Stem cell stories that caught our eye: spina bifida, review of heart clinical trials, tracking cells and cell switches

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

Stem cells boost fetal surgery for spina bifida. Fetal surgery to correct the spinal defect that causes spina bifida has revolutionized treatment for the debilitating birth defect in the past few years. But for one of the researchers who pioneered the surgery it was only a half fulfilled hope. While the surgery let most of the treated kids grow up without cognitive deficits it did not improve their ability to walk.

spina_bifida-webNow that researcher, Diana Farmer at the University of California, Davis, has found a way to complete the job. Though it has only been used in an animal model so far, she found that when you engineer a stem cell patch that you insert into the gap before you push the protruding spinal cord back in its place during surgery, the animals are able to walk within a few hours of birth.

Specifically, she used a type of stem cell found in the placenta that has been shown to protect nerves. She incased those cells in a gel and placed them on a scaffold to hold them in place after transplant. All six lambs that had surgery plus the cell transplant walked. None of the ones who just had surgery did.

“Fetal surgery provided hope that most children with spina bifida would be able to live without (brain) shunts,” Farmer said. “Now, we need to complete that process and find out if they can also live without wheelchairs.”

CIRM awarded Farmer’s team funds in March to carry this work forward and prepare it for a possible clinical trial. The animal study appeared in Stem Cells Translational Medicine this week and the university’s press release was picked up by HealthCanal.

Thorough, digestible review of heart trials. Kerry Grens, writing in The Scientist, has produced the most complete and understandable review of the clinical trials using stem cells to treat heart disease that I have read. More important she provides significant detail about the three large Phase 3 trials that are ongoing that could provide make-or-break outcomes for using bone marrow stem cells for patients developing heart failure.

The bulk of the piece focuses on research using various types of mesenchymal stem cells found in bone marrow. All three of the late stage clinical trials use those cells, two use cells from the patient’s own marrow and one uses cells from donors. Grens uses a broad spectrum of the research community describe what we currently know about how those cells may work and more importantly, what we don’t know. The experts provide a good point-counter-point on why there are so many clinical trials when we don’t really know those stem cells’ “method of action,” why they might make someone’s heart stronger.

However she leads and ends with work CIRM funds at Cedars-Sinai and Capricor Therapeutics in Los Angeles. That work uses cells derived from the heart called cardiosphere-derived cells. Early trials suggested these cells might be better at reducing scar tissue and triggering regrowth of heart muscle. Those cells are currently being tested in a Phase 2 study to try to get a better handle on exactly what their benefit might be.

Monitoring stem cells after transplants. Early attempts to use stem cells as therapies have been hampered by an inability to see where the cells go after transplant and if they stay the desired location and function. A team at Stanford has used some ingenious new technologies to get over this hurdle, at least in laboratory animals.

Using a homegrown technology that recently won a major innovation prize for a Stanford colleague, optogenetics, the team was able to selectively activate the transplanted cells. Then they used the older technology, functional Magnetic Resonance Imaging (fMRI), to see if the cells were working. Because cell transplants in the brain have led to some of the most difficult to interpret results in humans, they chose to work with nerve stem cells transplanted into the brains of rats. The work was partially funded by CIRM.

Starting with iPS type stem cells made from Parkinson’s patients’ skin, they inserted a gene for a protein that is sensitive to certain wavelengths of light. They then matured those cells into nerve stem cells and implanted them along with a tube that could transmit the right wavelength of light. Over the course of many months they measured the activity of the cells via fMRI with and without the light stimulation. Because the fMRI measures blood flow it by default detects active nerve cells that require more nutrients from blood than inactive cells. Senior researcher, Jin Hyung Lee described the value of this imaging in the university’s press release picked up by HealthCanal:

“If we can watch the new cells’ behaviors for weeks and months after we’ve transplanted them, we can learn — much more quickly and in a guided way rather than a trial-and-error fashion — what kind of cells to put in, exactly where to put them, and how.”

Understanding cell’s switchboard may speed therapy. Cells function by switching genes on and off. Learning which switches to hit to maximize stem cells’ ability to multiply and mature into desired cell types has occupied a significant part of the stem cell research community for years. Now, a team at the Salk Institute has shown that two known genetic switches pack an additive punch when working together.

