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Artificial blood made from human stem cells could plug the donations hole

By Dr. Matthew Watson

"It's a tiny wee finger prick test," says senior nurse Patsy Scouse to calm the nervous first-time donor having his hemoglobin levels tested at a blood donation centre in Edinburgh.

The Scottish National Blood Transfusion Service receives donations from about four percent of the UK's population. Currently, stocks are stable, although the service is always trying to recruit new donors.

The collection may take place in a clinical environment, the nurse says, but the clinic "wants this experience, especially for first-time donors, to be really positive so they can go out and feel they've done a really good thing."

But the service is also working on potential new technologies to secure blood supplies in the future, including "artificial blood."

Mass-produced and clean

Mark Turner, medical director of the Blood Transfusion Service, is looking into how blood could be synthesized in the future.

"We've known for some time that it's possible to produce red blood cells from so called adult stem cells, but you can't produce large amounts of blood in that way because of the restrictive capacity of those cells to proliferate," he explains. What scientists can do, he adds, is to derive pluripotent stem cells - stem cell lines - either from embryos or from adult tissue.

These cells are processed in the laboratory to produce larger numbers of cells, Turner told DW.

"It may be possible in due course to manufacture blood on a very large scale, but we're a very long way from that at the present time," he says. "At the moment, our focus is on trying to achieve production of red blood cells which are of the right kind of quality and safety, that they would be fit for human trials."

From the lab to clinical trials

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Bright Idea: Scientists Use Laser Lights to Regrow Teeth

By Dr. Matthew Watson

Scientists have a new way to repair teeth, and they say their concept - using laser light to entice the body's own stem cells into action - may offer enormous promise beyond just dentistry in the field of regenerative medicine.

The researchers used a low-power laser to coax dental stem cells to form dentin, the hard tissue similar to bone that makes up most of a tooth, demonstrating the process in studies involving rats and mice and using human cells in a laboratory.

They did not regenerate an entire tooth in part because the enamel part was too tricky. But merely getting dentin to grow could help alleviate the need for root canal treatment, the painful procedure to remove dead or dying nerve tissue and bacteria from inside a tooth, they said.

"I'm a dentist by training. So I think it has potential for great impact in clinical dentistry," researcher Praveen Arany of the National Institute of Dental and Craniofacial Research, part of the U.S. National Institutes of Health, said on Friday.

Arany expressed hope that human clinical trials could get approval in the near future.

"Our treatment modality does not introduce anything new to the body, and lasers are routinely used in medicine and dentistry, so the barriers to clinical translation are low," added Harvard University bioengineering professor David Mooney.

"It would be a substantial advance in the field if we can regenerate teeth rather than replace them." Using existing regeneration methods, scientists must take stem cells from the body, manipulate them in a lab and put them back into the body.

This new technique more simply stimulates action in stem cells that are already in place. Scientists had long noticed that low-level laser therapy can stimulate biological processes like rejuvenating skin and stimulating hair growth but were not sure of the mechanisms.

Arany noted the importance of finding the right laser dose, saying: "Too low doesn't work and too high causes damage."

First published May 30 2014, 2:24 PM

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Coaxing iPS cells to become more specialized prior to transplantation cuts rejection risk

By NEVAGiles23

PUBLIC RELEASE DATE:

30-May-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center

STANFORD, Calif. For many scientists, the clinical promise of stem cells has been dampened by very real concerns that the immune system will reject the transplanted cells before they could render any long-term benefit. Previous research in mice has suggested that even stem cells produced from the subject's own tissue, called iPS cells, can trigger an immune attack.

Now researchers at the Stanford University School of Medicine have found that coaxing iPS cells in the laboratory to become more-specialized progeny cells (a cellular process called differentiation) before transplantation into mice allows them to be tolerated by the body's immune system.

"Induced pluripotent stem cells have tremendous potential as a source for personalized cellular therapeutics for organ repair," said Joseph Wu, MD, PhD, director of the Stanford Cardiovascular Institute. "This study shows that undifferentiated iPS cells are rejected by the immune system upon transplantation in the same recipient, but that fully differentiating these cells allows for acceptance and tolerance by the immune system without the need for immunosuppression."

The findings are described in a paper to be published online May 30 in Nature Communications. Wu is senior author of the paper. Postdoctoral scholars Patricia Almeida, PhD, and Nigel Kooreman, MD, and assistant professor of medicine Everett Meyer, MD, PhD, share lead authorship.

In a world teeming with microbial threats, the immune system is a necessary watchdog. Immune cells patrol the body looking not just for foreign invaders, but also for diseased or cancerous cells to eradicate. The researchers speculate that the act of reprogramming adult cells to pluripotency may induce the expression of cell-surface molecules the immune system has not seen since the animal (or person) was an early embryo. These molecules, or antigens, could look foreign to the immune system of a mature organism.

Previous studies have suggested that differentiation of iPS cells could reduce their tendency to inflame the immune system after transplantation, but this study is the first to closely examine, at the molecular and cellular level, why that might be the case.

"We've demonstrated definitively that, once the cells are differentiated, the immune response to iPS-derived cells is indistinguishable from its response to unmodified tissue derived from elsewhere in the body," said Kooreman.

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Low-power laser triggers stem cells to repair teeth

By JoanneRUSSELL25

Ranking among the X-Men probably isn't all that it's cracked up to be, but who wouldn't want their uncanny ability to regenerate lost bone or tissue? New research into tooth repair and stem cell biology, from a cross-institution team led by David Mooney of Harvard's Wyss Institute, may bring such regeneration one step closer to reality or at the very least, give us hope that we can throw away those nasty dentures.

The researchers employed a low-power laser to trigger human dental stem cells to form dentin, a hard bone-like tissue that is one of four major components of teeth (the others being enamel, pulp, and cementum). This kind of low-level light therapy has previously been used to remove or stimulate hair growth and to rejuvenate skin cells, but the mechanisms were not well understood, results varied, and evidence of its efficacy was largely anecdotal.

