Theres a lot to be said for being in the right place at the right time, but could Air Supplys long-time success be the result or a chance meeting or was the cosmos working overtime on a little something called destiny? Maybe, but one thing is for surenone of it would have been possible at all without their hard work and tenacity to make it happen.The two Russells, Graham Russell and Russell Hitchcock, happened to be cast in the same Sydney, Australian production of Jesus Christ Superstar in 1975, and everything changed after that.

Many an audience member has probably asked himself if a fine looking group of ladies about to take the stage could possibly do justice to one of the most popular rock bands in the world. Its a legitimate question considering its not easy music to play, so a person cant help but wonder if the music will be taken as seriously as the people in the audience do. However, once the guitars are plugged in and the girls dig into those first few chords, the obvious answer to that question is, oh, hell, yes.

Many a cook tries their hand at duplicating foods they love in restaurants and specialty shops, telling themselves, it cant be that difficult. Often times, theyre right. It can be doneand its pretty simple. However, sometimes, its not as easy as it looks.Mexican food for example looks easy because ingredients are simple, sauces are often slow-cooked and meat is marinated, making this comfort food one of Americas favorite. Recipes are often handed down and each time theyre prepared, a spice might be tweaked or flavor added, depending on taste and preference.

Its been 40 years since Elvis Presley died (August 16, 1977) and millions of people still have the date circled in red on their calendars. People still remember and they still mourn. Some internet sites have gone to the extent of estimating what he would look like now, if he were still here in the physical.This time of year Memphis fills up with more people than usual as crowds in large numbers make their pilgrimages to Graceland for visits to his home while tribute shows pop up all around the country to remember the huge icon that he was.

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I didnt want it to affect my job as a BBC correspondent covering religious affairs. But in 2015 I went numb down one side of my body for several weeks. A scan showed multiple lesions, and a specialist confirmed I had relapsing-remitting MS. It felt like a life sentence. My family wasnt surprised wed long known it was a possibility. No tears were shed; my parents are of the stiff-upper-lip generation.

The next drug failed to stop another relapse. I wanted to keep reporting for as long as possible, but last September I finally stepped down frommy job, and my bosses helped me find other options involving less travel and with more predictable hours.

My MS seemed to be moving from relapsing-remitting to secondary progressive, as my body became less able to repair the brain damage caused by each relapse. So, after months of research, I decided to take a risk and have an autologous hematopoietic stem cell transplant (HSCT) a chemotherapy treatment that wipes out then regrows your immune system at a private clinic in Mexico.

HSCT has long been used to treat blood cancers, but its use in autoimmune diseases like MS is still undergoing trials. It destroys the malfunctioning cells thought to be responsible for damaging the myelin sheath, while stem cells harvested from your bone marrow are given back to shorten your time without a working immune system.

HSCT holds the most promise for people having regular MS attacks and its now offered to some MS patients at a few NHS hospitals in England under tight criteria. I didnt qualify, but I met several others who had been helped by it.

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'I approached my 50th birthday unable to balance or speak' - Telegraph.co.uk

In 2013, University of Virginia researcher Michael McConnell published research that would forever change how scientists study brain cells.

McConnell and a team of nationwide collaborators discovered a genetic mosaic in the brains neurons, proving that brain cells are not exact replicas of each other, and that each individual neuron contains a slightly different genetic makeup.

McConnell, an assistant professor in the School of Medicines Department of Biochemistry and Molecular Genetics, has been using this new information to investigate how variations in individual neurons impact neuropsychiatric disorders like schizophrenia and epilepsy. With a recent $50,000 grant from the Bow Foundation, McConnell will expand his research to explore the cause of a rare genetic disorder known as GNAO1 so named for the faulty protein-coding gene that is its likely source.

GNAO1 causes seizures, movement disorders and developmental delays. Currently, only 50 people worldwide are known to have the disease. The Bow Foundation seeks to increase awareness so that other probable victims of the disorder can be properly diagnosed and to raise funds for further research and treatment.

UVA Today recently sat down with McConnell to find out more about how GNAO1 fits into his broader research and what his continued work means for all neuropsychiatric disorders.

Q. Can you explain the general goals of your lab?

A. My lab has two general directions. One is brain somatic mosaicism, which is a finding that different neurons in the brain have different genomes from one another. We usually think every cell in a single persons body has the same blueprint for how they develop and what they become. It turns out that blueprint changes a little bit in the neurons from neuron to neuron. So you have slightly different versions of the same blueprint and we want to know what that means.

The second area of our work focuses on a new technology called induced pluripotent stem cells, or iPSCs. The technology permits us to make stem cell from skin cells. We can do this with patients, and use the stem cells to make specific cell types with same genetic mutations that are in the patients. That lets us create and study the persons brain cells in a dish. So now, if that person has a neurological disease, we can in a dish study that persons disease and identify drugs that alter the disease. Its a very personalized medicine approach to that disease.

Q. Does cell-level genomic variety exist in other areas of the body outside the central nervous system?

A. Every cell in your body has mutations of one kind or another, but brain cells are there for your whole life, so the differences have a bigger impact there. A skin cell is gone in a month. An intestinal cell is gone in a week. Any changes in those cells will rarely have an opportunity to cause a problem unless they cause a tumor.

Q. How does your research intersect with the goals of the Bow Foundation?

A. Let me back up to a little bit of history on that. When I got to UVA four years ago, I started talking quite a lot with Howard Goodkin and Mark Beenhakker. Mark is an assistant professor in pharmacology. Howard is a pediatric neurologist and works with children with epilepsy. I had this interest in epilepsy and UVA has a historic and current strength in epilepsy research.

We started talking about how to use iPSCs the technology that we use to study mosaicism to help Howards patients. As we talked about it and I learned more about epilepsy, we quickly realized that there are a substantial number of patients with epilepsy or seizure disorders where we cant do a genetic test to figure out what drug to use on those patients.

Clinical guidance, like Howards expertise, allows him to make a pretty good diagnosis and know what drugs to try first and second and third. But around 30 percent of children that come in with epilepsy never find the drug that works, and theyre in for a lifetime of trial-and-error. We realized that we could use iPSC-derived neurons to test drugs in the dish instead of going through all of the trial-and-error with patients. Thats the bigger project that weve been moving toward.

The Bow Foundation was formed by patient advocates after this rare genetic mutation in GNAO1 was identified. GNAO1 is a subunit of a G protein-coupled receptor; some mutations in this receptor can lead to epilepsy while others lead to movement disorders.

Were still trying to learn about these patients, and the biggest thing the Bow Foundation is doing is trying to address that by creating a patient registry. At the same time, the foundation has provided funds for us to start making and testing iPSCs and launch this approach to personalized medicine for epilepsy.