Both those signaling processes, one called Wnt and one called Activin, are needed for stem cells to mature into specific adult tissue. The Salk team led by Kathy Jones found that when working together the two signals activate some 200 genes. Wnt seems to load the cellular equipment needed for copying the cells and Activin increases the speed and efficiency of the process. In an institute press release picked up by Science Newsline, Jones discussed the practical implications of the finding:

“Now we understand stem cell differentiation at a much finer level by seeing how these cellular signals transmit their effects in the cells. Understanding these details is important for developing more robust stem cell protocols and optimizing the efficiency of stem cell therapies.”

Charting a new, faster way to fund science and help patients

Change is never easy. In fact, sometimes it can be downright hard. But change is also essential if you want to grow, to get faster and better.

When we launched CIRM 2.0 we set out to produce a better, faster, more effective and efficient way to deliver stem cell therapies to patients with unmet medical needs. Yesterday we got a chance to see how those changes are starting to play out. And it was very encouraging.

Our Grants Working Group (GWG – we love our acronyms at CIRM. See!) is the independent panel of experts that we bring in to review all the applications for agency funding. They come from all over the US, except California, and Monday was the first chance they got to meet in person and vote on our new 2.0 applications.

The day began with a really in-depth look at how 2.0 works and how it differs quite dramatically from the old system. One of the things that always impresses me about the GWG is the extraordinary quality of the questions they ask and the level of detail they want to help them make the best possible decisions. While we would never divulge any applicant’s confidential or proprietary information, we were able to hold much of the meeting in open session – furthering our commitment to transparency.

I think Sen. Art Torres, the Vice Chair and a Patient Advocate member of our governing Board, summed it up best in a note that he sent to the CIRM Team following the meeting:

“Yesterday was a historic day for CIRM.  It was one of the best meetings I have attended and gave me renewed confidence in speaking to the public of how we continue to be responsible stewards of the taxpayers’ dollars while at the same time keeping patients as our number one priority.

I cannot speak for all the patient advocates but I think they were all impressed with the candor and meaningful dialogue that took place.

It also gave the GWG members time to bond in a very welcoming setting to express their ideas and their commitments.  I do not recall ever having a session with GWG members where they shared their personal views other than their reviews of a proposed grant.  It was revealing about how we can work more closely together with our common bonds.”

The results of the review of the first two applications under CIRM 2.0 will go to the Board for a vote on May 21, but the more important outcome will be the long-term benefit to the way we work. The in-person meeting helped the members of the GWG really understand how the changes to the way they work will speed up our ability to fund the most promising science.

This is all new, so it’s likely we’ll hit some bumps along the way. And as we roll out our new versions of 2.0 that cover funding Discovery (or basic) and Translational research later this year we’ll probably have more adjustments to make. You can’t change this much this fast and not run into problems.

But as the meeting yesterday showed so clearly, with the right team behind you even the biggest changes can be taken in stride.

Pioneering treatments: planning first-in-human stem cell clinical trials

Sometimes the reason for the most complex of projects can be boiled down to the most simple of phrases.

Dr. John Adams, Dr. Catriona Jamieson & Dr. John Zaia at the Alpha Stem Cell Clinic network meeting

(left to right) Dr. John Adams, Dr. Catriona Jamieson & Dr. John Zaia at the Alpha Stem Cell Clinic network meeting

At a meeting last week to help plan for our Alpha Stem Cell Clinic network there were lots of great presentations and discussions about the role of the network, how to structure it, what its goals would be. But in the end it was all beautifully, and succinctly, summed up by Dr. Catriona Jamieson who said: “This is great for humanity and this is why we have to do it.”

Dr. Jamieson is heading the University of California, San Diego (UCSD) part of the network. Other partners in this program are City of Hope, UC Los Angeles (UCLA) and UC Irvine (UCI). The goal is to create a network of stem cell-focused clinics that will attract and conduct high quality clinical trials. The stem cell agency is investing $24 million to help create that network.

Why do we need this? Well, stem cells are a whole new way of treating disease, one that requires new skills and expertise, and a new way of working with patients so they understand exactly what is happening.

Many of these clinical trials will be the first time these therapies have been tested in people so Shirley Johnson, RN, the Chief Nursing Officer overseeing the City of Hope program, says you need to have specially trained staff involved.

“We really look to our research patients as being our heroes and particularly our patients that are participating in those first-in-human studies. So having nurses who understand the study protocols, who understand the potential side effects that might be occurring, the symptoms that might be manifested are critical points as we think about first-in-human studies and those things that might occur, and then how best to respond to them.”