The new work is the first to document the molecular mechanism involved, thus laying the foundations for controlled treatment protocols in not only restorative dentistry but also avenues like bone regeneration and wound healing. "The scientific community is actively exploring a host of approaches to using stem cells for tissue regeneration efforts," said Wyss Institute Founding Director Don Ingber. "Dave [Mooney] and his team have added an innovative, noninvasive, and remarkably simple but powerful tool to the toolbox."

To test the team's hypothesis, Praveen Arany, an assistant clinical investigator at the National Institutes of Health, drilled holes in the molars of rats and mice, then treated them with low-dose lasers and temporary caps. Around 12 weeks later, tests confirmed that the laser treatments triggered enhanced dentin formation.

Performing dentistry on rat teeth takes extreme precision and is actually harder than the same procedure on human teeth (Image: ames Weaver, Harvard's Wyss Institute)

Further experiments were conducted on microbial cultures in the laboratory, where they found that a regulatory cell protein called transforming growth factor beta-1 (TGF-1) was activated in a chemical domino effect that in turn caused the stem cells to form dentin. The good news there is that TGF-1 is more or less ubiquitous, with key roles in many biological processes such as immune response, wound healing, development, and malignancies.

This means we could one day see the technique used to do far more than help repair teeth. But first it needs to clear planned human clinical trials, so for now you'll have to make do with dentures, canes and all manner of other prosthetics while the likes of Wolverine prance around with self-healing bodies.

A paper on the research was recently published in the journal Science Translational Medicine.

Source: Wyss Institute at Harvard

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Researchers Use Light To Coax Stem Cells To Repair Teeth

By LizaAVILA

A Harvard-led team is the first to demonstrate the ability to use low-power light to trigger stem cells inside the body to regenerate tissue, an advance they reported in Science Translational Medicine. The research, led by Wyss Institute Core Faculty member David Mooney, Ph.D., lays the foundation for a host of clinical applications in restorative dentistry and regenerative medicine more broadly, such as wound healing, bone regeneration, and more.

The team used a low-power laser to trigger human dental stem cells to form dentin, the hard tissue that is similar to bone and makes up the bulk of teeth. What's more, they outlined the precise molecular mechanism involved, and demonstrated its prowess using multiple laboratory and animal models.

A number of biologically active molecules, such as regulatory proteins called growth factors, can trigger stem cells to differentiate into different cell types. Current regeneration efforts require scientists to isolate stem cells from the body, manipulate them in a laboratory, and return them to the bodyefforts that face a host of regulatory and technical hurdles to their clinical translation. But Mooney's approach is different and, he hopes, easier to get into the hands of practicing clinicians.

"Our treatment modality does not introduce anything new to the body, and lasers are routinely used in medicine and dentistry, so the barriers to clinical translation are low," said Mooney, who is also the Robert P. Pinkas Family Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences (SEAS). "It would be a substantial advance in the field if we can regenerate teeth rather than replace them."

The team first turned to lead author and dentist Praveen Arany, D.D.S., Ph.D., who is now an Assistant Clinical Investigator at the National Institutes of Health (NIH). At the time of the research, he was a Harvard graduate student and then postdoctoral fellow affiliated with SEAS and the Wyss Institute.

Arany took rodents to the laboratory version of a dentist's office to drill holes in their molars, treat the tooth pulp that contains adult dental stem cells with low-dose laser treatments, applied temporary caps, and kept the animals comfortable and healthy. After about 12 weeks, high-resolution x-ray imaging and microscopy confirmed that the laser treatments triggered the enhanced dentin formation.

"It was definitely my first time doing rodent dentistry," said Arany, who faced several technical challenges in performing oral surgery on such a small scale. The dentin was strikingly similar in composition to normal dentin, but did have slightly different morphological organization. Moreover, the typical reparative dentin bridge seen in human teeth was not as readily apparent in the minute rodent teeth, owing to the technical challenges with the procedure.

"This is one of those rare cases where it would be easier to do this work on a human," Mooney said.

Next the team performed a series of culture-based experiments to unveil the precise molecular mechanism responsible for the regenerative effects of the laser treatment. It turns out that a ubiquitous regulatory cell protein called transforming growth factor beta-1 (TGF-1) played a pivotal role in triggering the dental stem cells to grow into dentin. TGF-1 exists in latent form until activated by any number of molecules.

Here is the chemical domino effect the team confirmed: In a dose-dependent manner, the laser first induced reactive oxygen species (ROS), which are chemically active molecules containing oxygen that play an important role in cellular function. The ROS activated the latent TGF-1complex which, in turn, differentiated the stem cells into dentin.

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Forget the dentist's drill, use lasers to heal teeth

By Sykes24Tracey

Open wide, this won't hurt a bit. That might actually be true if the dentist's drill is replaced by a promising low-powered laser that can prompt stem cells to make damaged hard tissue in teeth grow back. Such minimally invasive treatment could one day offer an easy way to repair or regrow our pearly whites.

When a tooth is chipped or damaged, dentists replace it with ceramic or some other inert material, but these deteriorate over time.

To find something better, researchers have begun to look to regenerative medicine and in particular to stem cells to promote tissue repair. Most potential stem cell therapies require the addition of growth factors or chemicals to coax dormant stem cells to differentiate into the required cell type. These chemicals would be applied either directly to the recipient's body, or to stem cells that have been removed from the body and cultured in a dish for implantation.

But such treatments have yet to make it into the doctor's clinic because the approach needs to be precisely controlled so that the stem cells don't differentiate uncontrollably.

Praveen Arany at the National Institute of Dental and Craniofacial Research in Bethesda, Maryland, and his colleagues wondered whether they could use stem cells to heal teeth, but bypass the addition of chemicals by harnessing the body's existing mechanisms.

"Everything we need is in the existing tooth structure the adult stem cells, the growth factors, and exactly the right conditions," says Arany.

So they tried laser light, because it can promote regeneration in heart, skin, lung, and nerve tissues.

To mimic an injury, Arany's team used a drill to remove a piece of dentin the hard, calcified tissue beneath a tooth's enamel that doesn't normally regrow from the tooth of a rat. They then shone a non-ionising, low-power laser on the exposed tooth structure and the soft tissue underneath it. This allowed the light to reach the dental stem cells deep inside the pulp of the tooth.

Twelve weeks after a single 5-minute treatment, new dentin had formed in the cavity. Similar dentin production was seen in mice and in cultured human dental stem cells.