In the GNAO1 patients, we expect to be able to study their neurons in a dish and understand why they behave differently, why the electrical activity in their brain is different or why they develop differently.

Q. What other more widespread disorders, in addition to schizophrenia and epilepsy, are likely to benefit from your research?

A. Im part of a broader project called the Brain Somatic Mosaicism Network that is conducting research on diseases that span the neuropsychiatric field. Our lab covers schizophrenia, but other nodes within that network are researching autism, bipolar disorder, Tourette syndrome and other psychiatric diseases where the genetic cause is difficult to identify. Thats the underlying theme.

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Researcher Seeks to Unravel the Brain's Genetic Tapestry to Tackle Rare Disorder - University of Virginia

LOS ANGELES In the fight against cardiovascular disease, a new super-weapon is now even closer to deployment and its capabilities are turning out to be beyond expectations.

One of the most notorious killers facing humanity, cardiovascular disease, is responsible for about about 1 in every 3 deaths in the U.S., according to the American Heart Association. A new study aimed at combating the disease finds that stem cells, the controversial darlings of modern biomedical research, are not only showing promise in treating heart failure, but in rats are actually reversing problems associated with old age.

The way the cells work to reverse aging is fascinating, says Dr. Eduardo Marbn,one of the studys primary investigators, in a press release. They secrete tiny vesicles that are chock-full of signaling molecules such as RNA and proteins. The vesicles from young cells appear to contain all the needed instructions to turn back the clock.

Marbn, who serves as director of the Cedars-Sinai Heart Institute, explains this latest study builds on previous lab work and human trials which have shown promise in treating heart failure using cardiac stem cell infusions.

The specific type of stem cells used in the study are known as cardiosphere-derived cells or CDCs. The process to grow these cells was initially developed when Marbn was part of the Johns Hopkins University faculty.

While the latest research involving CDCs indicates possibilities that have previously been in the realm of science fiction, the scientists leading the charge urge restraint in face of the excitement.

This study didnt measure whether receiving the cardiosphere-derived cells extended lifespans, so we have a lot more work to do, says Dr. Lilian Grigorian-Shamagian, the studys first author. We have much to study, including whether CDCs need to come from a young donor to have the same rejuvenating effects and whether the extracellular vesicles are able to reproduce all the rejuvenating effects we detect with CDCs.

Nevertheless, the latest results of stem cell infusions in rats are startling. Not only did rats that received the CDCs experience improved heart function, they also had lengthened heart cell telomeres.

Telomeres, the protective caps at the ends of chromosomes, normally shrink with age. As telomere shrinkage is one of the most studied and least understood phenomenons associated with aging, the effect of CDCs on them is especially fascinating.

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Whats more, the researchers said the rats who received the treatment also had their exercise capacity increase by about 20 percent. They also regrew hair faster than rats that didnt receive the cells.

With these thrilling results only the latest in recent stem cell headlines, researchers caution the public that most treatments are still not ready for prime time.

Indeed, a recent Reuters article warned that stem cell therapy still is not approved to treat heart failure in the U.S., yet many unscrupulous clinics are offering questionable services anyway and charging tens of thousands of dollars for it. In some cases, researchers quoted in the article said these labs may not even be injecting stem cells, but rather a useless and dangerous mix of cellular debris.

The article also noted two patients died and another went blind after stem cell injection procedures in Florida clinics.

Still, the legitimate doctors and scientists working to push the frontier of medicine forward are very optimistic about the real possibilities of the therapy. The Cedars-Sinai team said they are also studying the use of stem cells in treating patients with Duchenne muscular dystrophy and patients with heart failure with preserved ejection fraction, a condition that affects more than 50 percent of all heart failure patients.

Their research on CDCs effects on aging was published this month in the European Heart Journal.

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Study: Cardiac Stem Cell Injections Reverse Effects of Aging - Study Finds

Representational image

Washington D.C. : A study has recently revealed that vitamin C may tell faulty stem cells in the bone marrow to mature and die normally, instead of multiplying to cause blood cancers.

According to researchers, certain genetic changes are known to reduce the ability of an enzyme called TET2 to encourage stem cells to become mature blood cells, which eventually die, in many patients with certain kinds of leukemia.

The new study found that vitamin C activated TET2 function in mice engineered to be deficient in the enzyme.

Corresponding study author Benjamin G. Neel said, "We're excited by the prospect that high-dose vitamin C might become a safe treatment for blood diseases caused by TET2-deficient leukemia stem cells, most likely in combination with other targeted therapies."

The results suggested that changes in the genetic code (mutations) that reduce TET2 function are found in 10 percent of patients with acute myeloid leukemia (AML), 30 percent of those with a form of pre-leukemia called myelodysplastic syndrome, and in nearly 50 percent of patients with chronic myelomonocytic leukemia.

The study results revolve around the relationship between TET2 and cytosine, one of the four nucleic acid "letters" that comprise the DNA code in genes.

To determine the effect of mutations that reduce TET2 function in abnormal stem cells, the team genetically engineered mice such that the scientists could switch the TET2 gene on or off.

The findings indicated that vitamin C did the same thing as restoring TET2 function genetically. By promoting DNA demethylation, high-dose vitamin C treatment induced stem cells to mature, and also suppressed the growth of leukemia cancer stem cells from human patients implanted in mice.

"Interestingly, we also found that vitamin C treatment had an effect on leukemic stem cells that resembled damage to their DNA," said first study author Luisa Cimmino.

"For this reason, we decided to combine vitamin C with a PARP inhibitor, a drug type known to cause cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients with ovarian cancer," Cimmino added.

The findings appear in journal Cell.

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Vitamin C may help genes to kill blood cancer stem cells - ETHealthworld.com

18 Aug 2017

Astrocytes are more than bystanders in neurotransmissionthey take an active role in synaptic activity. However, their functions are hard to study because the cells are difficult to grow in vitro and its hard to coax them to mature from progenitors. Now, researchers from the labs of Sergiu Paca and Ben Barres, both at Stanford University School of Medicine, California, report that astrocytes come of age in spherical balls of human brain cells cultured in a dish for almost two years. As reported in the August 16 Neuron, these astrocytes develop much like those from real brains, undergoing similar transcriptomic, morphologic, and functional changes. Studying the processes involved in this astrocyte maturation will help researchers understand neurodevelopmental disorders such as autism and schizophrenia, researchers say, and might even shed light on problems in adultbrains.

That these 3D cultures can be maintained for such a long time allows us to capture an interesting transition in astrocytes, said Paca. We are starting to appreciate aspects of human brain development to which we would not otherwise haveaccess.