One of the reasons we are creating the Alpha Stem Cell Clinic network is because it fits in perfectly with our mission of accelerating the development of stem cell therapies to help patients with unmet medical needs. The network will not just focus on planning and carrying out clinical trials, but will also focus on how those treatments will be paid for, so that life-changing therapies won’t cost patients an arm and a leg.

Dr. John Adams, who heads the UCLA-UCI program, says there will be many obstacles to overcome, but that this is an exciting time:

“The idea behind the Alpha Clinics is to provide an infrastructure to accelerate and make it dead easy for the researchers doing this work to get their work done efficiently, effectively and faster, so that it’s more beneficial for the patients who are undergoing the treatment. And certainly it will allow us to collect more data, and better data, during the course of these clinical trials.”

The data gathered in these trials, and the lessons learned in doing them, will then be shared with others in the network to help create a system of best practices, to make it easier to carry out future clinical trials.

As Dr. John Zaia, who heads the program at City of Hope says: “This is really the beginning of a new era, the era of regenerative medicine.”

You can read more about our Alpha Stem Cell Clinic network, and find links to the individual programs here.

Brain’s Own Activity Can Fuel Growth of Deadly Brain Tumors, CIRM-Funded Study Finds

Not all brain tumors are created equal—some are far more deadly than others. Among the most deadly is a type of tumor called high-grade glioma or HGG. Most distressingly, HGG’s are the leading cause of brain tumor death in both children and adults. And despite extraordinary progress in cancer research as a whole, survival rates for those diagnosed with an HGG have yet to improve.


But recent research from Stanford University scientists could one day help move the needle—and give renewed hope to the patients and their families affected by this devastating disease.

The study, published today in the journal Cell, found that one key driver for HGG’s deadly diagnosis is that the tumor can be stimulated to grow by the brain’s own neural activity—specifically the nerve activity in the brain’s cerebral cortex.

Michelle Monje, senior author of the study that was funded in part by two grants from CIRM, was initially surprised by these results, as they run counter to how most types of tumors grow. As she explained in today’s press release:

“We don’t think about bile production promoting liver cancer growth, or breathing promoting the growth of lung cancer. But we’ve shown that brain function is driving these brain cancers.”

By analyzing tumor cells extracted from HGG patients, and engrafting it onto mouse models in the lab, the researchers were able to pinpoint how the brain’s own activity was driving tumor growth.

The culprit: a protein called neuroligin-3 that appeared to be calling the shots. There are four distinct types of HGGs that affect the brain in vastly different ways—and have vastly different molecular and genetic characteristics. Interestingly, says Monje, neuroligin-3 played the same role in all of them.

What was so disturbing to the research team, says Monje, is that neuroligin-3 is an essential protein for overall brain development. Specifically, it helps maintain healthy growth and repair of brain tissue over time. In order to grow, HGG tumors hijack this critical protein.

The research team came to this conclusion after a series of experiments that delved deep into the molecular mechanisms that guide both brain activity and brain tumor development. They first employed a technique called optogenetics, whereby scientists use genetic manipulation to insert light-sensitive proteins into the brain cells, or neurons, of interest. This allowed scientists to activate these neurons—or deactivate them—at the ‘flick of a switch.’

When applying this technique to the tumor-engrafted mouse models, the team could then see that tumors grew significantly better when the neurons were switched on. The next step was to narrow it down to why. Additional biochemical analyses and testing on the mouse models confirmed that neuroligin-3 was being hijacked by the tumor to spur growth.

And when they dug deeper into the connection between neuroligin-3 and cancer, they found something even more disturbing. A detailed look at the Cancer Genome Atlas (a large public database of the genetics of human cancers), they found that HGG patients with higher levels of neuroligin-3 in their brain had shorter survival rates than those with lower levels of the same protein.

These results, while highlighting the particularly nefarious nature of this class of brain tumors, also presents enormous opportunity for researchers. Specifically, Monje hopes her team and others can find a way to block or nullify the presence of neuroligin-3 in the regions surrounding the tumor, creating a kind of barrier that can keep the size of the tumor in check. 