It not quite the end of the dentist's intervention though, they would still need to cap the tooth to protect it, because the stem cells that produce enamel are not present in adults.

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Skin Cell Research Suggests Schizophrenia Begins in Womb

By raymumme

By Traci Pedersen Associate News Editor Reviewed by John M. Grohol, Psy.D. on May 25, 2014

Neurons generated from the skin cells of schizophrenia patients behave strangely in the early developmental stages, offering clues that might lead to earlier detection and treatment, according to scientists from the Salk Institute.

The study, published in the journal Molecular Psychiatry, supports the theory that the neurological dysfunction that eventually leads to schizophrenia may begin in the brains of fetuses.

This study aims to investigate the earliest detectable changes in the brain that lead to schizophrenia, said Fred H. Gage, Ph.D., professor of genetics at Salk. We were surprised at how early in the developmental process that defects in neural function could be detected.

Up until now, scientists could only study the disease by examining the brains of cadavers; but age, stress, medication, or drug abuse had often changed or damaged these brains, making it harder to figure out the where it all began.

The Salk scientists were able to go around this obstacle by using stem cell technologies. They took skin cells from patients, coaxed the cells back to an earlier stem cell form and then prompted them to grow into very early-stage neurons called neural progenitor cells (NPCs). These NPCs are similar to cells found in the brain of a fetus.

The researchers tested the cells in two ways: In one test, they looked at how far the cells moved and interacted with particular surfaces; in the other test, they looked at cell stress by imaging mitochondria, tiny organelles that generate energy for the cells.

On both tests, the NPCs from schizophrenia patients differed in significant ways from those taken from people without the disease.

In particular, cells taken from people with schizophrenia showed unusual activity in two major classes of proteins: those involved in adhesion and connectivity, and those involved in oxidative stress. Schizophrenia neural cells seemed to have aberrant migration (which may result in the poor connectivity seen later in the brain) and greater levels of oxidative stress.

These results support the current theory that eventsduring pregnancy can contribute to schizophrenia, even though symptoms typically dont begin until early adulthood. For example, previous research suggests that pregnant mothers who experience infection, malnutrition, or extreme stress are at greater risk of having children with schizophrenia.

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Cosmetic essentials for flawless you

By Dr. Matthew Watson

New Delhi, May 24 (IANS) It's that time of the year again when the sun shines the brightest only to take your skin's shine away! How about trying some different ways to get flawless skin?

Sangeeta Amladi, head medical services with Kaya Skin Clinic, shares tips that will help one look radiant during summer.

* Say goodbye to pigmentation and uneven skin tone with skin lightening miracles. This skincare treatment is designed to reduce tan and visibly lighten your skin, leaving it fresh and glowing.

* Sun is known to cause skin damage, including wrinkles and aging skin disorders. Some beauty brands are hence using a new miracle ingredient stem cell in anti-aging creams. Stem cells have a remarkable potential to not only repair the body internally and rejuvenate the skin cells but it also slow skin aging. This new technology is a breakthrough solution to flaunt an ageless beautiful skin.

* With the increased level of pollution, there is a growing need for detoxifying the skin. Detox mask contains active blend of antioxidants which exfoliates and deep clean the pores without over-drying the skin. This gentle treatment helps detoxify, hydrate, and rejuvenate skin thus giving it a natural glow.

* Dare to go backless this summer with 'Back' beauty! Pamper your back with a microdermabrasion therapy (a light cosmetic procedure) to sport that spotless and smooth back. This therapy cleanses, polishes and moisturizes the highly ignored skin on our back. It removes the layer of dead skin to reveal a radiant and attractive back

* With the sun soaking all the moisture from your skin, only drinking water is not sufficient to keep it moisturized. Moisturizer with ceramides is another new age product that helps maintain the skin's lipid balance. There are also some studies that have shown that these ceramide induced moisturizers treat eczema as well. A ceremide induced moisturizer is definitely an answer to pamper dry skin

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Functional nerve cells from skin cells

By NEVAGiles23

15 hours ago These are mature nerve cells generated from human cells using enhanced transcription factors. Credit: Fahad Ali

A new method of generating mature nerve cells from skin cells could greatly enhance understanding of neurodegenerative diseases, and could accelerate the development of new drugs and stem cell-based regenerative medicine.

The nerve cells generated by this new method show the same functional characteristics as the mature cells found in the body, making them much better models for the study of age-related diseases such as Parkinson's and Alzheimer's, and for the testing of new drugs.

Eventually, the technique could also be used to generate mature nerve cells for transplantation into patients with a range of neurodegenerative diseases.

By studying how nerves form in developing tadpoles, researchers from the University of Cambridge were able to identify ways to speed up the cellular processes by which human nerve cells mature. The findings are reported in the May 27th edition of the journal Development.

Stem cells are our master cells, which can develop into almost any cell type within the body. Within a stem cell, there are mechanisms that tell it when to divide, and when to stop dividing and transform into another cell type, a process known as cell differentiation. Several years ago, researchers determined that a group of proteins known as transcription factors, which are found in many tissues throughout the body, regulate both mechanisms.

More recently, it was found that by adding these proteins to skin cells, they can be reprogrammed to form other cell types, including nerve cells. These cells are known as induced neurons, or iN cells. However, this method generates a low number of cells, and those that are produced are not fully functional, which is a requirement in order to be useful models of disease: for example, cortical neurons for stroke, or motor neurons for motor neuron disease.

In addition, for age-related diseases such as Parkinson's and Alzheimer's, both of which affect millions worldwide, mature nerve cells which show the same characteristics as those found in the body are crucial in order to enhance understanding of the disease and ultimately determine the best way to treat it.

"When you reprogramme cells, you're essentially converting them from one form to another but often the cells you end up with look like they come from embryos rather than looking and acting like more mature adult cells," said Dr Anna Philpott of the Department of Oncology, who led the research. "In order to increase our understanding of diseases like Alzheimer's, we need to be able to work with cells that look and behave like those you would see in older individuals who have developed the disease, so producing more 'adult' cells after reprogramming is really important."

