StemCell Therapy

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3D-printed Patch Can Help Mend a 'Broken' Heart Technology Networks In this study, researchers from the University of Minnesota-Twin Cities, University of Wisconsin-Madison, and University of Alabama-Birmingham used laser-based 3D-bioprinting techniques to incorporate stem cells derived from adult human heart cells on ...

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3D-printed Patch Can Help Mend a 'Broken' Heart - Technology Networks

The Emperor of All Maladies

Cancer is when an aberrant mutation in a cell leads it to prolifically divide, causingabnormal cell growth that can potentially spread to other parts of the body if untreated. Cancer is the second leading cause of death globally, with one in every six deaths caused by a type of cancer in 2015, leading to 8.8 million deaths.

Because different mutations can cause cancer, and cancerous cells can develop in many different parts of the body, doctors are continually coming up with different strategies for treating the disease. With each passing year, research on the topic continues to progress. From personalized vaccines to mecha-suit sperm, weve been looking inevery possible nook and cranny in hopes of finding an effective therapy that can work better than what we have today.

Currently, we use a host of methods to treat cancer, including surgery, radiation therapy, chemotherapy, immunotherapy, targeted therapy, hormone therapy, stem cell transplant, and precision medicine. While some cancer patients receive only one treatment, these treatments are normally used in conjunction to increase the rate of success.

Since the 1960s, our efforts in tackling cancer have progressed significantly. Patients back in the day had a five-year survival rate of around 50 percent. With the advent of these new therapies, some the most commonly diagnosed cancers in the U.S. have 5-year-survival rates at around 75 percent.

Many are hopeful that these numbers will soon improve again, with studies concluding that, of allnew cancer therapies that make it intorandomized controlled trials, at least 25 to 50 percent will improve current therapies. In fact, this might be the case for a newpotential cancer treatment that uses nanoparticles.

The next step in cancer therapies might be quietly waiting for its time in the limelight in Seattle, Washington, at the Fred Hutchinson Cancer Research Center, where scientists have constructed biodegradable nanoparticles that can genetically program immune cells while inside the bodyto target cancer cells. The study was published on April 17 in Nature Nanotechnologyand focused on the effect that nanoparticle-programmed immune T cells had on leukemia in mouse models.

The nanoparticles carried genes that code for chimeric antigen receptors(CARs), which are proteins designed by scientists to help immune cells target and destroy cancer. Once the immune cells undergo this molecular modification, they turn into an army of cancer serial killers.

This new method can eliminate expensive and time-consuming steps that lag previous T cell cancer therapies. The current protocol is that theT cells are removed from the patient, genetically altered, regrown, and infused back into the patient. The biodegradable nanoparticles will eliminate the removal, regrowth, and infusion steps by accomplishing the reprogramming step over a time span of 24 to 48 hourswhile the T cells are in the body.

When the researchers compared the nanoparticle-based method to current immunotherapy methods that require the T cells to be removed, researchers noticed that leukemia-induced mice lived an additional 58 days on average when compared to the mice that received the current treatment.

While these results are exciting, the researchers are looking to make the process safer before they move into human trials. But if this new technique is approved for humans, it could have many more applications. Scientists are looking to adapt the method for diseaseslike hepatitis, HIV, or even solid tumors.

By quickly arming patients immune cells to fed off disease, this new treatment could lower healthcare costs and improve the quality of patients lives.

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In the Future, Cells Reprogrammed Inside Our Bodies Will Fight Cancer for Us - Futurism

Newswise Johns Hopkins researchers today published new evidence refuting the long-held scientific belief that the gut nerve cells were born with are the same ones we die with.

In a report published in the journal Proceedings of the National Academy of Sciences, the investigators say the findinghas profound implications for the understanding and treatment of disorders and diseases that affect the digestive system.

Pankaj Jay Pasricha, M.B.B.S., M.D., professor of medicine and director of the Johns Hopkins Center for Neurogastroenterology, and Subhash Kulkarni, M.S., Ph.D., assistant professor at the Johns Hopkins University School of Medicine, led a research team that discovered the birth-and-death cycle of the neurons that form the network of millions of nerve cells throughout the digestive tract.

Previous studies have suggested that a healthy adult gut generates few or no new neurons. According to Pasricha, the Johns Hopkins study demonstrates that a healthy adult small intestine loses and regenerates about five percent of its nerve cells every day, or a third of them every week.

Scientific dogma believed that gut neurons dont regenerate and that this brain, known as the enteric nervous system, remained relatively static shortly after birth, Pasricha says. We now have proof that, not only do they regenerate, but the whole network turns completely over every few weeks in adult animals.

The enteric nervous system controls and regulates vital gastrointestinal functions such as digestion, immunity and inflammation. After the brain, the digestive tract contains the largest nervous system in the human body.

"The yin and the yang of neuronal loss and birth keeps us going," Kulkarni says.

Pasricha, Kulkarni and their team confined their research to the small intestines of healthy adult mice. Using a variety of techniques, they found proteins associated with neural cell death and were able to observe the loss of neurons. Their work provided irrefutable evidence of ongoing neuronal death due to apoptosis in the adult gut.

This significant rate of nerve cell loss left the research team with the question of how the gut maintains its relatively constant number of neurons.

"There could be only one answer," says Kulkarni. "The high turnover of neurons in the gut could only be reconciled by birth of newborn neurons, or neurogenesis."

Despite years of research, proof of neurogenesis in the healthy digestive system has been elusive. Scientists knew that the numbers of enteric neurons in a healthy small intestine remain remarkably constant for most of the adult life. While previous studies have shown that the adult gut contains cells that can generate neurons in lab settings outside of living organisms, finding whether such cells truly give birth to neurons in healthy adult animals eluded scientists for years.

Pasricha says the key to finding the process came when the team focused on tracing and following the behavior of cells that expressed Nestin, a protein typically associated with brain stem cells.

After years of staking out these Nestin-expressing cells and studying their location, behavior and fate in the adult gut tissue, the research team found that some of them, called enteric neural precursor cells, generated new neurons rapidly, shoring up and maintaining the large neuronal population that would otherwise dwindle fast in light of ongoing neuronal death.

The study also shows that any aberration that tilts the cells' birth-and-death balance may cause disease.

"Although previous studies have shown that regeneration of adult neurons may happen in an injured gut," Kulkarni says, "by and large, this appeared a relatively isolated and rare phenomenon. We now provide evidence that this happens continually and robustly in the adult healthy gut. It helps explain how this nervous system maintains itself, despite constant exposure to dietary factors, toxins, microbes and mechanical forces.

We didnt believe it ourselves, at first, Pasricha, whose lab has been working on these neural stem cells for many years, says of the findings. It's an extraordinary result; the mice get an entirely new brain in the gut every few weeks."

He cautions that their study was limited to the mouse small intestine and that further research is necessary to determine whether other species -- including humans -- and other regions of the gut experience the same cellular birth and death processes. Such studies are underway in Pasrichas Johns Hopkins lab.

The researchers hope the findings will help identify new regenerative and other therapies for gastrointestinal motility disorders like achalasia, gastroparesis, pseudo-obstruction, colonic inertia and other problems related to the digestive system.

"And as we dig deeper into this research," says Kulkarni, "we will gain new insights into a whole host of other diseases that affect not just the gut, but other organ systems with which this nervous system communicates, such as the brain."

Additional authors of the article are Jenna Leser, Ya-Yuan Fu, Liansheng Liu, Qian Li, Monalee Saha, Cuiping Li, Michael Anderson, Xinzhong Dong and Hongjun Song of The Johns Hopkins University School of Medicine; Manish J. Butte of the University of California, Los Angeles; E. Michelle Southard-Smith of Vanderbilt University Medical Center; Raj P. Kapur of Seattle Children's Hospital; Maria-Adelaide Micci of the University of Texas Medical Branch; Changsik Shin and Milena Bogunovic of the Pennsylvania State University; Shiue-Cheng Tang of the National Tsing Hua University; Grigori Enikolopov of Cold Spring Harbor Laboratory; Laren Becker of the Stanford University School of Medicine; Nikolai Rakhilin and Xiling Shen of Duke University.

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Hopkins Researchers Discover Birth-And-Death Life Cycle of Neurons in the Adult Mouse Gut - Newswise (press release)

Johns Hopkins researchers have published new evidence refuting the long-held scientific belief that the gut nerve cells we're born with are the same ones we die with.

In a report published in the journal Proceedings of the National Academy of Sciences, the investigators say the finding has profound implications for the understanding and treatment of disorders and diseases that affect the digestive system.

Pankaj Jay Pasricha M.B.B.S., M.D., , professor of medicine and director of the Johns Hopkins Center for Neurogastroenterology, and Subhash Kulkarni, M.S., Ph.D., assistant professor at the Johns Hopkins University School of Medicine, led a research team that discovered the birth-and-death cycle of the neurons that form the network of millions of nerve cells throughout the digestive tract.

Previous studies have suggested that a healthy adult gut generates few or no new neurons. According to Pasricha, the Johns Hopkins study demonstrates that a healthy adult small intestine loses and regenerates about five percent of its nerve cells every day, or a third of them every week.

"Scientific dogma believed that gut neurons don't regenerate and that this 'brain,' known as the enteric nervous system, remained relatively static shortly after birth," Pasricha says. "We now have proof that, not only do they regenerate, but the whole network turns completely over every few weeks in adult animals."

The enteric nervous system controls and regulates vital gastrointestinal functions such as digestion, immunity and inflammation. After the brain, the digestive tract contains the largest nervous system in the human body.

"The yin and the yang of neuronal loss and birth keeps us going," Kulkarni says.

Pasricha, Kulkarni and their team confined their research to the small intestines of healthy adult mice. Using a variety of techniques, they found proteins associated with neural cell death and were able to observe the loss of neurons. Their work provided irrefutable evidence of ongoing neuronal death due to apoptosis in the adult gut.