The breakthrough is that they can develop human astrocytes very close to maturity in their 3D culture models, said Doo Yeon Kim, Massachusetts General Hospital, Charlestown, who uses 3D culture models to study pathological process that occur in Alzheimers disease. Some researchers are using 3D cultures to model other neurodegenerative disorders, such as ALS, and still others are planning to use cultured astrocytes for cell therapy. If astrocytes are not mature enough in culture, patterns [we see] may not be the same as in the diseased brain, saidKim.

This developing human astrocyte (red), which comes from a 350-day-old cortical spheroid, is taking shape as a mature cell. [Image courtesy of Sloan et al.Neuron]

A few years back, Pacas group developed a method for differentiating human induced pluripotent stem cells (hiPSCs) into a 3D culture of brain cells. They used special dishes that the cells could not easily attach to, coaxing them to stick to each other instead. Under these conditions the iPSCs balled up into neural spheroids that grew to about 4 mm in diameter. A cocktail of growth factors early on encouraged them to form excitatory pyramidal cells like those in the cortex, and the cells spontaneously organized into layers. These cortical spheroids survived a year or more and spontaneously grew astrocytes in addition to neurons (Paca et al., 2015). Not long after, the Barres lab reported that astrocytes in the adult human brain look different from those isolated from fetuses. They called the latter astrocyte progenitor cells (APCs). Each had their own transcriptional patterns and functions (Jan 2016 news). Together, Barres and Paca wondered if it was possible to see the APCs morph into mature astrocytes in these long-lived corticalspheroids.

To find out, first author Steven Sloan and colleagues examined spheroids generated from iPSCs derived from healthy human fibroblasts. Sloan grew the spheroids for about 20 months. Along the way, he took samples, isolated the astrocytes, and compared them to those isolated from fetal and postnatal humanbrain.

At about 100 days in culture, astrocytes began to sprout spontaneously from within the mostly neuronal milieu of the cortical spheroids. At first, these cells were simple, adorned by few branches and expressing genes akin to those active in APCs. But as the spheroids reached about 250 days, the astrocytes therein looked more mature, having numerous processes. After this point, APC gene expression tapered off and the astrocytes started producing proteins typical of matureastrocytes.

Astrocytes also underwent functional changes as they matured. Early versions divided in fast and furious fashion, much like their counterparts from the fetal tissue. That division slowed as the spheroids aged. Dividing APCs dropped from 35 percent of all astrocytes at day 167 to 3 percent at day 590. Taken from the spheroids at day 150 and cultured in a 2D layer, immature astrocytes also harbored a voracious appetite for added synaptosomes, much like immature astrocytes recently characterized in mice (see image below; Dec 2013 conference news on Chung et al., 2013). However, that hunger waned as astrocytes approached the 590-daymark.

At the older end of the spectrum, mature astrocytes seemed to take on a supportive role, strengthening calcium signaling in nearbyneurons.

Studying the neurons and astrocytes in these cortical spheroids could be useful for addressing certain unanswered questions about human biology, said other researchers. This could be a very strong opportunity to understand what goes wrong in human genetic disorders that affect astrocyte function, said M. Kerry OBanion, University of Rochester Medical Center, New York. Its also possible that such cultures could reveal as yet unknown facets of familial mutations that cause Alzheimers disease, he suggested. However, given that these cultures take a long time to grow and develop, they are unlikely to completely supplant other types of cultures or faster-maturing animal models, hesaid.

Kim agreed, saying, The results are very exciting, but not practical yet for disease modeling." However, Kim hopes that researchers will make progress on accelerating the maturationprocess.

The Barres and Paca labs are trying just that with the spheroid. They will also analyze what they secrete to support neuronal signaling. In addition, they are exploring how to make the astrocytes reactive, as they often are in neurodegenerative diseases, such as Alzheimers. Doing so might reveal how such astrocytes interact withneurons.

An immature astrocyte taken from a 150-day-old spheroid gobbles up added synaptosomes (red). [Neuron, Sloan et al.2017]

To Pacas knowledge, these cortical spheroids are some of the longest human cell cultures ever reported. His group has continued to cultivate these clumps, with the oldest still going strong at day 850. Granted, these systems are missing many cell types: endothelial cells, oligodendrocytes, and microglia to name a few, he said. However, his lab has introduced new ways to add in other cells. Earlier this year, he reported 3D cultures of cortical glutamatergic neurons and GABAergic interneurons that fused together when they were placed side-by-side (Birey et al., 2017).

Clive Svendsen, Cedars-Sinai Medical Center in Los Angeles, California, saw clinical implications for this paper. It shows iPSC derived astrocytes can mature to an adult phenotype, he said. This further supports their use in clinical transplantation, as we are planning to do. His group has begun a Phase 1 clinical trial that implants human fetal astrocytes into the spinal cords of ALS patients.Gwyneth DickeyZakaib

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Brain Spheroids Hatch Mature Astrocytes - Alzforum

The study suggests it may encourage blood cancer stem cells to die.

Researchers say Vitamin C may "tell" faulty stem cells in the bone marrow to mature and die normally, instead of multiplying to cause blood cancers.

They explained that certain genetic changes are known to reduce the ability of an enzyme called TET2 to encourage stem cells to become mature blood cells, which eventually die, in many patients with certain kinds of leukaemia.

The new study, published online by the journal Cell. found that vitamin C activated TET2 function in mice engineered to be deficient in the enzyme.

Study corresponding author Professor Benjamin Neel, of the Perlmutter Cancer Centre in the United States, said: "We're excited by the prospect that high-dose vitamin C might become a safe treatment for blood diseases caused by TET2-deficient leukemia stem cells, most likely in combination with other targeted therapies."

He said changes in the genetic code that reduce TET2 function are found in 10 per cent of patients with acute myeloid leukaemia (AML), 30 per cent of those with a form of pre-leukaemia called myelodysplastic syndrome, and in nearly 50 per cent of patients with chronic myelomonocytic leukaemia.

Such cancers cause anaemia, infection risk, and bleeding as abnormal stem cells multiply in the bone marrow until they interfere with blood cell production, with the number of cases increasing as the population ages.

Prof Neel said the study results revolve around the relationship between TET2 and cytosine, one of the four nucleic acid "letters" that comprise the DNA code in genes.

To determine the effect of mutations that reduce TET2 function in abnormal stem cells, the researchers genetically engineered mice such that the scientists could switch the TET2 gene on or off.

Similar to the naturally occurring effects of TET2 mutations in mice or humans, using molecular biology techniques to turn off TET2 in mice caused abnormal stem cell behaviour.