By manipulating the signals which transcription factors send to the cells, Dr Philpott and her collaborators were able to promote cell differentiation and maturation, even in the presence of conflicting signals that were directing the cell to continue dividing.

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2 Reasons Why Growth Factors and Stem Cells are a Breakthough for Aging Skin, Says Sublime Beauty

By daniellenierenberg

St. Petersburg, FL (PRWEB) May 20, 2014

A breakthrough for rejuvenating aging skin today includes topical stem cells rich in Growth Factors. These are non-embryonic stem cells.

Collagen is lost during the aging process as production slows down, a contributing factor in the formation of wrinkles, lines, sagging and thinning of skin.

"A very effective way to reduce wrinkles, improve skin quality and boost collagen levels is through Human Fibroblast Conditioned Media," says Kathy Heshelow, founder of Sublime Beauty. "Human Fibroblast Conditioned Media contains key ingredients for rejuvenation of skinespecially natural Growth Factors and other proteins."

2 reasons why these Growth Factors are key for anti-aging skin care:

1) Growth Factors, when used topically, stimulate skin to create more collagen. Results include smoother, healthier skin with diminished wrinkles. Collagen is the structure holding up skin, essential for smoothness.

2) Growth Factors help to replace and regenerate the nutrients needed by skin for rejuvenation. It promotes skin tissue repair and strengthens the elastic fibers which give the skin its softness and suppleness.

"We added our stem cell serum to the Sublime Beauty line for those that wanted a higher end, scientific formula," says Heshelow. "Our serum is of high purity with no fillers and is made in the U.S under strict conditions."

Expensive to make, Heshelow says the Sublime Beauty serum is less expensive than many similar serums found on the market, which can range from $300 to $500. "Our serum retails under $160," Heshelow says.

Use twice daily and see first results in about 2 weeks.

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The Young Sperm, Poised for Greatness

By raymumme

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Newswise SALT LAKE CITY In the body, a skin cell will always be skin, and a heart cell will always be heart. But in the first hours of life, cells in the nascent embryo become totipotent: they have the incredible flexibility to mature into skin, heart, gut, or any type of cell.

It was long assumed that the joining of egg and sperm launched a dramatic change in how and which genes were expressed. Instead, new research shows that totipotency is a step-wise process, manifesting as early as in precursors to sperm, called adult germline stem cells (AGSCs), which reside in the testes.

The study was co-led by Bradley Cairns, Ph.D., University of Utah professor of oncological sciences, and Huntsman Cancer Institute investigator, and Ernesto Guccione, Ph.D., of the Agency for Science Technology and Research in Singapore. They worked closely with first author and Huntsman Cancer Institute postdoctoral fellow, Saher Sue Hammond, Ph.D. The research was published online in the journal Cell Stem Cell.

Typically, sperm precursors live a mundane life. They divide, making more cells like themselves, until they receive the signal instructing them to mature into sperm.

There is evidence, however, that these cells have the potential to do more. Under the unusual conditions that promote the cells to form dense cancerous masses called testicular teratomas, the young sperm transform into precursors of skin, muscle, and gut.

This realization prompted the investigators to examine the gene program within sperm precursors. They wondered, would it be like that of a cell that is destined to become a single cell type, or like that of a cell with the potential to become anything?

The answer, they found, is that the sperm precursors are somewhere in between. The most telling evidence is the status of a quartet of genes: Lefty, Sox2, Nanog, and Prdm14. When activated, the genes can trigger a cascade of events that give cells stem cell properties. In cells limited to becoming one cell type, the genes are silent.

Yet in sperm precursors, the genes bear a code of chemical tags, called methylation groups, indicating that the four genes are silenced, but poised to become active. In other words, embedded within these cells, is the potential to become totipotent.

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Herpes-loaded stem cells used to kill brain tumors

By Sykes24Tracey

Harvard Stem Cell Institute (HSCI) scientists at Massachusetts General Hospital have a potential solution for how to more effectively kill tumor cells using cancer-killing viruses. The investigators report that trapping virus-loaded stem cells in a gel and applying them to tumors significantly improved survival in mice with glioblastoma multiforme, the most common brain tumor in human adults and also the most difficult to treat.

The work, led by Khalid Shah, MS, PhD, an HSCI Principal Faculty member, is published in the Journal of the National Cancer Institute. Shah heads the Molecular Neurotherapy and Imaging Laboratory at Massachusetts General Hospital.

Cancer-killing or oncolytic viruses have been used in numerous phase 1 and 2 clinical trials for brain tumors but with limited success. In preclinical studies, oncolytic herpes simplex viruses seemed especially promising, as they naturally infect dividing brain cells. However, the therapy hasn't translated as well for human patients. The problem previous researchers couldn't overcome was how to keep the herpes viruses at the tumor site long enough to work.

Shah and his team turned to mesenchymal stem cells (MSCs) -- a type of stem cell that gives rise to bone marrow tissue -- which have been very attractive drug delivery vehicles because they trigger a minimal immune response and can be utilized to carry oncolytic viruses. Shah and his team loaded the herpes virus into human MSCs and injected the cells into glioblastoma tumors developed in mice. Using multiple imaging markers, it was possible to watch the virus as it passed from the stem cells to the first layer of brain tumor cells and subsequently into all of the tumor cells.

"So, how do you translate this into the clinic?" asked Shah, who also is an Associate Professor at Harvard Medical School.

"We know that 70-75 percent of glioblastoma patients undergo surgery for tumor debulking, and we have previously shown that MSCs encapsulated in biocompatible gels can be used as therapeutic agents in a mouse model that mimics this debulking," he continued. "So, we loaded MSCs with oncolytic herpes virus and encapsulated these cells in biocompatible gels and applied the gels directly onto the adjacent tissue after debulking. We then compared the efficacy of virus-loaded, encapsulated MSCs versus direct injection of the virus into the cavity of the debulked tumors."

Using imaging proteins to watch in real time how the virus combated the cancer, Shah's team noticed that the gel kept the stem cells alive longer, which allowed the virus to replicate and kill any residual cancer cells that were not cut out during the debulking surgery. This translated into a higher survival rate for mice that received the gel-encapsulated stem cells.