This significant rate of nerve cell loss left the research team with the question of how the gut maintains its relatively constant number of neurons.

"There could be only one answer," says Kulkarni. "The high turnover of neurons in the gut could only be reconciled by birth of newborn neurons, or neurogenesis."

Despite years of research, proof of neurogenesis in the healthy digestive system has been elusive. Scientists knew that the numbers of enteric neurons in a healthy small intestine remain remarkably constant for most of the adult life. While previous studies have shown that the adult gut contains cells that can generate neurons in lab settings outside of living organisms, finding whether such cells truly give birth to neurons in healthy adult animals eluded scientists for years.

Pasricha says the key to finding the process came when the team focused on tracing and following the behavior of cells that expressed Nestin, a protein typically associated with brain stem cells.

After years of "staking out" these Nestin-expressing cells and studying their location, behavior and fate in the adult gut tissue, the research team found that some of them, called "enteric neural precursor cells," generated new neurons rapidly, shoring up and maintaining the large neuronal population that would otherwise dwindle fast in light of ongoing neuronal death.

The study also shows that any aberration that tilts the cells' birth-and-death balance may cause disease.

"Although previous studies have shown that regeneration of adult neurons may happen in an injured gut," Kulkarni says, "by and large, this appeared a relatively isolated and rare phenomenon. We now provide evidence that this happens continually and robustly in the adult healthy gut. It helps explain how this nervous system maintains itself, despite constant exposure to dietary factors, toxins, microbes and mechanical forces."

"We didn't believe it ourselves, at first," Pasricha, whose lab has been working on these neural stem cells for many years, says of the findings. "It's an extraordinary result; the mice get an entirely new 'brain' in the gut every few weeks."

He cautions that their study was limited to the mouse small intestine and that further research is necessary to determine whether other species -- including humans -- and other regions of the gut experience the same cellular birth and death processes. Such studies are underway in Pasricha's Johns Hopkins lab.

The researchers hope the findings will help identify new regenerative and other therapies for gastrointestinal motility disorders like achalasia, gastroparesis, pseudo-obstruction, colonic inertia and other problems related to the digestive system.

"And as we dig deeper into this research," says Kulkarni, "we will gain new insights into a whole host of other diseases that affect not just the gut, but other organ systems with which this nervous system communicates, such as the brain."

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Researchers discover birth-and-death life cycle of neurons in the ... - Science Daily

Third in an occasional series on how Harvard researchers are tackling the problematic issues of aging.

If only, wrote an ancient Japanese poet, when one heard that Old Age was coming one could bolt the door.

Science is working on it.

Aging is as much about the physical processes of repair and regeneration and their slow-motion failure as it is the passage of time. And scientists studying stem cell and regenerative biology are making progress understanding those processes, developing treatments for the many diseases whose risks increase as we get older, while at times seeming to draw close to a broader anti-aging breakthrough.

If stem cells offer potential solutions, theyre also part of the problem. Stem cells, which can differentiate into many cell types, are important parts of the bodys repair system, but lose regenerative potency as we age. In addition, their self-renewing ability allows the mutations that affect every cell to accumulate across cellular generations, and some of those mutations lead to disease.

We do think that stem cells are a key player in at least some of the manifestations of age, said Professor of Stem Cell and Regenerative Biology David Scadden, co-director of the Harvard Stem Cell Institute. The hypothesis is that stem cell function deteriorates with age, driving events we know occur with aging, like our limited ability to fully repair or regenerate healthy tissue following injury.

When it comes to aging, certain tissue types seem to lead the charge, according to Professor of Stem Cell and Regenerative Biology Lee Rubin, who directs the Harvard Stem Cell Institutes Therapeutic Screening Center. Particular tissues nerve cells appear to be one somehow signal to others that its time to age. This raises the prospect, Rubin said, that aging might be reversed by treating these key tissue categories, rather than designing individual treatments for the myriad tissue types that make up the body.

The process of aging involves all tissues in your body and, while different things go wrong in each tissue, they go wrong at basically the same rate, Rubin said. We can think of it as a process that is somehow coordinated, or there are fundamental processes in each tissue that play out.

In addition to key tissues, certain chemical pathways like insulin signaling seem to be able to control aging, said Rubin, whose work has received backing from the National Institute of Neurological Disorders and Stroke, as well as private foundations. The insulin signaling pathway is a chemical chain reaction in which the hormone insulin helps the body metabolize glucose. Reducing it has been shown to greatly extend life span in flies and worms, Rubin said. Also, signaling doesnt have to be reduced in all tissues.

If you just reduce it in neurons, the whole fly or worm lives longer, Rubin said. Certain key tissues in those organisms, if you selectively manipulate those tissues, have a positive effect on a number of processes in other tissues.

Because it circulates throughout the body, blood is an obvious place to look for controlling or signaling molecules that prompt or coordinate aging. A key carrier of oxygen and nutrients, blood is also rich with other compounds, some of which appear to play a role in decline linked to age.

Scadden described recent work done separately by Ben Ebert, a professor of medicine working at Harvard-affiliated Brigham and Womens Hospital, and Steve McCarroll, the Dorothy and Milton Flier Associate Professor of Biomedical Science and Genetics, that identified age-related changes in the blood that can increase the risk of diseases we dont typically think of as blood diseases.

Another tantalizing study, published in 2013, used the blood of a young mouse to rejuvenate the organs of an older one. In these parabiotic experiments, conducted by Professor of Stem Cell and Regenerative Biology Richard Lee and Forst Family Professor of Stem Cell and Regenerative Biology Amy Wagers, the circulatory systems of the two mice were joined, allowing the blood of the young to flow through the older ones body. The older mouse showed improvements in muscle tone and heart function. Later, similar experiments done by Rubin also showed improvements in neuronal health and brain functioning.

The young mouses fate depended on the age of the older mouse, Rubin said. If the latter was middle-aged, the young mouse appeared to be fine. If the older mouse was very old, however, the young mouse did worse.

Rubin said the experiments suggest that blood contains both positive and negative factors that influence aging. It may be, he said, that both are always present, but that positive factors outweigh negative in the young and that negative factors increase as we age.

Researchers have identified but not yet confirmed candidate blood factors for the rejuvenating effects. What seems not in doubt is the overall effect of the young blood on the old mouse. Interest is intense enough that a California company, Alkahest, has begun experiments giving Alzheimers patients plasma from young blood in hopes of improving cognition and brain function.

Even if that approach works, Rubin said, there would be practical hurdles to the widespread administration of young peoples blood plasma to older patients. But with an active compound identified, a drug could be made available to restore at least some cognitive function in Alzheimers patients.

In addition to the overall process of aging, researchers at the Harvard Stem Cell Institute, as well as across the University and its affiliated institutions, are investigating an array of diseases whose incidence increases sometimes dramatically with age.

The list includes several of the countrys top causes of death heart disease, stroke, diabetes, and cancer as well as rarer conditions such as the lethal neurodegenerative disorder amyotrophic lateral sclerosis (ALS).

Two decades ago, when stem cell research hit mainstream consciousness, many thought its greatest promise would be in stem cells ability to grow replacement parts: organs and tissues for damage caused by trauma or disease.

The stem cell revolution is still developing, Scadden said, but so far has taken a different form than many expected. The dream of harnessing stem cells to grow replacement hearts, livers, and kidneys remains, but potentially powerful uses have emerged in modeling disease for drug discovery and in targeting treatment for personalized medicine.

We thought stem cells would provide mostly replacement parts. I think thats clearly changed very dramatically. Now we think of them as contributing to our ability to make disease models for drug discovery.

David Scadden

Researchers have taken from the sick easily accessible cells, such as skin or blood, and reprogrammed them into the affected tissue type nerve cells in the case of ALS, which most commonly strikes between 55 and 75, according to the National Institutes of Health (NIH).

These tissues are used as models to study the disease and test interventions. Work on ALS in the lab of Professor of Stem Cell and Regenerative Biology Kevin Eggan has identified a drug approved for epilepsy that might be effective against ALS. This application is now entering clinical trials, in collaboration with Harvard-affiliated Massachusetts General Hospital.

In the end, stem cells might have their greatest impact as a drug-discovery tool, Scadden said.

Much of stem cell medicine is ultimately going to be medicine, he said. Even here, we thought stem cells would provide mostly replacement parts. I think thats clearly changed very dramatically. Now we think of them as contributing to our ability to make disease models for drug discovery.

Also evolving is knowledge of stem cell biology. Our previous understanding was that once embryonic stem cells differentiated into stem cells for muscle, blood, skin, and other tissue, those stem cells remained flexible enough to further develop into an array of different cells within the tissue, whenever needed.

Recent work on blood stem cells, however, indicates that this plasticity within a particular tissue type may be more limited than previously thought, Scadden said. Instead of armies of similarly plastic stem cells, it appears there is diversity within populations, with different stem cells having different capabilities.

If thats the case, Scadden said, problems might arise in part from the loss of some of these stem cell subpopulations, a scenario that could explain individual variation in aging. Getting old may be something like the endgame in chess, he said, when players are down to just a few pieces that dictate their ability to defend and attack.

If were graced and happen to have a queen and couple of bishops, were doing OK, said Scadden, whose work is largely funded through the NIH. But if we are left with pawns, we may lose resilience as we age.

Scaddens lab is using fluorescent tags to mark stem cells in different laboratory animals and then following them to see which ones do what work. It might be possible to boost populations of particularly potent players the queens to fight disease.

Were just at the beginning of this, Scadden said. I think that our sense of stem cells as this highly adaptable cell type may or may not be true. What we observe when we look at a population may not be the case with individuals.