Prof Neel said, remarkably, the changes were reversed when TET2 expression was restored by a genetic trick.

Previous work had shown that vitamin C could stimulate the activity of TET2 and its relatives TET1 and TET3.

Because only one of the two copies of the TET2 gene in each stem cell is usually affected in TET2-mutant blood diseases, the researchers hypothesised that high doses of vitamin C, which can only be given intravenously, might reverse the effects of TET2 deficiency by turning up the action of the remaining functional gene.

They found that vitamin C did the same thing as restoring TET2 function genetically.

By promoting DNA demethylation, high-dose vitamin C treatment induced stem cells to mature, and also suppressed the growth of leukaemia cancer stem cells from human patients implanted in mice.

Study first author Doctor Luisa Cimmino, of New York University Langone Health, said: "Interestingly, we also found that vitamin C treatment had an effect on leukaemic stem cells that resembled damage to their DNA.

"For this reason, we decided to combine vitamin C with a PARP inhibitor, a drug type known to cause cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients with ovarian cancer."

The researchers found that the combination had an enhanced effect on leukaemia stem cells, further shifting them from self-renewal back toward maturity and cell death.

Dr Cimmino said the results also suggest that vitamin C might drive leukaemic stem cells without TET2 mutations toward death, given that it turns up any TET2 activity normally in place.

Corresponding author Professor Iannis Aifantis, also of NYU Langone Health, added: "Our team is working to systematically identify genetic changes that contribute to risk for leukaemia in significant groups of patients.

"This study adds the targeting of abnormal TET2-driven DNA demethylation to our list of potential new treatment approaches."

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Blood cancer: High doses of vitamin C could encourage stem cells ... - Express.co.uk

HELENA ExplorationWorks is hosting the Be The Match bone marrow donor drive this week at the Great Northern Town Center.

The drive is intended to support those in need of bone marrow or blood stem cell transplants around the world. Its being held in conjunction with ExplorationWorks Kids Kicking Cancer Camp.

The camp is open to children who are directly affected by cancer in their lives. Campers had the opportunity to make a card for Be the Match child who is currently undergoing or awaiting treatment.

Our hope is that the kids attending our camp will be able to connect with the Be The Match kids on a level most other children wouldnt understand. Knowing someone else is fighting the same fight will hopefully be a healing activity for all of the kids involved, said ExplorationWorks Education Director Lauren Rivers.

John Philpott of Be the Match said that sadly, some of the Be The Match kids children are still waiting to be matched with a donor.

There are still thousands of patients every year who have to hear their doctor say theres no match for you, said Phillpott, One Montanan [donation] can mean the difference for one patient.

According to Be the Match, someone is diagnosed with blood cancer every three minutes and every 10 minutes someone dies from not receiving a transplant.

The Marrow Donor Registry Drive will continue at ExplorationWorks from 10 a.m. to 5 p.m. Friday and from 12:30 to 3 p.m. on Saturday.

Registration takes around 10 minutes to complete and only involves some paper work and a few cheek swabs. You must be between the ages of 18 and 44 in order to register.

For more information about bone marrow donation and how to register click here.

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Bone marrow drive held at ExplorationWorks - KTVH

The early heart tube of a chick embryo: cardiac and endothelial cells are made visible by specifically expressing fluorescent proteins under the control of the Nkx2.5 (green) and Isl1 (red) cardiovascular genes. Credit: Weizmann Institute of Science

One of the first organ systems to form and function in the embryo is the cardiovascular system: in fact, this developmental process starts so early that scientists still have many unresolved questions on the origin of the primitive heart and blood vessels. How do the first cells the progenitors that are destined to become part of this system participate in shaping the developed cardiovascular system?

Dr. Lyad Zamir, a former PhD student in the lab of Prof. Eldad Tzahor in the Weizmann Institute of Science's Department of Molecular Cell Biology, developed a method to image the earliest cardiovascular progenitors and track them and their descendants through the developing embryo in real time. His movies took place in fertilized chicken eggs, in which a complex network of blood vessels forms within the yolk sac to nourish the embryo. The findings of this research were recently published in eLife.

Working in collaboration with the lab of Prof. Richard Harvey of the Victor Chang Cardiac Research Institute and the University of New South Wales, both in Australia, Prof. Tzahor and Dr. Zamir focused on a gene called Nkx2-5. This gene encodes a transcription factor, which is a regulatory protein that controls the expression of other genes involved in the development of the heart. "The new study revealed that Nkx2-5, independently of its role in the development of the heart, plays a central role in the genesis of the very first blood vessels and indeed the formation of blood," says Prof. Tzahor.

Looking at the onset of Nkx2-5 expression, the team revealed the existence of progenitor cells called hemangioblasts. These cells give rise to both the blood and vascular progenitor cells those that lead to the formation of blood vessels. These unique cells are created from the mesoderm the middle layer of cells that appears in the very early developing embryo. Researchers have been hotly debating the existence of hemangioblasts and, if they do exist, their possible function.

In the chick embryo films, the researchers could see the hemangioblasts moving to create "blood islands," which form within the primitive embryonic vessels. The researchers were surprised to observe that some of the hemangioblast cells were moving into the heart, where they formed blood stem cells. This helped make sense of other studies revealing that the early heart tube contains cells that appear to assist in generating blood cells. The researchers also identified specialized Nkx2-5-expressing cells within the lining of the newly formed aorta, where they appeared to "bud off" to produce new blood cells. Later on in development, these specialized cells move into the liver, where they give rise to the blood-forming stem cells in the fetus.

Prof. Tzahor: "Even 20 years after one of the 'master genes' for heart development was discovered, we have managed to write a new story about its action, showing that it works briefly at a very early stage in development in the formation of vessels and blood before the main action takes place in the heart. We have provided solid evidence for the existence of these very early cells and their contribution to heart and vascular development."

Because these findings reveal the early origins of at least some of the blood-forming stem cells in the embryo, they may be especially helpful in research into diseases affecting the cardiovascular system.

Explore further: Kidney research leads to surprising discovery about how the heart forms

More information: Lyad Zamir et al. Nkx2.5 marks angioblasts that contribute to hemogenic endothelium of the endocardium and dorsal aorta, eLife (2017). DOI: 10.7554/eLife.20994

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The unexpected role of a well-known gene in creating blood - Medical Xpress

The old rats appeared newly invigorated after receiving their injections. As hoped, the cardiac stem cells improved heart function yet also provided additional benefits. The rats' fur fur, shaved for surgery, grew back more quickly than expected, and their chromosomal telomeres, which commonly shrink with age, lengthened.

The old rats receiving the cardiac stem cells also had increased stamina overall, exercising more than before the infusion.