"They survived because the virus doesn't get washed out by the cerebrospinal fluid that fills the cavity," Shah said. "Previous studies that have injected the virus directly into the resection cavity did not follow the fate of the virus in the cavity. However, our imaging and side-by-side comparison studies showed that the naked virus rarely infects the residual tumor cells. This could give us insight into why the results from clinical trials with oncolytic viruses alone were modest."

The study also addressed another weakness of cancer-killing viruses, which is that not all brain tumors are susceptible to the therapy. The researchers' solution was to engineer oncolytic herpes viruses to express an additional tumor-killing agent, called TRAIL. Again, using mouse models of glioblastoma -- this time created from brain tumor cells that were resistant to the herpes virus -- the therapy led to increased animal survival.

"Our approach can overcome problems associated with current clinical procedures," Shah said. "The work will have direct implications for designing clinical trials using oncolytic viruses, not only for brain tumors, but for other solid tumors."

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New Stem Cell Finding Bodes Well for Future Medical Use in Humans

By daniellenierenberg

Concerns that stem cells could cause cancer in recipients are fading further with a new study

New bone formation (stained bright green under ultra-violet light) was seen in monkeys given their own reprogrammed stem cells. Courtesy of Nature magazine

A major concern over using stem cells is the risk of tumors: but now a new study shows that It takes a lot of effort to get induced pluripotent stem (iPS) cells to grow into tumors after they have been transplanted into a monkey. The findings will bolster the prospects of one day using such cells clinically in humans.

Making iPS cells from an animal's own skin cells and then transplanting them back into the creature also does not trigger an inflammatory response as long as the cells have first been coaxed to differentiate towards a more specialized cell type. Both observations, published inCell Reports today, bode well for potential cell therapies.

It's important because the field is very controversial right now, saysAshleigh Boyd,a stem-cell researcher at University College London, who was not involved in the work. It is showing that the weight of evidence is pointing towards the fact that the cells won't be rejected.

Pluripotent stem cells can be differentiated into many different specialized cell types in culture and so are touted for their potential as therapies to replace tissue lost in diseases such as Parkinsons and some forms of diabetes and blindness. iPS cells, which are made by reprogramming adult cells, have an extra advantage because transplants made from them could be genetically matched to the recipient.

Researchers all over the world are pursuing therapies based on iPS cells, and a group in Japan began enrolling patients for a human study last year. But work in mice has suggested controversially that even genetically matched iPS cellscan trigger an immune response, and pluripotent stem cells can also form slow-growing tumors, another safety concern.

Closer to human Cynthia Dunbar, a stem-cell biologist at the National Institutes of Health in Bethesda, Maryland, who led the new study, decided to evaluate both concerns in healthy rhesus macaques. Human stem cells are normally only studied for their ability to form tumors in mice as a test of pluripotency if the animals immune systems are compromised, she says.

We really wanted to set up a model that was closer to human. It was somewhat reassuring that in a normal monkey with a normal immune system you had to give a whole lot of immature cells to get any kind of tumour to grow, and they were very slow growing.

Dunbar and her team made iPS cells from skin and white blood cells from two rhesus macaques, and transplanted the iPS cells back into the monkeys that provided them. It took 20 times as many iPS cells to form a tumor in a monkey, compared with the numbers needed in an immunocompromised mouse. Such information will be valuable for assessing safety risks of potential therapies, Dunbar says. And although the iPS cells did trigger a mild immune response attracting white blood cells and causing local inflammation iPS cells that had first been differentiated to a more mature state did not.

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Do products used in cosmetics work for the hair?

By Sykes24Tracey

A number of ingredients like ceramides, collagen, stem cells and antioxidants that are commonly associated with cosmetics are being featured in products for the hair. Do they work as well?

In the quest for a healthy and shining mane, a number of new products are being launched in the market on a regular basis. It has been observed that many of these are said to contain elements that are normally associated with skin care. Products with collagen, ceramides, hyaluronic acid, stem cells and so on have long been proven beneficial to plump up skin, reduce fine lines, lighten dark spots and keep skin healthy and radiant. However, recently a number of these have been seen in hair care products like shampoos and conditioners. The question remains though is of they work just as well on the mane. Copper peptides, for example is considered an effective skin regeneration ingredient and research shows it works well for the scalp too producing thicker, healthier hair. Ceramides can be effective in forming a protective coat around the hair shaft and strengthening it, while collagen helps hair hold onto moisture making it look thicker and fuller. Antioxidants are said to neutralise the free radicals preventing dullness of locks.

SCALP IS SIMILAR TO SKIN Tisha Kapur Khurana, beauty expert and executive director, Bottega di Lungavita explains similar ingredients can be used on the skin and hair sometimes because the scalp is covered with thicker skin similar to the rest of our body. It is a thick layer of skin with many sebaceous glands which produce oil or sebum to protect the hair. Collagen is a protein that is found in the body and is a necessity for good health. The collagen supplements let hair grow long and strong. It increases the body's natural hair-building proteins. Moreover, if applied to the scalp, it can reduce the look and dryness of grey hair. Even stem cells work as the hair follicles contain cells which may lead to successfully treating baldness. When buying a product you should always consider the hair type curly or straight as well as thick or fine and accordingly choose products, she says.

BE CAREFUL It is advisable not to use similar products for your hair and skin. Your skin is very tender and it needs really mild products to cleanse and clear the dirt and impurities. On the other hand, while you do need mild products for your hair as well, the shampoos and conditioners are mild but effective enough to cleanse the grime, dandruff and other impurities that get lodged in your scalp, explains Priti Mehta, founder and director, Omved. She adds, Standard cosmetics often include synthetic and sometimes even animal-derived ingredients. When you use natural options for your skin and hair, it is likely to help your skin feel and breathe better. Anything that has SLS, parabens, preservatives, fragrance, and colours to name a few listed on it should be avoided.

HAVE SOME BENEFITS Dr Apratim Goel, dermatologist, Cutis Skin Studio says some of these ingredients can work. Collagen or ceramides are larger molecules which are doubtful on skin as well. However these ingredients have been used regularly in hair care products. However, there is no controlled studies of efficacy of these ingredients in hair. Stem cells and antioxidants, though, do work for hair. Stem cell injections are a regular treatment for boosting hair growth. Further, plant stem cells are available as hair serums and give good results against hair loss. Regarding antioxidants, they are very important for hair care as hair especially coloured or treated locks are very prone to damage from sun as well as chemical exposure.