The replacement parts scenario for stem cells hasnt gone away. One example is in the work of Harvard Stem Cell Institute co-director and Xander University Professor Douglas Melton, who has made significant progress growing replacement insulin-producing beta cells for treatment of diabetes.

Another is in Lees research. With support from the NIH, Lee is working to make heart muscle cells that can be used to repair damaged hearts.

Trials in this area have already begun, though with cells not genetically matched to the patient. In France, researchers are placing partially differentiated embryonic stem cells on the outside of the heart as a temporary aid to healing. Another trial, planned by researchers in Seattle, would inject fully differentiated heart muscle cells into a patient after a heart attack as a kind of very localized heart transplant.

Lees approach will take longer to develop. He wants to exploit the potential of stem cell biology to grow cells that are genetically matched to the patient. Researchers would reprogram cells taken from the patient into heart cells and, as in the Seattle experiment, inject them into damaged parts of the heart. The advantage of Lees approach is that because the cells would be genetically identical to the patient, he or she could avoid antirejection drugs for life.

What were thinking about is longer-term but more ambitious, Lee said. Avoiding immune suppression could change the way we think about things, because it opens the door to many decades of potential benefit.

Change has been a constant in Lees career, and he says theres no reason to think that will slow. Patient populations are older and more complex, disease profiles are changing, and the tools physicians have at their disposal are more powerful and more targeted.

Many of our patients today wouldnt be alive if not for the benefit of research advances, he said. Cardiology has completely changed in the last 25 years. If you think its not going to change even more in the next 25 years, youre probably wrong.

When Lee envisions the full potential of stem cell science, he sees treatments and replacement organs with the power to transform how we develop and grow old.

It may not be there for you and me, but for our children or their children, ultimately, regenerative biology and stem cell biology have that kind of potential, he said. We imagine a world where it doesnt matter what mutations or other things youre born with, because we can give you a good life.

Lees not guessing at future longevity. Hes not even sure extending life span beyond the current record, 122, is possible. Instead, he cites surveys that suggest that most Americans target 90 as their expectation for a long, healthy life.

Thats about a decade more than we get now in America, Lee said. We have work to do.

Originally posted here:
Researchers study secrets of aging via stem cells - Harvard Gazette

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By Chris Centeno, M.D., CEO at Regenexx April 16, 2017

In 1897, Mark Twain was on a speaking tour in London when an American newspaper started a rumor that he was gravely ill. This was soon followed by an obituary. When asked by an American reporter in London about his death, Twain quipped, The reports of my death have been greatly exaggerated. I feel thesame about C1-C2 facet injections. The radiofrequency mob has been trying hard to kill off cervical facet injections for years and C1-C2 is low hanging fruit, but like Twain, I have to report the death of this procedure has been greatly exaggerated.

Sometime around the turn of this last century, we began to see the use of radiofrequency ablation (RFA) for neck pain due to damaged facet joints take off. What is RFA and what is a damaged facet joint?

You have 14 joints in the back part of your spine (7 on each side). These joints help to control neck motion. These little articulations about the size of a finger joint are commonly called facet joints. They can become injuredor can get arthritis like any other joint in your body. When this happens they can become chronically painful.

While the injection of anti-inflammatory steroid into these joints was the most common way to treat this pain, about 2000 or so we began to see the rise of another form of treatment called RFA. This procedure uses a probe that heats up to burn away nerves around the painful joint. The idea is that once these pain carrying wires are cut, the pain will stop because its no longer being transmitted to the brain. This works pretty well and has been well researched to help chronic neck pain caused by a damagedfacetjoint. However, as you mightimagine, you cant just burn nerves that carry pain signals and not have consequences. This procedure can cause the joint to become more damaged (a Charcot joint) and in my experience can cause a cycle where the patient needs to be treated every 5-18 months forever. In addition, my personal observation is that these patients get more brittle with time. By that, I mean that when their pain returns its worse and easier to provoke than before RFA was begun.

Radiofrequency is a great medical business. Not only do these patients need to come back every so often for a repeat treatment, but insurance companies pay more for RFA than a simple facet injection. In addition, theres a third party vendorwho gets to charge outrageous prices for disposable needles and new RF probes, which means that theres lots of moolaharound to sponsor conferences, pay physician thought leaders, and medical directors. Hence, knowing that money talks in medicine, its not hard to figure out why those thought leaders have been trying to get rid of facet injections (i.e. injecting a substance into the joint rather than burning the nerves around the joint). as the idea competes with RFA. However, with the advent of orthobiologics like PRP and stem cells, everything changes.

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Reports of the Death of the C1-C2 Facet Injection have Been Greatly Exaggerated - OrthoSpineNews

April 17, 2017 by Hannah L. Robbins SMN protein (red) is necessary for the survival of spinal cord neurons (motor neurons) responsible for breathing and all movement. Harvard researchers have found a compound that stabilized this protein in mouse and human motor neurons. This may lead to the development of new treatments for motor neuron diseases including Spinal Muscular Atrophy and Lou Gehrigs disease. Credit: Natalia Rodriguez-Muela

Harvard Stem Cell Institute (HSCI) researchers have identified a compound that helps protect the cells destroyed by spinal muscular atrophy (SMA), the most frequent fatal genetic disease in children under 2 years of age.

SMA is a neurodegenerative disease targeting motor neurons, the long nerve cells that relay messages from the brain to the muscles and that are, consequently, responsible for bodily movements, including walking, swallowing, and even breathing. Patients with milder forms of SMA experience muscle wasting that may confine them to a wheelchair, while the more severe forms cause paralysis and death before the second birthday.

About one in 50 people are genetic carriers of the disease.

Because of a dysfunctional gene, many motor neurons in SMA patients are unable to produce adequate amounts of a protein called survival of motor neuron (SMN). The deficiency causes cellular stress and eventually cell death. Rather than fixing the gene, which has been the strategy of many labs looking to develop SMA therapies, the Harvard team has identified a compound that helps stabilize the SMN protein both in human neurons in a dish and in mouse models.

The findings were published in the journal Cell Reports.

"This discovery opens up new lines of drug interrogation," said Lee Rubin, HSCI principal faculty member and the senior author on the study. Rubin's lab, which operates out of in Harvard's Department of Stem Cell and Regenerative Biology, uses induced pluripotent stem cells (iPS cells) to make human models of neurological diseases.

In 2015, Rubin made a variety of neuronal types from the iPS cells of SMA patients in order to determine why motor neurons in particular were targeted, and found they experienced a fatal stress response similar to motor neurons affected by amyotrophic lateral sclerosis (ALS), the late-onset neurodegenerative disease more commonly known as Lou Gehrig's disease.

Additionally, some SMA-affected motor neurons were dying before others, though all of the neurons had the same genetic mutations and were experiencing the same stressful environment.

"Clearly, some motor neurons were surviving, so the next question was whether this is random or if there is a molecular explanation," Rubin said.

Early on in their most recent study, the researchers found that within a single petri dish of motor neurons derived from an SMA patient, some produced up to four times as much SMN protein as their neighbors. Over time, those motor neurons with higher levels of SMN were more likely to survive after exposure to toxic environments and stressors.

When the team analyzed motor neurons derived from ALS patients, they found similar results: Motor neurons with higher levels of SMN were likelier to survive than those with lower levels.

"The surprise was when we looked in a control culture and also saw differences between the individual neurons," Rubin said.

"It is clear that the SMN protein is necessary for all motor neuron survival, not just motor neurons targeted by ALS or SMA," said Natalia Rodrguez-Muela, a postdoctoral fellow in Rubin's lab and co-first author on the paper. The results suggest that if the team could increase the amount of SMN protein in any single motor neuron, they would be able to rescue the cell.

During a cell's life span, proteins are constantly being made and degraded, made and degraded again. To interrupt the process of breaking down the SMN protein, the researchers looked at a family of proteins called Cullins, which act as a part of the cell machinery that regulates protein degradation.

In 2011, the Rubin lab had determined that an enzyme called GSK3b helps control SMN stability. Nearly all proteins degraded by GSK3b are flagged for degradation by a pathway that involves a specific member of the Cullin family. Rubin said the researchers hypothesized that if they could block that Cullin-mediated process, the SMN proteins would not be flagged for degradation and would remain stable longer.

The researchers, led by co-first author Nadia Litterman, then dosed human and murine motor neurons with a compound known to block the specific Cullin and found that exposure to the compound made SMN proteins more stable and more abundant. As a consequence, the compound promoted survival of all motor neurons, both in human cells in the dish and in mouse models.

Additionally, mice with SMA, even the more severe forms of the disease, had some of their symptoms improve after exposure to the compound.

"This process points to an unexplored therapeutic direction that could benefit patients of not one, but two separate diseases," Rubin said.

Explore further: Hope against disease targeting children

More information: Natalia Rodriguez-Muela et al. Single-Cell Analysis of SMN Reveals Its Broader Role in Neuromuscular Disease, Cell Reports (2017). DOI: 10.1016/j.celrep.2017.01.035

Journal reference: Cell Reports

Provided by: Harvard University

This story is published courtesy of the Harvard Gazette, Harvard University's official newspaper. For additional university news, visit Harvard.edu.

Harvard Stem Cell Institute (HSCI) researchers studying spinal muscular atrophy (SMA) have found what they term "surprising similarities" between this childhood disorder that attacks motor neurons and amyotrophic lateral ...

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A new study from the Icahn School of Medicine at Mount Sinai provides important insights into how the body regulates its production of heat, a process known as thermogenesis that is currently intensely studied as a target ...

Cornell University researchers have produced for the first time an image of P2X7, a receptor associated with chronic pain. Visualizing the shape of the receptor has also allowed them to make a second groundbreaking discovery: ...