A new approach to killing blood cancer

It’s not often that you get a therapy named after you, particularly one that has so much promise for helping to save lives. So when researchers at the University of California, San Diego Moores Cancer Center named the treatment Cirmtuzumab after us it’s understandable we should feel just a little pride. After all, we provided the funding and support needed to develop it. Now Cirmtuzumab is being used in a clinical trial to treat chronic lymphocytic leukemia (CLL) a deadly blood cancer. Cirmtuzumab is a monoclonal antibody drug and is designed to attach itself to a protein called ROR1 that CLL cells need to survive and spread. The idea is that if you block ROR1, you can block the growth of the cancer. Ivanhoe Broadcasting, a company that syndicates medical stories to TV stations around the US, recently featured this trial. You can see that report here. kipps2013Dr. Thomas Kipps, who is heading the trial, told Ivanhoe that CLL is an important disease to target: “This is the most common adult leukemia in western societies. We have early data now to suggest this antibody may be effective at preventing the relapse and metastasis of cancer.” It’s always encouraging when a promising therapy moves out of the lab and into clinical trials. Reaching this point is the culmination of years, sometimes decades, of hard work and while this is an important milestone, it’s just the first step in a long journey. But now we get to put it to the test and see if it will work in people. If it does, then that will be something to be truly proud of.

Stem cell stories that caught our eye: Hair stem cells, amniotic fluid cells for repair and fixing kids’ faulty genes

Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.

With hair, lose a few to grow more.
A team at the University of Southern California has shown that if you pull out a couple hundred hairs in just the right pattern you could trigger a thousand or more hairs to grow. It is the latest example of several we have written about that show stem cells react very acutely to their environment.

The researcher had known that hair follicle injury affects the adjacent environment and that environment can influence hair growth. They teamed up with a University of California, Irvine, expert on “quorum sensing,” a field that the USC press release defined as “how a system responds to stimuli that affects some, but not all members”. They tested various patterns of hair follicle damage caused by plucking hairs on the back of a mouse. They eventually found the pattern and spacing that turned the 200 hairs loss into a thousand-strand gain.

The stem cells that reside at the base of hair follicles are a common tool for studying stem cell behavior because they are easy to get at. And while this work could eventually produce real cosmetic benefits for folks follicularly challenged like myself, the real payoff could come from finding similar quorum affects in stem cells in other organs, which the senior researcher, Cheng-Ming Chuong, notes in the release picked up by Epoch Times:

“The implication of the work is that parallel processes may also exist in the physiological or pathogenic processes of other organs, although they are not as easily observed as hair regeneration.”

Baby’s amniotic fluid as source of repairs. The amniotic fluid that surrounds a growing baby carries cells shed by the fetus that doctors use to diagnose problems, but it also has some valuable stem cells, actually a few types of stem cells. Even though those cells are characteristically adult stem cells, because they have recently crossed the line from embryo to adult, they seem to be more versatile than adult stem cells, and since they match the baby could be the perfect cell for repairing birth defects.

Mature blood vessels form after two weeks in a mouse, with red blood cells flowing at the bottom right.

Mature blood vessels form after two weeks in a mouse, with red blood cells flowing at the bottom right.

Scientists at Rice University and Texas Children’s hospital have reported that when you seed those stem cells into the gel scaffolds commonly used for tissue engineering, the resulting tissues do a better job of growing blood vessels. And without the nutrients brought by new vessels, repair tissues will not survive. They now hope to use this new technique in their ongoing efforts to grow heart muscle patches for children born with heart defects.

The university’s press release was picked up by ScienceDaily. It looks like the fluid and cells normally thrown away after a prenatal test, might become a valuable resource.

Genetically correcting childhood disease.
Last week Stanford organized a multi-day symposium called Childx with an impressive array of speakers from around the world talking about how to improve child health. It ended with a special session on the rapid advances being made by combining stem cell science and gene therapy.

“It’s not just science fiction anymore,” Stanford’s Matthew Porteus, told the audience. “We can correct mutations that cause childhood disease.”

The university’s Scope blog summed up the session in a post this week. It discusses progress in sickle cell anemia, severe combined immune deficiency (SCID) and epidermolysis bullosa, among others. The piece also has a voice from industry cautioning that many hurdles remain before any of these therapies can be scaled up to broad use.

But my email this morning had a potent reminder that enough scientists are getting on this bandwagon to make it happen. The subject line of a sales pitch was “Boost transduction with 20 % off Lentiviral Particles,” which referred to the viral units used to carry genes into cells hoping they with take up residence there and function, aka transduction.