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Stem Cells Make Heart Disease-on-a-Chip

By Dr. Matthew Watson

Harvard scientists have merged stem cell and organ-on-a-chip technologies to grow, for the first time, functioning human heart tissue carrying an inherited cardiovascular disease. The research appears to be a big step forward for personalized medicine because it is working proof that a chunk of tissue containing a patient's specific genetic disorder can be replicated in the laboratory.

The work, published in May 2014 in Nature Medicine, is the result of a collaborative effort bringing together scientists from the Harvard Stem Cell Institute, the Wyss Institute for Biologically Inspired Engineering, Boston Children's Hospital, the Harvard School of Engineering and Applied Sciences, and Harvard Medical School. It combines the organs-on-chips expertise of Kevin Kit Parker, PhD, and stem cell and clinical insights by William Pu, MD.

A release from Harvard explains that using their interdisciplinary approach, the investigators modeled the cardiovascular disease Barth syndrome, a rare X-linked cardiac disorder caused by mutation of a single gene called Tafazzin, or TAZ. The disorder, which is currently untreatable, primarily appears in boys, and is associated with a number of symptoms affecting heart and skeletal muscle function.

The researchers took skin cells from two Barth syndrome patients, and manipulated the cells to become stem cells that carried these patients' TAZ mutations. Instead of using the stem cells to generate single heart cells in a dish, the cells were grown on chips lined with human extracellular matrix proteins that mimic their natural environment, tricking the cells into joining together as they would if they were forming a diseased human heart. The engineered diseased tissue contracted very weakly, as would the heart muscle seen in Barth syndrome patients. The investigators then used genome editinga technique pioneered by Harvard collaborator George Church, PhDto mutate TAZ in normal cells, confirming that this mutation is sufficient to cause weak contraction in the engineered tissue. On the other hand, delivering the TAZ gene product to diseased tissue in the laboratory corrected the contractile defect, creating the first tissue-based model of correction of a genetic heart disease. The release quotes Parker as saying, "You don't really understand the meaning of a single cell's genetic mutation until you build a huge chunk of organ and see how it functions or doesn't function. In the case of the cells grown out of patients with Barth syndrome, we saw much weaker contractions and irregular tissue assembly. Being able to model the disease from a single cell all the way up to heart tissue, I think that's a big advance."

Furthermore, the scientists discovered that the TAZ mutation works in such a way to disrupt the normal activity of mitochondria, often called the power plants of the cell for their role in making energy. However, the mutation didn't seem to affect overall energy supply of the cells. In what could be a newly identified function for mitochondria, the researchers describe a direct link between mitochondrial function and a heart cell's ability to build itself in a way that allows it to contract. "The TAZ mutation makes Barth syndrome cells produce an excess amount of reactive oxygen species or ROSa normal byproduct of cellular metabolism released by mitochondriawhich had not been recognized as an important part of this disease," said Pu, who cares for patients with the disorder. "We showed that, at least in the laboratory, if you quench the excessive ROS production then you can restore contractile function," Pu added. "Now, whether that can be achieved in an animal model or a patient is a different story, but if that could be done, it would suggest a new therapeutic angle." His team is now trying to translate this finding by doing ROS therapy and gene replacement therapy in animal models of Barth syndrome to see if anything could potentially help human patients. At the same time, the scientists are using their human 'heart disease-on-a-chip' as a testing platform for drugs that are potentially under trial or already approved that might be useful to treat the disorder.

"We tried to thread multiple needles at once and it certainly paid off," Parker said. "I feel that the technology that we've got arms industry and university-based researchers with the tools they need to go after this disease." Both Parker and Pu, who first talked about collaborating at a 2012 Stockholm conference, credit their partnership and scientific consilience for the success of this research. Parker asserted that the 'organs-on-chips' technology that has been a flagship of his lab only worked so fast and well because of the high quality of Pu's patient-derived cardiac cells. "When we first got those cells down on the chip, Megan, one of the joint first authors, texted me 'this is working,'" he recalled. "We thought we'd have a much harder fight." "When I'm asked what's unique about being at Harvard, I always bring up this story," Pu said. "The diverse set of people and cutting-edge technology available at Harvard certainly made this study possible." The researchers also involved in this work include: Joint first authors Gang Wang, MD, of Boston Children's Hospital, and Megan McCain, PhD, who earned her degree at the Harvard School of Engineering and Applied Sciences and is now an assistant professor at the University of Southern California. Amy Roberts, MD, of Boston Children's Hospital, and Richard Kelley, MD, PhD, at the Kennedy Krieger Institute provided patient data and samples, and Frdric Vaz, PhD, and his team at the Academic Medical Center in the Netherlands conducted additional analyses. Technical protocols were shared by Kenneth Chien, MD, PhD, at the Karolinska Institutet.

Kevin Kit Parker, PhD, is the Tarr Family Professor of Bioengineering and Applied Physics in Harvard's School of Engineering and Applied Sciences, a Core Faculty member of the Wyss Institute for Biologically Inspired Engineering, and a Principal Faculty member of the Harvard Stem Cell Institute. William Pu, MD, is an Associate Professor at Harvard Medical School, a member of the Department of Cardiology at Boston Children's Hospital, and an Affiliated Faculty member of the Harvard Stem Cell Institute. George Church, PhD, is a Professor of Genetics at Harvard Medical School and a Core Faculty member of the Wyss Institute of Biologically Inspired Engineering. The work was supported by the Barth Syndrome Foundation, Boston Children's Hospital, the National Institutes of Health, and charitable donations from Edward Marram, Karen Carpenter, and Gail Federici Smith.

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Stem cell technology points to early indicators of schizophrenia

By NEVAGiles23

Using new stem cell technology, scientists at the Salk Institute have shown that neurons generated from the skin cells of people with schizophrenia behave strangely in early developmental stages, providing a hint as to ways to detect and potentially treat the disease early.

The findings of the study, published online in April's Molecular Psychiatry, support the theory that the neurological dysfunction that eventually causes schizophrenia may begin in the brains of babies still in the womb.