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Scientists find evidence that ALS and SMA could be treated with a common drug - Medical Xpress

by MARK SHERMAN and MARIA DANILOVA, Associated Press

In this photo taken Jan. 26, 2016, the empty playground at Trinity Lutheran Church in Columbia, Mo. Justice Neil Gorsuch's first week hearing Supreme Court arguments features a case that's giving school choice advocates hope for an easier use of public money for private, religious schools in dozens of states. The long-delayed argument Wednesday, April 19, 2017, deals with whether Missouri should pay for a soft surface at the church playground. (Annaliese Nurnberg/Missourian via AP)

WASHINGTON (AP) Justice Neil Gorsuch's first week on the Supreme Court bench features an important case about the separation of church and state that has its roots on a Midwestern church playground. The outcome could make it easier to use state money to pay for private, religious schooling in many states.

The justices on Wednesday will hear a Missouri church's challenge to its exclusion from a state program that provides money to use ground-up tires to cushion playgrounds. Missouri is among roughly three dozen states with constitutions that explicitly prohibit using public money to aid a religious institution, an even higher wall separating government and religion than the U.S. Constitution erects.

Trinity Lutheran Church of Columbia, Missouri, says its exclusion is discrimination that violates its religious freedoms under the U.S. Constitution.

If the justices agree, "the decision could have implications far beyond scrap tires and playgrounds," said Michael Bindas of the Institute for Justice, which is backing the church. "It has the potential to remove one of the last legal clouds hanging over school choice."

That prospect worries groups of public school teachers and others who oppose vouchers and other forms of public aid for private schooling.

Adding to the intrigue is the long delay between when the Supreme Court agreed to hear Trinity Lutheran's appeal, a month before Justice Antonin Scalia died in February 2016, and the argument. The span of more than 15 months suggests the justices were concerned they might divide 4-4. Indeed, the case wasn't scheduled for argument until after President Donald Trump nominated Gorsuch for the seat.

The timing of the argument "heightened our concern that the court has held this case for so long," said Alice O'Brien, general counsel of the National Education Association, which opposes state aid to private schools.

Missouri's new governor, Republican Eric Greitens, injected some uncertainty into the high court case on Thursday, when he directed state agencies to allow religious groups and schools to receive taxpayer money for playgrounds and other purposes. The court on Friday asked both the church and the state to tell it whether the governor's announcement affects the case.

A lawyer for the church said in an interview with The Associated Press that the case would be unaffected because Greitens' policy change does not resolve the legal issue. But a top aide to state Attorney General Josh Hawley told the AP that state lawyers were evaluating whether the new policy would affect the case.

Should the court decide to go forward, Gorsuch's votes and opinions in religious liberty cases as a judge on the federal appeals court in Denver would seem to make him more inclined to side with the church, and potentially provide the decisive, tie-breaking vote if the rest of the court is divided between liberals and conservatives, Bindas said.

The case arose from an application the church submitted in 2012 to take part in Missouri's scrap tire grant program, which reimburses the cost of installing a rubberized playground surface made from recycled tires. The money comes from a fee paid by anyone who buys a new tire. The church's application to resurface the playground for its preschool and daycare ranked fifth out of 44 applicants.

But the state's Department of Natural Resources rejected the application, pointing to the part of the state constitution that says "no money shall ever be taken from the public treasury, directly or indirectly, in aid of any church, sect or denomination of religion."

A recycled scrap tire is not religious, the church said in its Supreme Court brief. "It is wholly secular," the church said.

Leslie Hiner, vice president of programs at Ed Choice, a school voucher advocacy group said, "It is difficult to understand that a little school could not participate in a safety measure determined by the state because somehow safety of children is conflated with religious purpose."

But the question of where the dividing line should be between church and state is complicated, said the NEA's O'Brien.

The Supreme Court has upheld some school voucher programs and state courts have ratified others. But "in many instances challenges to voucher programs have succeeded based on state court views that their constitutions draw a different line than does the federal constitution," O'Brien said.

Thirty states and the District of Columbia have some form of school choice, including vouchers, tax credits and education savings accounts, according to Ed Choice.

The justices could themselves draw a line that decides the case in Missouri without saying anything more broadly about school choice.

But that issue already is looming at the high court in appeals from a Colorado Supreme Court ruling that blocked the nation's first county-initiated voucher program in Douglas County, Colorado.

The Missouri church and some of the groups backing it have invoked what they describe as anti-Catholic bias that motivated the adoption of the Missouri provision and similar measures in other states in the late 1800s. They are similar to the proposed 1875 Blaine Amendment to the U.S. Constitution that would have prohibited the allocation of public school funds to religious institutions.

"Both the Colorado and Missouri Blaine Amendments share discriminatory, anti-Catholic origins that make their contemporary use to compel religious discrimination particularly unacceptable," lawyer Paul Clement wrote on behalf of the Colorado county.

But 10 legal and religious historians said in a separate court filing that there is no evidence that "anti-Catholic or anti-religious animus" played a role in the adoption of the Missouri constitutional provision. And they said anti-Catholicism was a minor factor behind the Blaine Amendment. The broader debate was about the future of American education, they said.

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Supreme Court , including Gorsuch, to hear church-state case - WJLA

Scientists have created a revolutionary 3D-bioprinted patch that can help heal scarred heart tissue after a heart attack. The discovery is a major step forward in treating patients with tissue damage after a heart attack, researchers at University of Minnesota in the US said. During a heart attack, a person loses blood flow to the heart muscle and that causes cells to die.

Our bodies can not replace those heart muscle cells so the body forms scar tissue in that area of the heart, which puts the person at risk for compromised heart function and future heart failure. Researchers used laser-based 3D-bioprinting techniques to incorporate stem cells derived from adult human heart cells on a matrix that began to grow and beat synchronously in a dish in the lab.

When the cell patch was placed on a mouse following a simulated heart attack, the researchers saw significant increase in functional capacity after just four weeks. Since the patch was made from cells and structural proteins native to the heart, it became part of the heart and absorbed into the body, requiring no further surgeries. This is a significant step forward in treating the No 1 cause of death in the US, said Brenda Ogle, an associate professor at the University of Minnesota.

We feel that we could scale this up to repair hearts of larger animals and possibly even humans within the next several years, said Ogle. Ogle said that the research is different from previous ones as the patch is modelled after a digital, three- dimensional scan of the structural proteins of native heart tissue. The digital model is made into a physical structure by 3D printing with proteins native to the heart and further integrating cardiac cell types derived from stem cells.

Only with 3D printing of this type can we achieve one micron resolution needed to mimic structures of native heart tissue, researchers said. We were quite surprised by how well it worked given the complexity of the heart. We were encouraged to see that the cells had aligned in the scaffold and showed a continuous wave of electrical signal that moved across the patch, Ogle said.

Ogle said they are already beginning the next step to develop a larger patch that they would test on a pig heart, which is similar in size to a human heart. The study was published in the journal Circulation Research.

Publish date: April 16, 2017 12:57 pm| Modified date: April 16, 2017 12:57 pm

Tags: 3D-Bioprint, Brenda Ogle, cells, Heart, heart attack, heart failure, Journal Circulation Research, scientists, structural proteins, University of Minnesota

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Scientists have made a 3D-printed patch that can help heal the damaged heart tissue - Tech2 (blog)

A team of biomedical engineering researchers, led by the University of Minnesota, has created a revolutionary 3D-bioprinted patch that can help heal scarred heart tissue after a heart attack. The discovery is a major step forward in treating patients with tissue damage after a heart attack.

The research study is published today in Circulation Research, a journal published by the American Heart Association. Researchers have filed a patent on the discovery.

According to the American Heart Association, heart disease is the No. 1 cause of death in the U.S. killing more than 360,000 people a year. During a heart attack, a person loses blood flow to the heart muscle and that causes cells to die. Our bodies cant replace those heart muscle cells so the body forms scar tissue in that area of the heart, which puts the person at risk for compromised heart function and future heart failure.

In this study, researchers from the University of Minnesota-Twin Cities, University of Wisconsin-Madison, and University of Alabama-Birmingham used laser-based 3D-bioprinting techniques to incorporate stem cells derived from adult human heart cells on a matrix that began to grow and beat synchronously in a dish in the lab.

Watch a video of the cells beating on the patch.

When the cell patch was placed on a mouse following a simulated heart attack, the researchers saw significant increase in functional capacity after just four weeks. Since the patch was made from cells and structural proteins native to the heart, it became part of the heart and absorbed into the body, requiring no further surgeries.

This is a significant step forward in treating the No. 1 cause of death in the U.S., said Brenda Ogle, an associate professor of biomedical engineering at the University of Minnesota. We feel that we could scale this up to repair hearts of larger animals and possibly even humans within the next several years.

Ogle said that this research is different from previous research in that the patch is modeled after a digital, three-dimensional scan of the structural proteins of native heart tissue. The digital model is made into a physical structure by 3D printing with proteins native to the heart and further integrating cardiac cell types derived from stem cells. Only with 3D printing of this type can we achieve one micron resolution needed to mimic structures of native heart tissue.

We were quite surprised by how well it worked given the complexity of the heart, Ogle said. We were encouraged to see that the cells had aligned in the scaffold and showed a continuous wave of electrical signal that moved across the patch.

Ogle said they are already beginning the next step to develop a larger patch that they would test on a pig heart, which is similar in size to a human heart.

The research was funded by the National Science Foundation, National Institutes of Health, University of Minnesota Lillehei Heart Institute, and University of Minnesota Institute for Engineering in Medicine.