CIRM has bet big on this avenue of research investing more than $110 million in nine projects that combine stem cells and gene manipulation and are either in the clinic or soon will be. We will be launching a new series of posts on “Genes + Cells” next week.

Mutation Morphs Mitochondria in Models of Parkinson’s Disease, CIRM-Funded Study Finds

There is no singular cause of Parkinson’s disease, but many—making this disease so difficult to understand and, as a result, treat. But now, researchers at the Buck Institute for Research on Aging have tracked down precisely how a genetic change, or mutation, can lead to a common form of the disease. The results, published last week in the journal Stem Cell Reports, point to new and improved strategies at tackling the underlying processes that lead to Parkinson’s.

Mitochondria from iPSC-derived neurons. On the left is a neuron derived from a healthy individual, while the image on the right shows a neuron derived from someone with the Park2 mutation, the most common mutation in Parkinson's disease (Credit: Akos Gerencser)

Mitochondria from iPSC-derived neurons. On the left is a neuron derived from a healthy individual, while the image on the right shows a neuron derived from someone with the Park2 mutation, the most common mutation in Parkinson’s disease (Credit: Akos Gerencser)

The debilitating symptoms of Parkinson’s—most notably stiffness and tremors that progress over time, making it difficult for patients to walk, write or perform other simple tasks—can in large part be linked to the death of neurons that secrete the hormone dopamine. Studies involving fruit flies in the lab had identified mitochondria, cellular ‘workhorses’ that churn out energy, as a key factor in neuronal death. But this hypothesis had not been tested using human cells.

Now, scientists at the Buck Institute have replicated the process in human cells, with the help of stem cells derived from patients suffering from Parkinson’s, a technique called induced pluripotent stem cell technology, or iPSC technology. These newly developed neurons exactly mimic the disease at the cellular level. This so-called ‘disease in a dish’ is one of the most promising applications of stem cell technology.

“If we can find existing drugs or develop new ones that prevent damage to the mitochondria we would have a potential treatment for PD,” said Dr. Xianmin Zeng, the study’s senior author, in a press release.

And by using this technology, the Buck Institute team confirmed that the same process that occurred in fruit fly cells also occurred in human cells. Specifically, the team found that a particular mutation in these cells, called Park2, altered both the structure and function of mitochondria inside each cell, setting off a chain reaction that leads to the neurons’ inability to produce dopamine and, ultimately, the death of the neuron itself.

This study, which was funded in part by a grant from CIRM, could be critical in the search for a cure for a disease that, as of yet, has none. Current treatment regimens aimed at slowing or reducing symptoms have had some success, but most begin to fail overtime—or come with significant negative side effects. The hope, says Zeng, is that iPSC technology can be the key to fast-tracking promising drugs that can actually target the disease’s underlying causes, and not just their overt symptoms. Hear more from Dr. Xianmin Zeng as she answers your questions about Parkinson’s disease and stem cell research:

Why TED Talks are ChildX’s Play

When the TED (Technology, Entertainment, Design) talks began in 1984 they were intended to be a one-off event. So much for that idea! Today they are a global event, with TED-sponsored conferences held everywhere from Scotland to Tanzania and India. They have also spawned a mini-industry of copycat events. Well, their slogan is “Ideas Worth Spreading” so in a way they only have themselves to blame for having such a great idea.

Dr. Maria Grazia Roncarolo

Dr. Maria Grazia Roncarolo

The latest place for that idea to take root is Stanford, which is holding a TED-style event focused on critical issues facing child and maternal health. The event – April 2nd and 3rd at Stanford – is called ChildX where x = medicine + technology + innovative treatment + wellbeing. ChildX will bring together some of the leading experts in the field for a series of thoughtful, powerful presentations on the biggest problems facing child and maternal health, and the most exciting research aimed at resolving those problems. One of the main tracks during the two-day event is a section on stem cell and gene therapy. It will raise a number of key questions including:

  • What advances have occurred to enable these therapies to move from science fiction less than a decade ago to the promise of next generation transformative therapeutics?
  • In coming years, how will these therapies allow children with presently incurable diseases to become children living free of disease and reaching their maximum potential?