"It's extremely exciting," said Dr. Eduardo Marbn, primary investigator on the research and director of the Cedars-Sinai Heart Institute. Witnessing "the systemic rejuvenating effects," he said, "it's kind of like an unexpected fountain of youth."

"We've been studying new forms of cell therapy for the heart for some 12 years now," Marbn said.

Some of this research has focused on cardiosphere-derived cells.

"They're progenitor cells from the heart itself," Marbn said. Progenitor cells are generated from stem cells and share some, but not all, of the same properties. For instance, they can differentiate into more than one kind of cell like stem cells, but unlike stem cells, progenitor cells cannot divide and reproduce indefinitely.

Since heart failure with preserved ejection fraction is similar to aging, Marbn decided to experiment on old rats, ones that suffered from a type of heart problem "that's very typical of what we find in older human beings: The heart's stiff, and it doesn't relax right, and it causes fluid to back up some," Marbn explained.

He and his team injected cardiosphere-derived cells from newborn rats into the hearts of 22-month-old rats -- that's elderly for a rat. Similar old rats received a placebo injection of saline solution. Then, Marbn and his team compared both groups to young rats that were 4 months old. After a month, they compared the rats again.

Even though the cells were injected into the heart, their effects were noticeable throughout the body, Marbn said

"The animals could exercise further than they could before by about 20%, and one of the most striking things, especially for me (because I'm kind of losing my hair) the animals ... regrew their fur a lot better after they'd gotten cells" compared with the placebo rats, Marbn said.

The rats that received cardiosphere-derived cells also experienced improved heart function and showed longer heart cell telomeres.

Why did it work?

The working hypothesis is that the cells secrete exosomes, tiny vesicles that "contain a lot of nucleic acids, things like RNA, that can change patterns of the way the tissue responds to injury and the way genes are expressed in the tissue," Marbn said.

It is the exosomes that act on the heart and make it better as well as mediating long-distance effects on exercise capacity and hair regrowth, he explained.

Looking to the future, Marbn said he's begun to explore delivering the cardiac stem cells intravenously in a simple infusion -- instead of injecting them directly into the heart, which would be a complex procedure for a human patient -- and seeing whether the same beneficial effects occur.

Dr. Gary Gerstenblith, a professor of medicine in the cardiology division of Johns Hopkins Medicine, said the new study is "very comprehensive."

"Striking benefits are demonstrated not only from a cardiac perspective but across multiple organ systems," said Gerstenblith, who did not contribute to the new research. "The results suggest that stem cell therapies should be studied as an additional therapeutic option in the treatment of cardiac and other diseases common in the elderly."

Todd Herron, director of the University of Michigan Frankel Cardiovascular Center's Cardiovascular Regeneration Core Laboratory, said Marbn, with his previous work with cardiac stem cells, has "led the field in this area."

"The novelty of this bit of work is, they started to look at more precise molecular mechanisms to explain the phenomenon they've seen in the past," said Herron, who played no role in the new research.

One strength of the approach here is that the researchers have taken cells "from the organ that they want to rejuvenate, so that makes it likely that the cells stay there in that tissue," Herron said.

He believes that more extensive study, beginning with larger animals and including long-term followup, is needed before this technique could be used in humans.

"We need to make sure there's no harm being done," Herron said, adding that extending the lifetime and improving quality of life amounts to "a tradeoff between the potential risk and the potential good that can be done."

Capicor hasn't announced any plans to do studies in aging, but the possibility exists.

After all, the cells have been proven "completely safe" in "over 100 human patients," so it would be possible to fast-track them into the clinic, Marbn explained: "I can't tell you that there are any plans to do that, but it could easily be done from a safety viewpoint."

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Cardiac stem cells rejuvenate rats' aging hearts, study says - CNN

Anika Therapeutics, Inc. ANIK , a global medical technology company, specializing on integrated orthopedics medicines , has made a development with its proprietary hyaluronic acid (HA) technology. The company recently published favorable data on evaluating the usefulness of HYALOFAST, a non-woven biodegradable HA-based scaffold for treatment of cartilage lesions of the knee joint.

The study was based on 40 patients with full thickness cartilage lesions of the knee joint. 20 among them were aged above 45 and the remaining, below the figure. Per the company, all patients were implanted with HYALOFAST, soaked in bone marrow aspirate concentrate (BMAC), containing mesenchymal stem cells (MSCs) and prospectively evaluated for four years.

Data from the trial demonstrated that treatment outcomes were equally effective for both the age groups. This is more encouraging for the fact that it is difficult to treat patients above 45 years of age with traditional surgical approaches such as microfracture. Based on the findings, the company claimed that irrespective of a patient's age, HYALOFAST in combination with autologous adult mesenchymal stem cells (MSCs), can be successfully used as a treatment option for cartilage lesions.

With this breakthrough, we expect the market adoption of HYALOFAST to increase significantly, boosting Anika Therapeutics' sales performance. Notably, HYALOFAST is commercially available in more than 15 countries worldwide and has been used in more than 11,000 patients so far. Also, this trial result should advance the company's procedure of regulatory submission of HYALOFAST in the US. Under 'FastTRACK' Phase III trial, it is currently enrolling patients across the U.S. and Europe.

Demand for therapeutics-based treatment in the field of integrated orthopedics medicines and traumatic conditions, is growing in leaps and bounds these days. Per a recent report by Market Research Engine in this regard, global Orthopedic Devices Market will witness a CAGR of 5% from 2016 to 2022 and is projected to reach $47.50 billion by 2022.

Some of the big names in the orthopedic device market with promising growth potential are Stryker Corporation SYK , Smith & Nephew plc SNN and Orthofix International N.V. OFIX .

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Many doctors tell patients and families that recovery does not occur after spinal cord injury. This is not true. Recovery is the rule, not the exception after spinal cord injury.

Segmental recovery. Most patients recover 1-2 segments below the injury site, even after so-called complete spinal cord injuries. For example, a person with a C4/5 injury may have deltoid function on admission and then recover biceps (C5), wrist extensors (C6), and perhaps even triceps (C7) after several months, and the associated dermatomes.

Recovery due to methylprednisolone. The second National Acute Spinal Cord Injury Study (NASCIS 2) showed that patients with complete spinal cord injuries and who did not receive the high-dose steroid methylprednisolone recovered on average 8% of motor function they had lost. If they received methylprednisolone within 8 hours after injury, they recovered on average 21% of what they had lost. In contrast, people with incomplete spinal cord injury recovered on average 59% of motor function and 75% if treated with high dose methylprednisolone.