"This study aims to investigate the earliest detectable changes in the brain that lead to schizophrenia," says Fred H. Gage, Salk professor of genetics. "We were surprised at how early in the developmental process that defects in neural function could be detected."

Currently, over 1.1 percent of the world's population has schizophrenia, with an estimated three million cases in the United States alone. The economic cost is high: in 2002, Americans spent nearly $63 billion on treatment and managing disability. The emotional cost is higher still: 10 percent of those with schizophrenia are driven to commit suicide by the burden of coping with the disease.

Although schizophrenia is a devastating disease, scientists still know very little about its underlying causes, and it is still unknown which cells in the brain are affected and how. Previously, scientists had only been able to study schizophrenia by examining the brains of patients after death, but age, stress, medication or drug abuse had often altered or damaged the brains of these patients, making it difficult to pinpoint the disease's origins.

The Salk scientists were able to avoid this hurdle by using stem cell technologies. They took skin cells from patients, coaxed the cells to revert back to an earlier stem cell form and then prompted them to grow into very early-stage neurons (dubbed neural progenitor cells or NPCs). These NPCs are similar to the cells in the brain of a developing fetus.

The researchers generated NPCs from the skin cells of four patients with schizophrenia and six people without the disease. They tested the cells in two types of assays: in one test, they looked at how far the cells moved and interacted with particular surfaces; in the other test, they looked at stress in the cells by imaging mitochondria, which are tiny organelles that generate energy for the cells.

On both tests, the Salk team found that NPCs from people with schizophrenia differed in significant ways from those taken from unaffected people.

In particular, cells predisposed to schizophrenia showed unusual activity in two major classes of proteins: those involved in adhesion and connectivity, and those involved in oxidative stress. Neural cells from patients with schizophrenia tended to have aberrant migration (which may result in the poor connectivity seen later in the brain) and increased levels of oxidative stress (which can lead to cell death).

These findings are consistent with a prevailing theory that events occurring during pregnancy can contribute to schizophrenia, even though the disease doesn't manifest until early adulthood. Past studies suggest that mothers who experience infection, malnutrition or extreme stress during pregnancy are at a higher risk of having children with schizophrenia. The reason for this is unknown, but both genetic and environmental factors likely play a role.

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New Stem Cell Research Points to Early Indicators of Schizophrenia

By Dr. Matthew Watson

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Newswise LA JOLLAUsing new stem cell technology, scientists at the Salk Institute have shown that neurons generated from the skin cells of people with schizophrenia behave strangely in early developmental stages, providing a hint as to ways to detect and potentially treat the disease early.

The findings of the study, published online in April's Molecular Psychiatry, support the theory that the neurological dysfunction that eventually causes schizophrenia may begin in the brains of babies still in the womb.

"This study aims to investigate the earliest detectable changes in the brain that lead to schizophrenia," says Fred H. Gage, Salk professor of genetics. "We were surprised at how early in the developmental process that defects in neural function could be detected."

Currently, over 1.1 percent of the world's population has schizophrenia, with an estimated three million cases in the United States alone. The economic cost is high: in 2002, Americans spent nearly $63 billion on treatment and managing disability. The emotional cost is higher still: 10 percent of those with schizophrenia are driven to commit suicide by the burden of coping with the disease.

Although schizophrenia is a devastating disease, scientists still know very little about its underlying causes, and it is still unknown which cells in the brain are affected and how. Previously, scientists had only been able to study schizophrenia by examining the brains of patients after death, but age, stress, medication or drug abuse had often altered or damaged the brains of these patients, making it difficult to pinpoint the disease's origins.

The Salk scientists were able to avoid this hurdle by using stem cell technologies. They took skin cells from patients, coaxed the cells to revert back to an earlier stem cell form and then prompted them to grow into very early-stage neurons (dubbed neural progenitor cells or NPCs). These NPCs are similar to the cells in the brain of a developing fetus.

The researchers generated NPCs from the skin cells of four patients with schizophrenia and six people without the disease. They tested the cells in two types of assays: in one test, they looked at how far the cells moved and interacted with particular surfaces; in the other test, they looked at stress in the cells by imaging mitochondria, which are tiny organelles that generate energy for the cells.

On both tests, the Salk team found that NPCs from people with schizophrenia differed in significant ways from those taken from unaffected people.

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New Stem Cell Research Points to Early Indicators of Schizophrenia

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'Heart Disease-On-A-Chip' Made From Patient Stem Cells

By daniellenierenberg

Image Caption: Researchers use modified RNA transfection to correct genetic dysfunction in heart stem cells derived from Barth syndrome patients. The series of images show how inserting modified RNA into diseased cells causes the cells to produce functioning versions of the TAZ protein (first image: in green) that correctly localize in the mitochondria (second image: in red). When the images are merged to demonstrate this localization, green overlaps with red, giving the third image a yellow color. Credit: Gang Wang and William Pu/Boston Children's Hospital

[ Watch The Video: Cardiac Tissue Contractile Strength Differences Shown Using Heart-On-A-Chip ]

Harvard University

Harvard scientists have merged stem cell and organ-on-a-chip technologies to grow, for the first time, functioning human heart tissue carrying an inherited cardiovascular disease. The research appears to be a big step forward for personalized medicine, as it is working proof that a chunk of tissue containing a patients specific genetic disorder can be replicated in the laboratory.

The work, published in Nature Medicine, is the result of a collaborative effort bringing together scientists from the Harvard Stem Cell Institute, the Wyss Institute for Biologically Inspired Engineering, Boston Childrens Hospital, the Harvard School of Engineering and Applied Sciences, and Harvard Medical School. It combines the organs-on-chips expertise of Kevin Kit Parker, PhD, and stem cell and clinical insights by William Pu, MD.

Using their interdisciplinary approach, the investigators modeled the cardiovascular disease Barth syndrome, a rare X-linked cardiac disorder caused by mutation of a single gene called Tafazzin, or TAZ. The disorder, which is currently untreatable, primarily appears in boys, and is associated with a number of symptoms affecting heart and skeletal muscle function.