In addition to Ogle, other biomedical engineering researchers who were part of the team include Molly E. Kupfer, Jangwook P. Jung, Libang Yang, Patrick Zhang, and Brian T. Freeman from the University of Minnesota; Paul J. Campagnola, Yong Da Sie, Quyen Tran, and Visar Ajeti from the University of Wisconsin-Madison; and Jianyi Zhang, Ling Gao, and Vladimir G. Fast from the University of Alabama,

To read the full research paper entitled Myocardial Tissue Engineering With Cells Derived from Human Induced-Pluripotent Stem Cells and a Native-Like, High-Resolution, 3-Dimensionally Printed Scaffold, visit the Circulation Research website.

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3D-printed patch can help mend a broken heart - UMN News

As we baby boomers confront various health issues as we age, its good to keep abreast of medical advances that may offer us hope or, in some cases, maybe just a dose of amusement.

Interestingly, some of these developments were the stuff of science fiction when we were growing up. Take a look:

Silly Putty can help track blood pressure

When we boomers were kids, one of the coolest things you could do with Silly Putty was press it on comics and transfer the image. Now researchers have discovered this polymer can measure blood pressure, pulse and respiration rate. The scientists added grapheneconsidered the thinnest and strongest material to existto Silly Putty, then measured if electrical current would pass through it. They found G-putty was 250 times more sensitive than a typical metal-based sensor and, when placed on a subjects chest, was able to measure how much blood was pushing on artery walls. Who knew?

Speed bumps can help diagnose appendicitis

Apparently, how much pain patients experience when theyre driven over a speed bump is a highly reliable clinical indicator of acute appendicitis. According to a study published in the medical journal BMJ, Asking about speed bumps may contribute to clinical assessment and could be useful in telephone assessment of patients. So if you feel increased abdominal pain when going over a speed bump, maybe you should keep driving straight to the hospitalbecause delayed surgery for acute appendicitis can lead to severe infection, even death. Not funny.

Surgeons want to transplant a human head

A Russian tech geek, a Chinese surgeon and an Italian neurosurgeon walk into an operating roomsounds like the opening line of a joke, right? Well, according to an article in the Washington Post, these three folks want to be involved in the first human head transplant (the Russian is volunteering his head because hes got a fatal genetic disorder). The neurosurgeon says the transplant could happen as early as this year (probably in China since its unlikely to get US or EU approval) and has a 90 percent plus chance of success. It would require 80 surgeons (none named Frankenstein) and cost tens of millions of dollars. Im still wrapping my head around this one

Robot to care for the elderly at home

Remember Rosie, the household robot from The Jetsons? Well, researchers at Rice University and IBM are working on an in-home assistant for elders who wish to age in place named MERAthe Multi-purpose Eldercare Robot Assistant. MERA will monitor an individuals heart rate and respiration, and can detect if someone falls, automatically calling a caregiver or 911. People using the device can also ask it health-related questionslike what are the signs of a stroke or heart attackand MERA shares these messages with caregivers or providers. The device is powered by Watson, IBMs artificial intelligence and analytical softwareand Jeopardy champion. Wonder if MERA plays any games

Part-human, part-pig creature grown in lab

Remember The Island of Doctor Moreau, or Jeff Goldblum in The Fly? Well,according to STAT, a national medical newsletter from Boston Globe Media, scientists recently announced they produced a human-pig chimeraa hybrid created by fusing a sperm and egg from different species. The researchers injected pig embryos with human stem cells, and the chimeras began to grow organs containing human cells. These creatures werent allowed to develop past the fetal stage, but the experiment suggests hybrids might someday be used to grow organs for transplant, easing a dire shortage. Hmmethical considerations aside, what human-animal combos would you like to see?

Got stomach acid? It might be the battery of the future

Also according to STAT, biomedical engineers at Brigham and Womens Hospital believe your churning stomach acid could power ingestible medical devices like long-acting drug-delivery capsules or sensors that can detect blood or toxins. The acid allows electrons to move between two metals, producing a small amount of current, like a battery. In an animal study, an ingestible thermometer was able to poweritself for about six days while transmitting measurements every 12 seconds. Better lay off the antacids, huh?

When you think about it, it is pretty amazing what the human mind has brought to life, inspiring this haiku:

Medicine is like science fiction: its the art of the possible.

What do you think? Are there other medical advances that wereor still seemlike science fiction to you? If you could have a head transplant, whose would you want? Conversely, who would you donate your head to? Please share

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6 unusual medical advances baby boomers might appreciate - Bangor Daily News

April 14, 2017 A team of biomedical engineering researchers has created a revolutionary 3-D-bioprinted patch that can help heal scarred heart tissue after a heart attack. Two of the researchers involved are biomedical engineering Associate Professor Brenda Ogle (right) and Ph.D. student Molly Kupfer (left). Credit: Patrick O'Leary, University of Minnesota

A team of biomedical engineering researchers, led by the University of Minnesota, has created a revolutionary 3D-bioprinted patch that can help heal scarred heart tissue after a heart attack. The discovery is a major step forward in treating patients with tissue damage after a heart attack.

The research study is published today in Circulation Research, a journal published by the American Heart Association. Researchers have filed a patent on the discovery.

According to the American Heart Association, heart disease is the No. 1 cause of death in the U.S. killing more than 360,000 people a year. During a heart attack, a person loses blood flow to the heart muscle and that causes cells to die. Our bodies can't replace those heart muscle cells so the body forms scar tissue in that area of the heart, which puts the person at risk for compromised heart function and future heart failure.

In this study, researchers from the University of Minnesota-Twin Cities, University of Wisconsin-Madison, and University of Alabama-Birmingham used laser-based 3D-bioprinting techniques to incorporate stem cells derived from adult human heart cells on a matrix that began to grow and beat synchronously in a dish in the lab.

When the cell patch was placed on a mouse following a simulated heart attack, the researchers saw significant increase in functional capacity after just four weeks. Since the patch was made from cells and structural proteins native to the heart, it became part of the heart and absorbed into the body, requiring no further surgeries.

"This is a significant step forward in treating the No. 1 cause of death in the U.S.," said Brenda Ogle, an associate professor of biomedical engineering at the University of Minnesota. "We feel that we could scale this up to repair hearts of larger animals and possibly even humans within the next several years."

Ogle said that this research is different from previous research in that the patch is modeled after a digital, three-dimensional scan of the structural proteins of native heart tissue. The digital model is made into a physical structure by 3D printing with proteins native to the heart and further integrating cardiac cell types derived from stem cells. Only with 3D printing of this type can we achieve one micron resolution needed to mimic structures of native heart tissue.

"We were quite surprised by how well it worked given the complexity of the heart," Ogle said. "We were encouraged to see that the cells had aligned in the scaffold and showed a continuous wave of electrical signal that moved across the patch."

Ogle said they are already beginning the next step to develop a larger patch that they would test on a pig heart, which is similar in size to a human heart.

Explore further: Tissue engineering advance reduces heart failure in model of heart attack

More information: Ling Gao et al, Myocardial Tissue Engineering With Cells Derived From Human-Induced Pluripotent Stem Cells and a Native-Like, High-Resolution, 3-Dimensionally Printed ScaffoldNovelty and Significance, Circulation Research (2017). DOI: 10.1161/CIRCRESAHA.116.310277

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Patching a damaged heart with a patient's own muscle stem cells improves symptoms of heart failure, according to a Phase I clinical trial reported in Journal of the American Heart Association, the Open Access Journal of the ...

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A team of biomedical engineering researchers, led by the University of Minnesota, has created a revolutionary 3D-bioprinted patch that can help heal scarred heart tissue after a heart attack. The discovery is a major step ...

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(HealthDay)Strokes are typically associated with the elderly, but new research suggests that strokes are increasingly happening to Americans under 65.

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3-D-printed patch can help mend a 'broken' heart - Medical Xpress

Harvard Gazette

Harvard scientists find evidence that ALS and SMA could be treated with a common drug Harvard Gazette Harvard Stem Cell Institute (HSCI) researchers have identified a compound that helps protect the cells destroyed by spinal muscular atrophy (SMA), the most frequent fatal genetic disease in children under 2 years of age. SMA is a neurodegenerative ...

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Harvard scientists find evidence that ALS and SMA could be treated with a common drug - Harvard Gazette

April 14, 2017 Before stem cells (green) give rise to eggs and sperm, they make DND1, a molecule that helps prevent the cells from being eliminated. Credit: Rockefeller University

The first days of an embryo's development are a busy time for the molecules that regulate gene expression. A vast number of specific genes need to be turned on and off at precisely the right time for cells to end up in the proper place and in the appropriate quantity.

Researchers at the Rockefeller University have untangled how a molecule called DND1 enables the proper formation of eggs and spermessential parts of any species that reproduces sexually. Published in Nature, the findings suggest that a pool of stem cells, which will ultimately give rise to eggs and sperm, can only survive if DND1 is around. The protein prevents a host of factors related to cell death and inflammation from killing these stem cells off.

"We already knew that mutations in the DND1 gene can cause a substantial loss of germline stem cells and male sterilityand now we know why," says Thomas Tuschl, head of the Laboratory of RNA Molecular Biology and Howard Hughes Medical Institute Investigator. Tuschl led the study with Markus Hafner, a former postdoctoral fellow in the Tuschl lab who is now at the National Institutes of Health, and research associate Masashi Yamaji.

For a gene to be expressed, it must be copied from DNA to so-called messenger RNA (mRNA), which brings it outside of the nucleus. The mRNA then recruits the necessary building blocks to make a protein. There are many places along a gene's journey to becoming a protein where regulators can step in to either ramp up or tone down the resulting level of protein in a cell. DND1 is one of these regulators, and scientists used to think its function is to increase the stability of mRNA.

However, Tuschl and colleagues found that it does just the opposite: DND1 binds to sites made up of a specific code on mRNA, and attracts a complex responsible for destabilizing the targeted mRNAs, thereby halting further protein production. That code can be repeated throughout an mRNA sequence, and the researchers found that more repeats of this code meant more of a chance that the mRNA would be eliminated.

