth they divided the mice into two groups. One group received daily injections of a sulforaphane solution over a further period of two weeks, and another group was injected with a ‘control’ salt solution. After this time they extracted the tumours from the mice and examined how cancer stem cells were affected. They then re-implanted living cancer cells extracted from the sulforaphane-treated and control-treated tumours into a secondary group of mice to monitor how the tumours would grow.

What were the basic results?

The researchers found that incubating breast cancer cell lines with sulforaphane reduced the size and number of breast cancer stem cells. It also reduced the number of cells that were positive for the  aldehyde dehydrogenase enzyme thought to enrich cancer stem cells. In the mice, daily injection with sulforaphane for two weeks reduced the number of aldehyde dehydrogenase-positive cells. It also eliminated breast cancer stem cells. When these sulforaphane-treated tumour cells were then re-implanted into the second group of mice, tumour growth was prevented.

How did the researchers interpret the results?

The researchers concluded that sulforaphane inhibits breast cancer stem cells and limits their rate of  self-renewal. They say that their findings ‘support the use of sulforaphane for the chemoprevention of breast cancer stem cells’, and they warrant further clinical evaluation.

Conclusion

This valuable laboratory research has found that sulforaphane, a natural compound found in broccoli and broccoli sprouts, does appear to have some anti-cancer properties. In human breast cancer cells in the laboratory, and in mice that had been injected with these cancer cells, directly treating the cells with sulforaphane was found to prevent the growth of breast cancer stem cells and thereby halt progression of the tumour.

These findings will undoubtedly lead to further research into the possible uses of this compound in preventing and treating cancer by targeting this stem cell population – an action that current chemotherapy and radiotherapy regimes are reportedly incapable of doing, and which could play a role in non-responsive or relapsing of tumours.

However, this research is in the very early stages, and there are no immediate implications for breast cancer treatment or prevention. Most importantly, it cannot be assumed that eating broccoli is comparable to applying the sulforaphane compound directly to cancer cells under controlled conditions.

Links to the science

Li Y, Zhang T, Korkaya H, et al. Sulforaphane, a dietary component of broccoli/broccoli sprouts, inhibits breast cancer stem cells. Clinical cancer research 2010; Published online first April 13

Murthy will collaborate with researchers to develop stem cell isolation technologies.

Photo by Mary Knox Merrill.

GoogleNews.com, May 6, 2010  –  Shashi Murthy, assistant professor of chemical engineering at Northeastern University, has been awarded a three-year $1.9 million grant from the National Institutes of Health (NIH) to develop innovative techniques for isolating and cultivating stem cells for use in the replacement of damaged tissue.
 
An international team of researchers led by Murthy will design and build small devices to extract cell types that help to grow new tissue for cardiac muscle or skin, for example, or repair diseased or non-functional tissue.
 
Stem cells and cells that resemble stem cells are present in every tissue of the human body. Under certain conditions, these cells have the capacity to repair damaged tissue.
 
Murthy explains, “Stem cells play a critical role in the development of the human body and all its parts. Our goal is to advance regenerative-medicine technologies by more effectively extracting and cultivating stem cells to multiply and develop into new tissue.”

His team will develop a new family of devices, called microfluidic systems, which will enable greater efficiency and accuracy in the separation of stem cells from a small tissue or blood sample.
 
One focus of this work—to be pursued in collaboration with Rebecca Carrier, another assistant professor of chemical engineering at Northeastern—is the isolation of intestinal stem cells. These cells are extremely challenging to separate, since they tend not to survive after they’re extracted from their native environment.
 
As part of the grant, Murthy will also collaborate with several scientists from research institutions throughout North America. Working with Milica Radisic, an assistant chemical-engineering professor at the University of Toronto, Murthy will explore ways of repairing diseased heart tissue by obtaining cardiac stem cells from normal tissue and implanting these cells into damaged tissue.

In collaboration with John Mayer and Juan Melero-Martin, doctors at Children’s Hospital Boston, Murthy will investigate blood-vessel tissue repair by extracting cells capable of repairing the tissue and implanting them into damaged blood vessels.

And Murthy will team up with Martin Yarmush and Yaakov Nahmias, researchers at Massachusetts General Hospital and Shriners Burn Hospital, to study how stem cells extracted from hair follicles in normal skin can repair severely burned skin by growing new hair follicles and sweat glands.

For more information, please contact Jenny Catherine Eriksen at 617-373-2802 begin_of_the_skype_highlighting,      end_of_the_skype_highlior at j.eriksen@neu.edu.