The moderator for that discussion is Dr. Maria Grazia Roncarolo, and you can hear her talking about the most recent advances in the clinical use of stem cell and gene therapies on this podcast. Anytime you get a chance to hear some of the most compelling speakers in their field talk about exciting innovations that could shape the future, it’s worth taking the time to listen.

Goodnight, Stem Cells: How Well Rested Cells Keep Us Healthy

Plenty of studies show that a lack of sleep is nothing but bad news and can contribute to a whole host of health problems like heart disease, poor memory, high blood pressure and obesity.


Even stem cells need rest to stay healthy

In a sense, the same holds true for the stem cells in our body. In response to injury, adult stem cells go to work by dividing and specializing into the cells needed to heal specific tissues and organs. But they also need to rest for long-lasting health. Each cell division carries a risk of introducing DNA mutations—and with it, a risk for cancer. Too much cell division can also deplete the stem cell supply, crippling the healing process. So it’s just as important for the stem cells to assume an inactive, or quiescent, state to maintain their ability to mend the body. Blood stem cells for instance are mostly quiescent and only divide about every two months to renew their reserves.

Even though the importance of this balance is well documented, exactly how it’s achieved is not well understood; that is, until now. Earlier this week, a CIRM-funded research team from The Scripps Research Institute (TSRI) reported on the identification of an enzyme that’s key in controlling the work-rest balance in blood stem cells, also called hematopoietic stem cells (HSCs). Their study, published in the journal Blood, could point the way to drugs that treat anemias, blood cancers, and other blood disorders.

Previous studies in other cell types suggested that this key enzyme, called ItpkB, might play a role in promoting a rested state in HSCs. Senior author Karsten Sauer explained their reasoning for focusing on the enzyme in a press release:

“What made ItpkB an attractive protein to study is that it can dampen activating signaling in other cells. We hypothesized that ItpkB might do the same in HSCs to keep them at rest. Moreover, ItpkB is an enzyme whose function can be controlled by small molecules. This might facilitate drug development if our hypothesis were true.”

Senior author Karsten Sauer is an associate professor at The Scripps Research Institute.

Senior author Karsten Sauer is an associate professor at The Scripps Research Institute.

To test their hypothesis, the team studied HSCs in mice that completely lacked ItpkB. Sure enough, without ItpkB the HSCs got stuck in the “on” position and continually multiplied until the supply of HSCs stores in the bone marrow were exhausted. Without these stem cells, the mice could no longer produce red blood cells, which deliver oxygen to the body or white blood cells, which fight off infection. As a result the animals died due to severe anemia and bone marrow failure. Sauer used a great analogy to describe the result:

“It’s like a car—you need to hit the gas pedal to get some activity, but if you hit it too hard, you can crash into a wall. ItpkB is that spring that prevents you from pushing the pedal all the way through.”

With this new understanding of how balancing stem cell activation and deactivation works, Sauer and his team have their sights set on human therapies:

“If we can show that ItpkB also keeps human HSCs healthy, this could open avenues to target ItpkB to improve HSC function in bone marrow failure syndromes and immunodeficiencies or to increase the success rates of HSC transplantation therapies for leukemias and lymphomas.”

The eyes have it: a video guide to stem cells

We are visual creatures. Our eyes are essential tools in getting information to our brain to help us learn and understand. For example, visuals are processed about 60,000 times faster in the brain than text is, and some 60 percent of us are visual learners, meaning we respond better to visual information than to plain text.

ben paylorThat’s why a series of 8 videos, just completed by Ben Paylor and Mike Long at InfoShots, are so wonderful. They are fun, simple and engaging videos that help make some of the complex science around stem cells readily understandable thanks to the use of eye-catching animation and simple, everyday English.

The videos are short, all around one minute (less time than it takes to make a cup of tea). Each video has a single theme – ‘What is a stem cell”, “What is stem cell tourism” – and they are all masterful at walking you through different aspects of stem cell research.

The last video in the series is about neural stem cells, which is highly appropriate considering this is Brain Awareness Week, a worldwide celebration of the brain.

The videos are a reminder that the most effective communication is often the most direct, cutting through the clutter and getting to the heart of the subject. The beauty of these is that Ben and Mike are keen to share them with as many people as possible and have made them available to anyone who wants to watch them or use them as a teaching tool.

Finally, credit for the videos also has to go to the Canada’s Stem Cell Network and the Canadian Stem Cell Foundation, which helped fund them.