The researchers also identified all of the mRNAs that DND1 targets, which included genes related to inflammation, differentiation, and cell deathgenes whose activity is supposed to be turned off at this point in development. When a cell shuts down these genes, it stops producing their mRNAs. However, mRNAs that were copied earlier may still be floating around, ready to build a protein.

"We think that DND1 helps to sharpen the transition from one developmental stage to the next by targeting mRNAs that should have already been turned off, and clearing them from the cell," says Yamaji. "By halting the production of proteins that otherwise promote cell death, DND1 allows germline stem cells to grow and be maintained in proper numbers."

Explore further: Protein production in differentiating stem cells is more complex than previously thought

More information: Masashi Yamaji et al. DND1 maintains germline stem cells via recruitment of the CCR4NOT complex to target mRNAs, Nature (2017). DOI: 10.1038/nature21690

Journal reference: Nature

Provided by: Rockefeller University

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The first days of an embryo's development are a busy time for the molecules that regulate gene expression. A vast number of specific genes need to be turned on and off at precisely the right time for cells to end up in the ...

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Shooting the messenger: how one protein allows germ cells to develop - Phys.Org

Saving cells: Before stem cells (green) give rise to eggs and sperm, they make DND1, a molecule that helps prevent the cells from being eliminated.

The first days of an embryos development are a busy time for the molecules that regulate gene expression. A vast number of specific genes need to be turned on and off at precisely the right time for cells to end up in the proper place and in the appropriate quantity.

Researchers at the Rockefeller University have untangled how a molecule called DND1 enables the proper formation of eggs and spermessential parts of any species that reproduces sexually. Published in Nature, the findings suggest that a pool of stem cells, which will ultimately give rise to eggs and sperm, can only survive if DND1 is around. The protein prevents a host of factors related to cell death and inflammation from killing these stem cells off.

We already knew that mutations in the DND1 gene can cause a substantial loss of germline stem cells and male sterilityand now we know why, says Thomas Tuschl, head of the Laboratory of RNA Molecular Biology and Howard Hughes Medical Institute Investigator. Tuschl led the study with Markus Hafner, a former postdoctoral fellow in the Tuschl lab who is now at the National Institutes of Health, and research associate Masashi Yamaji.

For a gene to be expressed, it must be copied from DNA to so-called messenger RNA (mRNA), which brings it outside of the nucleus. The mRNA then recruits the necessary building blocks to make a protein. There are many places along a genes journey to becoming a protein where regulators can step in to either ramp up or tone down the resulting level of protein in a cell. DND1 is one of these regulators, and scientists used to think its function is to increase the stability of mRNA.

However, Tuschl and colleagues found that it does just the opposite: DND1 binds to sites made up of a specific code on mRNA, and attracts a complex responsible for destabilizing the targeted mRNAs, thereby halting further protein production. That code can be repeated throughout an mRNA sequence, and the researchers found that more repeats of this code meant more of a chance that the mRNA would be eliminated.

The researchers also identified all of the mRNAs that DND1 targets, which included genes related to inflammation, differentiation, and cell deathgenes whose activity is supposed to be turned off at this point in development. When a cell shuts down these genes, it stops producing their mRNAs. However, mRNAs that were copied earlier may still be floating around, ready to build a protein.

We think that DND1 helps to sharpen the transition from one developmental stage to the next by targeting mRNAs that should have already been turned off, and clearing them from the cell, says Yamaji. By halting the production of proteins that otherwise promote cell death, DND1 allows germline stem cells to grow and be maintained in proper numbers.

The study was supported, in part, by the Starr Cancer Foundation, the Starr Foundation, National Cancer Institute, National Institutes of Health, National Center for Advancing Translational Sciences, the Vilcek Foundation, and the Transformative Research Award Program.

Excerpt from:
Shooting the messenger: how one protein allows germ cells to develop - The Rockefeller University Newswire

Mar 12, 2017; Tampa, FL, USA; New York Yankees pitcher James Kaprielian (88) looks on from the dugout at George M. Steinbrenner Field. Mandatory Credit: Kim Klement-USA TODAY Sports

Yankees In Line To Sweep The Series With Rays Hell Yes! by Steve Contursi

Yankees: In the Blink Of An Eye, A Fledging Career Is In Jeopardy by Steve Contursi

Yankees top pitching prospectand sixth-best prospect in the entire farm system (perMLB Pipeline) will have surgery to repair the torn ulnar collateral ligament in his right throwing elbow on Tuesday of next week.

After being examined by Dr. Neal ElAttrache in Los Angeles, the prognosis was grim, as the results were in line with what the team concluded following the first MRI and dye test they performed back in Tampa.

Though Yankees general manager Brian Cashman wouldnt talk about Kaprielians ulnar collateral ligament or the possibility of Tommy John surgery, he did, however, point out the obvious.

Clearly, you dont bounce around the country if the surgical option isnt on the table, Cashman said. Its either the surgical option or continue to pitch through it. Hes basically gonna take a day or two to talk to his family and his agency and get back to us about what hed like to see happen.

Its understandable that Kaprielian asked the Yankees for a few days to mull over his options. After all, this isnt the first problem hes experienced from his million dollar arm. Kaprielian missed all but two starts last season, after being shut down with a strained right flexor tendon.

Oftena precursor to Tommy John surgery, Kaprielian pitched well in the offseason instructional league, Arizona Fall League, and even parts of this Spring Training.

While many within the organization were hopeful he would reach the big leagues at some point this season, Kaprielian will now likely be out of action until the midway point of 2018.

Fellow top pitching prospect, Alex Reyes of the St. Louis Cardinals, recently faced the same frustrating decision.

After sustaining a torn UCL in 2016, Los Angeles Angels righty Garrett Richards went in an opposite direction in regards to his recovery. Richards began biometrics surgery in early May of last year, which involves stem cells being directly injected into the affected area. And though he missed the remainder of the 2016 season, Richards did return this springand was said to be throwing in the mid to upper 90s before hitting the DL with a biceps strain, just a few days ago.

But thats the worry about pitchers who dont get TJ surgery the first time around. Other parts of the arm overcompensate to make up for the instability in the UCL. Sure, you can mostly stabilize the muscles around the injured ligament, as Yankees ace Masahiro Tanaka has done, but it can lead to a laundry list of other maladies.

If I were the Yankees, I would have told Tanaka the same thing when he sustained the injury back in 2014 at age 25. Get the surgery rehab come back strong and lets put this issue to rest.

I fully understand Tanaka had his best statistical season in 2016, but what is his prognosis long-term?

Tanaka wants to play, especially if he intends to optout after this season. But whoever signs him to a multimillion dollar deal this offseason is doing so, knowing there is a real possibility that Tanaka could very well miss 12-18 months with one wrong pitch.

Sure, all pitchers assume some sort of risk each time they take the mound, but how in your right mind can you pay someone $100M plus when you know theyre already hurt? Id rather sign a guy like Yu Darvish, who has already proven he is recovered from TJ surgery (even if he is a few years older).

According to The American Sports Medicine Institute (ASMI), nearly 30 percent of all big league pitchers have at one time undergone Tommy John. The successful return rate for pitchers currently stands between 85 to 95 percent. For those wondering about players who have undergone two TJs well, theyve actually come back78.7 percent of the time.

All in all, this type of surgery is no longer a career death sentence. Its a second chance for a once promising player to redefine himself as an athlete, especially at such a young age.

Want your voice heard? Join the Yanks Go Yard team!

Obviously, its a disappointment for the team and its fans, but its the right move for the injured player, and thats all that really matters.

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HSCT veterans, current patients, and the doctors and staff of the A.A. Maximov center in Moscow are in shock as they grieve and mourn the loss of a stem cell sister.

Sadly, Kristen Dyson, who had been giving updates of her progress on Facebook, suffered a serious and rare reaction after her first day of stem cell infusion, following chemotherapy.

Several days later, after valiant efforts of doctors and nurses in intensive care, Kristen, of Nichol Hills, Oklahoma, U.S., died.

I spent almost a week at the center six months ago, and have first-hand experience of the great care given by the medical team. I also benefited from the wonderful family spirit enjoyed by both the team and those going through the treatment.

Head of the centers transplant procedure is Denis Fedorenko, MD, and when we spoke this week he talked movingly about what happened.

He said: Everyone here is full of sorrow and we are all grieving for Kristen. Everyone who has HSCT here is a friend, not a patient. We have lost a friend, a sister.

Kristen is in our thoughts at this sad time, as is her family husband Bryan, son Brayden and daughter Brooklyn, Fedorenko said.

I asked about Kristens illness and he said Kristen had relapsing MS that was diagnosed in 2003, but it had since developed into secondary progressive. She had been treated with interferon and Gilenya, but the disease was progressing quickly. Her disability had worsened from 5.5 to 6.5 on the EDSS scale. She had no other health problems.

So, what happened? Fedorenko explained: The first indication of any problem was after her first day of stem cell infusion (when her own stem cells were being returned after chemotherapy). Despite days of intensive care, the toxic effect of chemotherapy is thought to have provoked an irreversible, progressive heart reaction.

In more than 700 stem cell transplants we have carried out since 2005, this was our first case of a heart reaction. We are devastated and Kristens passing has led us improve our safety protocols. Starting this week, we are implementing an additional new protocol to evaluate the heart both before and after chemotherapy, he said.

What really impresses me, though, is that since Kristin died, five people in the center decided to continue with their stem cell infusions. Their stem cell new life birthday was yesterday (April 11), when they first paid tribute to their lost sister.

I am sure you want to know how many people with MS who have had HSCT in Moscow have died. Well, including Kristin, the answer is two. Thats two out of 700, or less than 0.3%, in 12 years.