Recovery of postural reflexes. Most people with cervical or upper thoracic spinal cord injury are initially unable to control their trunk muscles. However, most will recover better trunk control over months or even years after injury.

Walking quads and paras. Most people with incomplete spinal cord injuries, i.e. ASIA C, will recover standing or walking. Walking recovery after complete spinal cord injuries, i.e. ASIA A, are rare but can occur in 5% of the cases. In the 1980s, less than 40% of spinal cord injuries admitted to hospital were incomplete. However, in the 1990s, over 60% of spinal cord injuries are incomplete and thus the incidence of walking quads or walking paras may be higher than most people think.

Both animal and human studies indicate that as little as 10% of spinal cord tracts can support substantial function, including locomotion. People often can walk even though a tumor has damaged 90% of their spinal cord. This is due to the redundancy and plasticity of the spinal cord. Multiple spinal pathways serve similar or overlapping functions. Plasticity refers to the ability of axons to sprout and make new connections. Because transected spinal cords are rare, most people have some spinal axons crossing the injury site. This is the basis of the hope that even slight regeneration of the spinal cord will restore substantial function.

Experimental Therapies for Subacute Spinal Cord Injury

Several experimental therapies are being tested in clinical trial for spinal cord injury during the first days or weeks after injury.

Monosialic ganglioside (GM1, Sygen). In 1991, Fred Geisler and colleagues reported that GM1 injected daily for 6 weeks after injury improve locomotor recovery 37 patients. Fidia Pharmaceutical subsequently tested this therapy in a large multicenter clinical trial in 800 patients, showing that the GM1 accelerated recovery during the first six weeks but did not significantly improve the extent of recovery at 6-12 months after injury. Note that this trial is no longer active. Although the drug is still available in Europe and South America, the company Fidia has been bought by another company. CareCure Forum (GM1) Link

Activated macrophage transplants. In 1998, Michal Schwartz at the Weizmann Institute reported that activated macrophages obtained from blood and transplanted to the spinal cord improve functional recovery in rats. The company Proneuron initiated phase 1 clinical trials to assess feasibility and safety of macrophage transplants in human spinal cord injury. Preliminary reports suggest that the treatment is feasible and safe. All the patients had complete thoracic spinal cord injury and received macrophage transplants within 2 weeks after injury. Three of the 8 patients recovered from ASIA A to ASIA C, more than the expected 5%. A phase 1 clinical trial is continuing at Erasmus Hospital in Brussels, Belgium. A phase 2 trial is being planned in two U.S. centers including Craig Hospital in Denver (CO) and Mt. Sinai in New York City (NY). CareCure Forum (Macrophage) Link

Alternating Current Electrical Stimulation. In 1999, Richard Borgens and colleagues at Purdue University reported that alternating currents applied to dog spinal cords stimulated regeneration and recovery of function in dogs with spinal cord injury. A clinical trial has commenced at Purdue University for people who are within 2 weeks after acute spinal cord injury. CareCure Forum (AC Stim) Link

AIT-082 (Neotrofin). This is a guanosine analog that can be taken orally and reportedly increases neurotrophins or neural growth factors in the brain and spinal cord. Neotherapeutics tested this drug in patients with Alzheimers disease. They started a multicenter clinical trial at Ranchos Los Amigos in Downey (CA), Gaylord Hospital in Wallingford (CT), and Thomas Jefferson Hospital in Philadelphia. The treatment must be started within 2 weeks after spinal cord injury. CareCure Forum (AIT-082) Link

Experimental Therapies for Chronic Spinal Cord Injury

Several therapies are being tested in clinical trials for chronic spinal cord injury, i.e. people whose neurological recovery has stabilized one or more years after injury. Many other treatments are being considered for clinical trial (see article on Advances in Spinal Cord Injury Therapy 25 November 2002).

4-aminopyridine (4-AP). This drug is a small molecule that blocks fast voltage sensitive potassium channel blockers. The drug can be obtained by physician prescription from compounding pharmacies in the United States. In addition, Acorda Therapeutics is carrying out a multicenter phase 3 clinical trial of a sustained release formulation of the drug in people who are more than one and a half years after incomplete spinal cord injury. The drug may improve conduction of demyelinated axons in the spinal cord and preliminary clinical trial results suggest that the drug may reduce spasticity and improve motor or sensory function in as many as a third of people with chronic spinal cord injury. See CareCure Forum (4-AP) Link

Fetal porcine stem cell transplants. Embryonic stem cells have attracted much attention. Several studies of human fetal cell transplants have been carried out in Sweden, Russia, and the United States, showing that transplanted fetal cells will engraft in human spinal cords. However, due in part of the lack of availability of adult human stem cells for transplantation and politics associated with the use of embryonic human stem cells, the first and only stem cell therapy trial for spinal cord injury in the United States used fetal stem cells from pigs. A phase 1 clinical trial at Washington University in St. Louis (MO) and Albany Medical Center in Albany (NY) has transplanted fetal stem obtained from pig fetuses and treated with antibodies to reduce the immune rejection. Sponsored by Diacrin, this trial is aiming to test 10 patients. See CareCure Forum (Diacrin) Link

Olfactory ensheathing glial transplants. Olfactory ensheathing glia (OEG) reside in the olfactory nerve and the olfactory bulb. They are believed to be why the olfactory nerve continuously regenerates in adults. OEG cells are made in the nasal mucosa and migrate up the nerve to the olfactory bulb. Several laboratories have shown that OEG transplants facilitate regeneration of the spinal cord. Three clinical trials have started in Lisbon (Portugal), Brisbane (Australia), and Beijing (China). In Lisbon, they are transplanting nasal mucosa obtained from the patient into the spinal cord. In Brisbane, they are culturing OEG cells from nasal mucosa and transplanting the cells to the spinal cord. In Beijing, they are culturing OEG from human fetal olfactory bulbs and transplanting into the spinal cord. See CareCure Forum Link (Brisbane) and CareCure Forum Link (Beijing)

Summary

Spinal cord injury is devastating, not only for the injured person but for families and friends. While much information is available on Internet, most of the material is scattered and out of date. This article summarizes answers to some of the most frequently asked questions by people who are encountering spinal cord injury for the first time. Spinal cord injury disconnects the brain from the body. This leads not only to loss of sensation and motor control below the injury site but may be associated with abnormal activities of the spinal cord both above and below the injury site, resulting in spasticity, neuropathic pain, and autonomic dysreflexia. Many functions of our body that we take for granted, such as going to the bathroom, sexual function, blood pressure and heart rate, digestion, temperature control and sweating, and other autonomic functions may not only be lost but may be abnormally active. Finally, contrary to popular notions about spinal cord injury, recovery is the rule and not the exception in spinal cord injury. The recovery takes a long time and may be slowed down or blocked by the muscle atrophy and learned non-use. Finally, there is hope. Many therapies have been shown to regenerate and remyelinate the spinal cord. Some of these are now in clinical trials and many more should be in clinical trial soon.