The researchers took skin cells from two Barth syndrome patients, and manipulated the cells to become stem cells that carried these patients TAZ mutations. Instead of using the stem cells to generate single heart cells in a dish, the cells were grown on chips lined with human extracellular matrix proteins that mimic their natural environment, tricking the cells into joining together as they would if they were forming a diseased human heart. The engineered diseased tissue contracted very weakly, as would the heart muscle seen in Barth syndrome patients.

The investigators then used genome editinga technique pioneered by Harvard collaborator George Church, PhDto mutate TAZ in normal cells, confirming that this mutation is sufficient to cause weak contraction in the engineered tissue. On the other hand, delivering the TAZ gene product to diseased tissue in the laboratory corrected the contractile defect, creating the first tissue-based model of correction of a genetic heart disease.

You dont really understand the meaning of a single cells genetic mutation until you build a huge chunk of organ and see how it functions or doesnt function, said Parker, who has spent over a decade working on organs-on-chips technology. In the case of the cells grown out of patients with Barth syndrome, we saw much weaker contractions and irregular tissue assembly. Being able to model the disease from a single cell all the way up to heart tissue, I think thats a big advance.

Furthermore, the scientists discovered that the TAZ mutation works in such a way to disrupt the normal activity of mitochondria, often called the power plants of the cell for their role in making energy. However, the mutation didnt seem to affect overall energy supply of the cells. In what could be a newly identified function for mitochondria, the researchers describe a direct link between mitochondrial function and a heart cells ability to build itself in a way that allows it to contract.

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'Heart Disease-On-A-Chip' Made From Patient Stem Cells

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Eczema may reduce skin cancer risk

By JoanneRUSSELL25

Eczema is one of the most common skin conditions, affecting up to 30% of people in the US. Symptoms include dry, itchy skin and rashes. But according to new research, having eczema may not be all that bad; it could reduce the risk of skin cancer.

In a study published in the journal eLife, researchers from Kings College London in the UK say that eczema, also known as atopic dermatitis, activates an immune response that sheds potentially cancerous cells from the skin, preventing tumor formation.

According to the research team, including Prof. Fiona Watt of the Centre for Stem Cells and Regenerative Medicine at Kings College, previous studies have suggested that eczema may reduce the risk of skin cancer.

However, they note that this association has proven difficult to confirm in human studies, as medication for eczema may influence cancer risk. Furthermore, symptoms of the condition vary in severity in each individual.

Eczema reduced tumor formation in mice models

For their study, the team genetically engineered mice to have skin defects commonly found in humans with eczema.

They did this by removing structural proteins in the outer layers of their skin, causing them to have an abnormal skin barrier.

The researchers then tested two cancer-causing chemicals in the genetically engineered mice, as well as in normal mice.

They found that the number of benign tumors in defected mice was six times lower than the number found in the normal mice.

Further investigation revealed that although both the defected and normal mice had equal susceptibility to mutations caused by the chemicals, the defected mice had an exaggerated inflammatory response that resulted in potentially cancerous cells being shed from the skin.

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Eczema may reduce skin cancer risk

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Stem cell progeny tell their parents when to turn on

By raymumme

20 hours ago A signal from Transit-Amplifying Cells (TACs) activates stem cells in the hair follicle, researchers have found. Both types of cells appear in green (top), with TACs clustered lower down. The researchers identified the signal as Sonic Hedgehog. In experiments, such as this one (bottom), they disabled the signal, interfering with hair growth and regeneration.

(Phys.org) Stem cells switch off and on, sometimes dividing to produce progeny cells and sometimes resting. But scientists don't fully understand what causes the cells to toggle between active and quiet states.

New research in Elaine Fuchs' Laboratory of Mammalian Cell Biology and Development focused on stem cells in the hair follicle to determine what switches them on. The researchers found cells produced by the stem cells, progeny known at Transit-Amplifying Cells or TACs, emit a signal that tells quiet hair follicle stem cells to become active.

"Many types of mammalian stem cells produce TACs, which act as an intermediate between the stem cells and their final product: fully differentiated cells in blood, skin and elsewhere," says Ya-Chieh Hsu, who conducted the research while as a postdoc in the lab and will soon move to Harvard University. "In the past, TACs were seen as a population of cells that sat by passively cranking out tissues. No one expected them to play a regulatory role."

Hsu and Fuchs went a step further to identify the signal sent out by the TACs. They pinpointed a cell-division promoting protein called Sonic Hedgehog, which plays a role in the embryonic development of the brain, eyes and limbs.

Stem cells are medically valuable because they have the potential to produce a number of specialized cells suitable for specific roles. Stem cells' production of these differentiated cells is crucial to normal maintenance, growth and repair. Many tissues have two populations of stem cells: one that divides rarely, known as the quiescent stem cells, and another that is more prone to proliferate, known as primed stem cells. Regardless of their proliferation frequency, most stem cells in humans do not directly produce differentiated progeny cells; instead, they give rise to an intermediate proliferating population, the TACs.

The hair follicle, the tiny organ that produces a hair, forms a narrow cavity down into the skin. It cycles between rounds of growth, destruction and rest. When entering the growth phase, the primed stem cell population is always the first to divide and generates the TACs clustered lower down in the hair follicle. Primed stem cell proliferation sets the stage for the next round of hair growth, a process which ensures hairs are replaced as they are lost over time. Proliferating TACs produce the hair shaft, as well as all the cells surrounding the hair underneath the skin, which make up the follicle itself.

At the outset, Hsu and Fuchs suspected a role for both the TACs and for Sonic Hedgehog in hair regeneration.

"We noticed that the primed stem cell population gets activated early and makes the TACs, while the quiescent stem cell population only becomes activated once TACs are generated. This correlation prompted us to look for a signal that is made by the TACs. Sonic Hedgehog is that signal, as we went on to demonstrate," explained Fuchs.

In experiments described this week in Cell, Hsu disabled TACs' ability to produce the Sonic Hedgehog protein by knocking out the gene responsible in the hair follicles of adult mice. As a result, the proliferation of hair follicle stem cells and their TACs are both compromised. They further showed that it is the quiescent stem cell population which requires Sonic Hedgehog directly for proliferation.

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Stem cell progeny tell their parents when to turn on

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