Fedorenko wouldnt discuss that figure, however. I dont want to talk about the low percentage. Kristins death is a tragedy. We are all friends and she is already missed here, at home and around the world, he said.

I cant finish this column without expressing my own sadness and sympathies for Kristins loss to her husband Bryan, their children and family members. Also, to Dr. Fedorenko and all the team in Moscow, and members of the HSCT community worldwide. My thoughts are with you all.

***

[You are invited to visit my personal MS, Health & Disability website at 50shadesofsun.com].

Note: Multiple Sclerosis News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Multiple Sclerosis News Today, or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to multiple sclerosis.

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Mourning Loss of Stem Cell Sister in Moscow HSCT Center - Multiple Sclerosis News Today

Forbes

Artificial Heart Transplants May Be The Future Of Medicine Forbes But the systems responsible for recreating body cells eventually halt to a stop, leading to a person's death. ... So far, the best way to supply 3D printers with biological ink is to obtain stem cells from biopsies, then allowing them to multiply on ...

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Artificial Heart Transplants May Be The Future Of Medicine - Forbes

Besides the traditional use of insects such as termites and grasshoppers as part of the Nigerian diet for their nutritive values, scientists have bioengineered these local delicacies in the treatment of cancer, diabetes, rheumatoid arthritis, Human Immuno-deficiency Virus (HIV), wounds among other benefits. CHUKWUMA MUANYA writes.

A study published in the Journal of Agriculture and Food Chemistry found that insects could provide as much magnesium, iron, and other nutrients as steak.

And researchers at the American Chemical Society (ACS) found grasshoppers and crickets to be a far better source of many nutrients, particularly iron, compared to beef.

Grasshoppers, mealworms, termites and crickets all had higher concentrations of chemically available calcium, copper and zinc than the sirloin.

In Nigeria, termites are usually roasted and eaten as food, mostly during the rainy season.

Indian researchers from Department of Biological Sciences, Presidency University, Kolkata; Department of Zoology, Darjeeling Government College, West Bengal; and Department of Zoology, Scottish Church College, Kolkata explored developments in bioengineering natural products from insects with potential use in modern medicines as well as in utilisation of insects as models for studying essential mammalian processes such as immune responses to pathogens.

The study was published in World Science News.

The researchers listed natural products derived from insects possess medicinal value:

Honey bee products used as medicine Bee products such as honey, venom have been used in folk medicine for thousands of years for treating wounds, ulcers, inflammation, infections, pain, allergies and cancer.

Bee venom therapy, the therapeutic application of bee venom have been used in traditional medicine to treat diseases, such as arthritis, rheumatism, pain, cancerous tumors and kin diseases. Bee venom contains a variety of peptides including melittin, apamin, adolapin, the mast cell-degranulating peptide, enzymes (phospolipase A2), biologically active amines (that is histamine and epinephrine) and nonpeptide components with a variety of pharmaceutical properties.

Cancer treatment Bee venom has been widely used in the treatment of tumours. Several cancer cells, including renal, lung, liver, prostate, mammary gland as well as leukemia cells can be targets of bee venom peptides such as melittin and phospholipase A2.

In recent study scientists reported that bee venom can induce apoptosis in cancer cells (in human leukemic U937cells) the key regulators in bee venom induced apoptosis are Bcl-2 and caspase-3 through down regulation of the ERK and Akt signal pathway. Melittin, a water-soluble toxic peptide derived from bee venom of Apis mellifera was reported to have inhibitory effects on hepatocellular carcinoma. Melittin inhibits tumor cell metastasis by reducing motility and migration via the suppression of Rac-1 dependent pathway, suggesting that melittin is a potent therapeutic agent for hepatocellular carcinoma. Melittin prevents liver cancer cells metastasis through inhibition of the Rac-1-dependent pathway.

Treatment for rheumatoid arthritis Bee venom induces apoptosis in rheumatoid synovial cells through a decrease in BCL2 expression and an increase in BAX and caspase-3 expression. Bee venom induces apoptosis through caspase-3 activation in synovial fibroblasts of patients with rheumatoid arthritis.

Controlling diabetes Hyperglycemia in diabetes leads to increased protein glycation resulting in structural and functional alteration in proteins. Recent studies showed that bee venom prevents glycation induced increasing in beta-sheet structure decreasing in free amino groups, altering in the secondary structure and heme degradation in the hemoglobin. Hence, bee venom has the potential to be used as a natural drug to prevent diabetes complications. Honeybee venom decreases the complications of diabetes by preventing haemoglobin glycation.

Antioxidant Free radicals are ubiquitous in our body and are generated by physiological processes, including aerobic metabolism and inflammatory responses, to eliminate invading pathogenic microorganisms. Target of free radicals in inflammation include Deoxyribonucleic Acid (DNA)/genetic material, proteins, Ribonucleic Acid (RNA) and lipids. An antioxidant is a molecule capable of slowing or preventing the oxidation of other molecules and so to prevent such changes. Oxidative stress is thought to contribute to the development of chronic and degenerative diseases such as cancer, autoimmune disorders, aging, rheumatoid arthritis, cardiovascular and neurodegenerative diseases. Propolis, pollen, honey have the highest antioxidant activities. Bee venom is a potent antioxidant and possesses radio-protecting actions.

Treatment for HIV Nanoparticles carrying a toxin found in bee venom can destroy Human immunodeficiency virus (HIV) while leaving surrounding cells unharmed, researchers at Washington University School of Medicine in St. Louis have shown. The finding is an important step toward developing a vaginal gel that may prevent the spread of HIV, the virus that causes AIDS. Bee venom contains a potent toxin called melittin that can poke holes in the protective envelope that surrounds HIV virus as well as other viruses. This melittin is loaded with nanoparticles, which do not harm surrounding normal cells. The nanoparticles attack an essential part of the virus structure.

Since melittin attacks double-layered membranes indiscriminately this concept is not limited to HIV. Many viruses, including hepatitis B and C rely on the same kind of protective envelope and would be vulnerable to melittin-loaded nanoparticles. Scientists also said that these nanoparticles are easy to manufacture in large enough quantities to supply them for future clinical trials.

Maggot products Maggot therapy is now commonly used for many types of infected wounds such as diabetic foot wounds, postoperative infections, bedsores, and leg ulcers, in the United States (US), Israel, and Europe. The larvae of the blowfly, Lucilia sericata, are frequently used although other species have also been tried such as Lucilia cuprina, Phormia regina, and Calliphora vicina. The use of L. sericata larvae for treating wounds has been recognised by the U.S. Food and Drug Administration and the United Kingdom (UK) Prescription Pricing Authority. Sterile maggots can therefore be officially prescribed.

Ant venom as medicine Ants have been used as medicine, owing to their special active substances such as citral, ATP, histamine, growth hormone, superoxide dismutase etc. Pachycondyla sennaarensis, the samsum ant venom possesses many pharmacological effects as reducing inflammation, relieving pain, inhibition of tumor growth, hepatitis treatment, liver protection. According to Bai et al., solenopsin A, a primary alkaloid obtained from fire ant Solenopsis invicta exhibits antiangiogenic activity; this toxin has the ability to inhibit a series of kinases involving in angiogenesis mechanism.

Polyrachisla mellidens, a medicinal ant used in Chinese medicine, was confirmed to exert potent analgesic and anti-inflammatory actions. Its therapeutic efficacy in the treatment of various inflammatory disorders had been reported.

Beetle products Many of the Blister beetles (Coleoptera: Meloidae) produce toxic defensive secretions, which upon contact with the skin cause blistering. One such toxin is cantharidin, which has been extracted from Mylabris caragnae, the dried bodies of which have been used in Chinese Folk Medicine since the 13th century for the removal of warts and forever 2000 years for the treatment of cancer.

Canthardin is a monoterpene derived from the bodies of several types of blister beetle, including Mylabris phalerata and M. cichorii (Chinese blister beetles) and this compound is stored in the beetle hemolymph and making up about five per cent of body dry weight. Cantharadin has been found to inhibit the growth of human leukemic cells in vitro. In contrast to other chemotherapeutic agents, cantharadin acts as leukemia progenitor and stem cells.

Several derivatives of cantharadin also retard the growth of prostate, oral, colon, cervical, gall bladder cancer cell lines.

Recently in the year 2007 Huang et al. showed that growth inhibition and killing of human colorectal cancer cells by cantharidin was both time- and dose-dependent. The cantharidin exposure reduced CDK1 kinase activity, which led to failure of the cells to progress from G2 to M phases in the cell cycle. In addition, the colorectal cells were killed by apoptosis, which was induced through the mitochondrial and death receptor pathways and activation of caspases.

Shou et al have studied other effects of cantharidin in human breast cancer cells. They reported that cantharidin resulted in apoptosis and reduced growth, adhesion and migration of the cancer cells.

Wasp venom in cancer therapy Scientists from the Institute for Biomedical Research (IRB) Barcelona have carried out successful in vitro tests using wasp venom to kill cancer cells. The peptide from wasp venom has the ability to form pores in the cell plasma membrane, penetrate into the cell and finally, cause its death either by necrosis or by triggering apoptosis. However, this powerful natural weapon can not only damage tumor cells but also affect healthy cells. As such the researchers designed a means of transporting the peptide to the tumour and making it accumulate in a specific and controlled manner. The system consists of a decorated carrier polymer with two components: a peptide that is bound to a tumor cell receptor and the cytotoxic peptide of the wasp venom.

In vitro experiments show that the substance is adequately distributed within the tumor cells and causes their death, while healthy cells, such as red blood cells, are not affected.

Wasp venom contains Polybia MPI (from venom of the social wasp Polybia paulista), which shows anti tumour activity. Polybia MPI is able to target non-polar lipid cell membrane, forming ion permeable channels, leading to depolarization irreversible cytolysis and finally cell death. It has been shown that Polybia MPI can significantly inhibit the proliferation of tumor cells and associated endothelial cells by membrane disrupting.