Recovery and TreatmentWise Young, MD, PhD

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Does recovery occur after spinal cord injury? | Answers ...

FREMONT, Calif., Aug. 14, 2017 (GLOBE NEWSWIRE) -- Asterias Biotherapeutics, Inc. (NYSE MKT:AST), a biotechnology company pioneering the field of regenerative medicine, today announced that Cancer Research UK, supported by Asterias technical personnel, has successfully completed manufacture of the first cGMP (current Good Manufacturing Practice) clinical grade lot of AST-VAC2, which meets all specifications for release. This lot will provide clinical trial material for patients enrolling in the first clinical study evaluating AST-VAC2 in non-small cell lung cancer.

The successful production of this first cGMP lot of AST-VAC2 is a major step towards initiating the upcoming study in non-small cell lung cancer, said Mike Mulroy, President and Chief Executive Officer. With its potential as a ready-to-use, off-the-shelf cancer immunotherapy, AST-VAC2 represents an exciting opportunity for Asterias in the rapidly evolving cancer immunotherapy sector.

Investigational therapies intended for human clinical applications must be manufactured in accordance with cGMP standards designed to help assure the safety and potency of drug products. To achieve cGMP standards, a product must be manufactured and released according to rigorous systems designed to ensure appropriate control of manufacturing facilities, equipment, raw materials, processes and testing procedures. Under the companys agreement with Cancer Research UK, Asterias has transferred its innovative laboratory scale AST-VAC2 manufacturing process to Cancer Research UKs Biotherapeutics Development Unit, which has developed and optimized the process for cGMP manufacture and is responsible for producing cGMP AST-VAC2 for use in the upcoming clinical study in non-small cell lung cancer.

About AST-VAC2

AST-VAC2 is an innovative immunotherapy product that contains mature dendritic cells derived from pluripotent stem cells. These non-patient specific (allogeneic) AST-VAC2 cells are engineered to express a modified form of telomerase, a protein widely expressed in tumor cells, but rarely found in normal cells. The modified form of telomerase permits enhanced stimulation of immune responses to the protein. The AST-VAC2 dendritic cells instruct the immune system to generate responses against telomerase which will target tumor cells. AST-VAC2 is based on a specific mode of action that is complementary and potentially synergistic to other immune therapies.

About Non-Small Cell Lung Cancer

Lung cancer (both small cell and non-small cell) is the leading cause of cancer-related death, accounting for about one-quarter of all cancer deaths and more than colorectal, breast, and prostate cancers combined. Non-small cell lung cancer (NSCLC) accounts for about 80% to 85% of lung cancers, according to the American Cancer Society. The three main types of NSCLC are adenocarcinoma, squamous cell carcinoma, and large cell carcinoma. The American Cancer Societys estimates for lung cancer in the United States for 2017 are: about 222,500 new cases of lung cancer, and about 155,870 deaths from lung cancer. Despite the large number of people afflicted by non-small cell lung cancer, patients remain vastly underserved due to a scarcity of effective treatments. According to statistics published by Cancer Research UK, the five year survival rate for lung cancer patients in England and Wales is less than 10%.

About Asterias Biotherapeutics

Asterias Biotherapeutics, Inc. is a biotechnology company pioneering the field of regenerative medicine. The company's proprietary cell therapy programs are based on its pluripotent stem cell and immunotherapy platform technologies. Asterias is presently focused on advancing three clinical-stage programs which have the potential to address areas of very high unmet medical need in the fields of neurology and oncology. AST-OPC1 (oligodendrocyte progenitor cells) is currently in a Phase 1/2a dose escalation clinical trial in spinal cord injury. AST-VAC1 (antigen-presenting autologous dendritic cells) is undergoing continuing development by Asterias based on promising efficacy and safety data from a Phase 2 study in Acute Myeloid Leukemia (AML), with current efforts focused on streamlining and modernizing the manufacturing process. AST-VAC2 (antigen-presenting allogeneic dendritic cells) represents a second generation, allogeneic cancer immunotherapy. The company's research partner, Cancer Research UK, plans to begin the first clinical trial of AST-VAC2 in non-small cell lung cancer in 2017. Additional information about Asterias can be found at http://www.asteriasbiotherapeutics.com.

About Cancer Research UK

Cancer Research UK is the worlds leading cancer charity dedicated to saving lives through research. Cancer Research UKs pioneering work into the prevention, diagnosis and treatment of cancer has helped save millions of lives. Cancer Research UK receives no government funding for its life-saving research. Every step it makes towards beating cancer relies on vital donations from the public. Cancer Research UK supports research into all aspects of cancer through the work of over 4,000 scientists, doctors and nurses.

FORWARD-LOOKING STATEMENTSStatements pertaining to future financial and/or operating and/or clinical research results, future growth in research, technology, clinical development, and potential opportunities for Asterias, along with other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements. Any statements that are not historical fact (including, but not limited to statements that contain words such as "will," "believes," "plans," "anticipates," "expects," "estimates") should also be considered to be forward-looking statements. Forward-looking statements involve risks and uncertainties, including, without limitation, risks inherent in the development and/or commercialization of potential products, uncertainty in the results of clinical trials or regulatory approvals, need and ability to obtain future capital, and maintenance of intellectual property rights. Actual results may differ materially from the results anticipated in these forward-looking statements and as such should be evaluated together with the many uncertainties that affect the businesses of Asterias, particularly those mentioned in the cautionary statements found in Asterias' filings with the Securities and Exchange Commission. Asterias disclaims any intent or obligation to update these forward-looking statements.

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Asterias Announces Major AST-VAC2 Development Milestone: First ... - GlobeNewswire (press release)

SOUTH SAN FRANCISCO, CA--(Marketwired - August 14, 2017) - VistaGen Therapeutics Inc. (NASDAQ: VTGN), a clinical-stage biopharmaceutical company focused on developing new generation medicines for depression and other central nervous system (CNS) disorders, today reported its financial results for its first fiscal quarter ended June 30, 2017.

The Company also provided an update on its corporate progress, clinical status and anticipated milestones for AV-101, its orally available CNS prodrug candidate in Phase 2 development, initially as a new generation treatment for major depressive disorder (MDD).