Fujiwara et al. isolated and determined the structure of anti cancer molecule from the outer envelop of the social wasp Vespa simillima. A biologically active quinone, 7,8-seco-para-ferruginone exhibited a growth inhibitory effect on rat liver cancer cells. The authors suggest that the cytotoxic activity is related to the morphological changes that induce apoptosis of the cells exposed to this molecule.

Moore et al. showed that cecropins are active against several mammalian lymphomas and leukemias in vitro and a preliminary in vivo study showed that cecropin B increases the survival time of mice bearing murine ascitic colon adenocarcinoma cells.

Suttmann et al. showed that cecropin A and B inhibit the viability proliferation of bladder cancer cells, but with no effect on fibroblasts. The selective antitumor action mechanism of these peptides depends on disruption of target cell membrane resulting in irreversible cytolysis and cell destruction. Both peptides may offer novel strategies for the treatment of bladder cancer cells with limited cytotoxic effects on benign cells.

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Insects employed to treat cancer, HIV - Guardian

A quick glance at your calendar will reveal that we're now in 2017. 2017, you may recall, is the year when contraversial surgeon Sergio Canavero has promised to perform the world's first human head transplant.

But just how feasible is a human head transplant? Is it the stuff of science fiction, or does it have a basis in current sceintific thinking? Read on for everything you need to know about 2017 most alarming scientific development.

A human head transplant is exactly what it sounds like taking one living head and putting it onto a new body.

But actually, thats a little misleading. In real terms, its a body transplant, as the head will be gaining a new body to control. However, as the term whole body transplant is already used to mean transferring the brain between bodies, calling it a head transplant makes it clear that the whole head is to be switched, brain included.

Until recently, a head transplant seemed totally implausible, but the Italian scientist Dr Sergio Canavero believes its possible, and intends to conduct the first surgery in 2017.

Canavero outlines the procedure in detail here, but these are the basics of the process. Remember: dont try this at home, kids.

The donor body and the head to be attached are first cooled down to 12-15C to ensure that the cells last longer than a few minutes without oxygen. The tissue around the neck is then cut, with the major blood vessels linked with tiny tubes. The spinal cord on each party is then severed cleanly with an extremely sharp blade.

"Post coma, Canavero believes the patient would immediately be able to move, feel their face and even speak with the same voice."

At this point, the head is ready to be moved, and the two ends of the spinal cord are fused using a chemical called polyethylene glycol, encouraging the cells to mesh. This chemical has been shown to prompt the growth of spinal cord nerves in animals, although Canavero suggests that introducing stem cells or olfactory ensheathing cells into the spinal cord could also be tried.

After the muscles and blood supply are successfully connected, the patient is kept in a coma for a month to limit movement of the newly fused neck, while electrodes stimulate the spinal cord to strengthen its new connections.

Following the coma, Canavero anticipates that the patient would immediately be able to move, feel their face and even speak with the same voice. He believes physiotherapy would allow the patient to walk within a year.

He explains his suggested methods in the TED talk below.

Sceptical would be a nice way of putting it. Horrified would, in most cases, be more accurate.

Dr Hunt Batjer has attracted headlines for being particularly blunt: I would not wish this on anyone. I would not allow anyone to do it to me as there are a lot of things worse than death.

Dr Jerry Silver witnessed the 1970s monkey head transplant experiment more on which later and describes the procedure as bad science, adding that just to do the experiments is unethical. This is a particular blow to Canavero, as he states that Silvers own work in reconnecting rats spinal cords should give hope to the human head transplant. Silver dismisses this: To sever a head and even contemplate the possibility of gluing axons back properly across the lesion to their neighbours is pure and utter fantasy in my opinion.

Dr Chad Gordon, professor of plastic and reconstructive surgery and neurological surgery at Johns Hopkins University, agrees that Canaveros claims are scientifically implausible. He told BuzzFeed: Theres no way hes going to hook up somebodys brain to someones spinal cord and have them be functional.

On the conservative side, were about 100 years away from being able to figure this out, he continued. If hes saying two, and hes promising a living, breathing, talking, moving human being? Hes lying.

Dr Paul Myers, associate professor of biology at the University of Minnesota at Morris, puts it even more explicitly: This procedure will not work... Try it with monkeys first. But he cant: the result would be, at best, a shambling horror, an animal driven mad with pain and terror, crippled and whimpering, and a poor advertisement for his experiment. And most likely what hed have is a collection of corpses that suffered briefly before expiring.

Others wonder whether Canavero might simply be enjoying the limelight with a PR stunt, including Dr Arthur Caplan, director of ethics at the NYU Langone Medical Centre. Describing the doctor as nuts, he explained to CNN: Their bodies would end up being overwhelmed with different pathways and chemistry than theyre used to, and theyd go crazy.

"We'll probably see a head on a robot before we see it on [another] body," he told Live Science.

Dr John Adler of Stanford University's school of medicine is slightly more optimistic... but not much more. "Conceptually, much of this could work, but the most favourable outcome will be little more than a Christopher Reeve level of function," he told Newsweek.

Canavero is aware of this criticism, claiming that silently hes received a lot of support from the medical community. Of Dr Batjers comments that the surgery would be a fate worse than death, Canavero is scathing. Hes a vascular surgeon. A vascular surgeon of the brain, yes, but he knows nothing, he argued. How can you say such a thing? Its incredible.

"The world is moving, the critics are dwindling. Of course, there will always be critics. Science teaches us that when you propose something groundbreaking, you must be confronted by criticism. If no critics really step forward, you are saying nothing special," he told Medical News Today.

No-one has ever attempted a human head transplant before, and attempts on animals have to put it charitably had limited success.

Image: from Motherboard, uploaded under fair use from a 1959 issue of Life

The photo above really does show a dog with two heads and its not a fake. This was the work of Soviet scientist Vladimir Demikhov, and for four days the hybrid of two dogs lived as normally as such a scientific horror could be expected to. Then they died.

Demikhov tried the experiment more than 24 times, but was unable to find a way of avoiding the dogs dying shortly after surgery. Although the results are horrifying to see, Demikhovs research did pave the way for human organ transplants.

"For four days this hybrid of two dogs lived as normally as such a scientific horror could be expected to. Then they died."

But back to the topic of head transplants. The first time a straight swap was successful, was by Dr Robert White, in an experiment on a rhesus monkey in 1970. I feel the need to qualify the word successful with quotation marks, because although the monkey did live, he didnt live very long. Eight days, to be exact, and as the spinal cord wasnt attached to its new body, the monkey was paralysed for its remaining days. However, it could indeed see, hear, smell and taste before the body rejected the foreign head.

According to Canavero in his paper on human head transplants, the monkey lived eight days and was, by all measures, normal, having suffered no complications. However, Dr Jerry Silver who worked in the same lab as Dr White has more haunting memories. He toldCBS: I remember that the head would wake up, the facial expressions looked like terrible pain and confusion and anxiety in the animal. The head will stay alive, but not very long. It was just awful. I dont think it should ever be done again.

More recently, Chinese doctor Xiaoping Ren claims to have conducted head transplants on more than 1,000 mice. The Wall Street Journal reports to have witnessed a mouse with a new head moving, breathing, looking around and drinking. But, crucially, none of these mice have lived longer than a few minutes.

Still, Dr Rens studies continue, and the latest reports are said to be promising, offering a possible answer to the risk of severe blood loss (or brain ischemia) during transplantation. The experimental method that we have described can allow for long-term survival, and thus assessment of transplant rejection and central nervous system recovery, bringing us one step closer to AHBR in man, the researchers wrote.

Ren himself has not ruled out taking part in the first human head transplant operation, according to the Daily Mail. "A human head transplant will be a new frontier in science. Some people say it is the last frontier in medicine. It is a very sensitive and very controversial subject but if we can translate it to clinical practice, we can save a lot of lives," he said.

"Many people say a head transplant is not ethical. But what is the essence of a person? A person is the brain not the body. The body is just an organ," he added.

In January 2016, Canavero told New Scientist that a head transplant had been successfully completed on a monkey in China, although details were sparse. "The monkey fully survived the procedure without any neurological injury of whatever kind," he said, although the article notes that the monkey only kept alive for 20 hours after the surgery for "ethical reasons," limiting its use as a comparison somewhat.

In September 2016, Canavero revealeda further trial of the head transplant on dogs.New Scientisthas seen video footage of a dog appearing to walk three weeks after its spinal cord was severed, with Canavero claiming that the outcome is the result of the same techniques he plans to use on Spiridonov next year.

However, speaking to a number of scientists for their view on the new evidence, New Scientistcould find few sceptics converted. "These papers do not support moving forward in humans," said Jerry Silver a neuroscientist at Cape Western Reserve University in Ohio.

"The dog is a case report, and you cant learn very much from a single animal without controls. They claim they cut the cervical cord 90 per cent but theres no evidence of that in the paper, just some crude pictures," added Silver.

You could say so, though Canavero doesn't see it quite like that. In fact, controversially he sees it more as a failure of other types of medicine, telling Medical News Today, "It will be about curing incurable neurological disorders for which other treatments have failed big time, so gene therapy,stem cells- they all just came to nothing. We have failed despite billions of dollars being poured into this sort of research."

"So actually, head transplant or body transplant, whatever your angle is, is actually a failure of medicine. It is not a brilliant success, a brilliant advancement to medical science. When you just haven't tackled biology, you don't know how to treat genes, you don't really understand, and you really need to resort to a body transplant, it means that you've failed. So this must not be construed as a success of medical research," he added.

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Human head transplant: Sergio Canavero considers the UK as the venue for 2017's most talked about operation - Alphr