"We anticipate several catalytic milestones in our clinical development, intellectual property and regulatory programs for AV-101 within the next 6 to 18 months. We remain highly focused on satisfying standard regulatory requirements and completing preparations for our planned AV-101 Phase 2 adjunctive treatment study in MDD. Our primary goal is to launch the study in January 2018 and complete it during 2018 to advance our efforts to provide a new generation treatment alternative to millions battling depression every day," commented Shawn Singh, Chief Executive Officer of VistaGen.

Mr. Singh continued, "In conjunction with our focused efforts to advance our AV-101 Phase 2 development program, we have continued to expand our intellectual property portfolio. Earlier this year the European Patent Office issued a Notice of Intention to Grant our European Patent Application regarding AV-101 for treatment of depression and reduction of dyskinesias associated with levodopa therapy for Parkinson's disease, a patent that will be in effect until at least January 2034. In addition, the U.S. Patent and Trademark Office recently allowed another important U.S. patent relating to stem cell technology held by VistaStem Therapeutics, our subsidiary using stem cell technology for drug rescue and regenerative medicine. The breakthrough technology under the allowed U.S. patent involves the stem cells from which all blood cells and most bone marrow cells are derived, technology with the potential to reach patients with a broad range of life-threatening diseases, including cancer, with CAR-T cell applications and foundational technology we believe may ultimately provide approaches for producing bone marrow stem cells for bone marrow transfusions. We are confident in our path forward through strategic collaborations, such as our agreement with the U.S. National Institute of Mental Health covering its full financial sponsorship of the ongoing Phase 2 study of AV-101 for MDD that Dr. Carlos Zarate Jr. and his team are conducting at the NIH's clinic in Bethesda, as well as our sublicense arrangement with BlueRock Therapeutics, a company established by Bayer AG and Versant Ventures, focused on regenerative medicine for heart disease. As we have historically, we believe we have surrounded ourselves with partners, supportive stockholders and corporate development and finance experts who share our confidence in our future and will assist us in securing key collaborations and raising sufficient capital to achieve our objectives, most notably the launch and completion in 2018 of our Phase 2 adjunctive treatment study of AV-101 for MDD. We look forward to creating value for our stakeholders in fiscal 2018 and beyond."

Potential Near-Term Milestones:

During the second half of 2017, the Company is pursuing the following objectives:

Further, the Company anticipates that the U.S. National Institute of Mental Health (NIMH) will complete the NIH-sponsored Phase 2 study of AV-101 in depression, with topline results during the first half of 2018.

Recent Operational Highlights:

Advancement of AV-101 as a Potential, Non-Opioid Treatment Alternative for Chronic Pain

Bolstered Clinical Team with Industry Expert

Intellectual Property Accomplishments

Capital Market Highlights

Financial Results for the Fiscal Quarter Ended June 30, 2017:

At June 30, 2017, the Company had a cash and cash equivalents balance of $1.6 million, compared to $2.9 million as of March 31, 2017. Between late-March 2017 and late-June 2017, in self-placed private placement transactions, the Company sold units consisting of unregistered common stock and common stock warrants to accredited investors, yielding approximately $1 million in net cash proceeds.

Net loss for the fiscal quarters ended June 30, 2017 and 2016 was approximately $2.3 million and $2.0 million, respectively, including non-cash expenses of approximately $0.5 million in each period.

Research and development expense totaled $1.1 million for the fiscal quarter ended June 30, 2017, compared with $0.8 million for the fiscal quarter ended June 30, 2016. The increase in year-over-year research and development expense was attributable to the Company's increased focus on the continuing non-clinical and clinical development of AV-101 and ongoing preparations to launch its AV-101 Phase 2 Adjunctive Treatment Study.

General and administrative expense increased slightly to $1.2 million in the fiscal quarter ended June 30, 2017, from $1.1 million in the fiscal quarter ended June 30, 2016 primarily because of increased headcount and employee-related expenses and non-cash stock compensation expense attributable to recent stock option grants, partially offset by a reduction in professional services fees.

About VistaGen

VistaGen Therapeutics, Inc. (NASDAQ: VTGN), is a clinical-stage biopharmaceutical company focused on developing new generation medicines for depression and other CNS disorders. VistaGen's lead CNS product candidate, AV-101, is in Phase 2 development, initially as a new generation oral antidepressant prodrug candidate for MDD. AV-101's mechanism of action is fundamentally differentiated from all FDA-approved antidepressants and atypical antipsychotics used adjunctively to treat MDD, with potential to drive a paradigm shift towards a new generation of safer and faster-acting antidepressants. AV-101 is currently being evaluated by the U.S. NIMH in a Phase 2 monotherapy study in MDD being fully funded by the NIMH and conducted by Dr. Carlos Zarate Jr., Chief, Section on the Neurobiology and Treatment of Mood Disorders and Chief of Experimental Therapeutics and Pathophysiology Branch at the NIMH. VistaGen is preparing to launch a 180-patient Phase 2 study of AV-101 as an adjunctive treatment for MDD patients with inadequate response to standard, FDA-approved antidepressants. Dr. Maurizio Fava of Harvard Medical School will be the Principal Investigator of the Company's Phase 2 adjunctive treatment study. AV-101 may also have the potential to treat multiple CNS disorders and neurodegenerative diseases in addition to MDD, including neuropathic pain, epilepsy, Huntington's disease, L-Dopa-induced dyskinesia associated with Parkinson's disease and other disorders where modulation of the NMDA receptors, activation of AMPA pathways and/or key active metabolites of AV-101 may achieve therapeutic benefit.

About VistaStem

VistaStem Therapeutics is VistaGen's wholly-owned subsidiary focused on applying human pluripotent stem cell (hPSC) technology, internally and with third-party collaborators, to discover, rescue, develop and commercialize (i) proprietary new chemical entities (NCEs), including NCEs with regenerative potential, for CNS and other diseases and (ii) cellular therapies involving stem cell-derived blood, cartilage, heart and liver cells. VistaStem's internal drug rescue programs are designed to utilize CardioSafe 3D, its customized cardiac bioassay system, to develop NCEs for VistaGen's pipeline. To advance potential regenerative medicine (RM) applications of its cardiac stem cell technology, in December 2016, VistaStem exclusively sublicensed to BlueRock Therapeutics LP, a next generation regenerative medicine company established in 2016 by Bayer AG and Versant Ventures, rights to certain proprietary technologies relating to the production of cardiac cells for the treatment of heart disease. In a manner similar to its exclusive sublicense agreement with BlueRock Therapeutics, VistaStem may pursue additional collaborations and potential RM applications of its stem cell technology platform, including using blood, cartilage, and/or liver cells derived from hPSCs, for (i) cell-based therapy, (ii) cell repair therapy, and/or (iii) tissue engineering.

For more information, please visit http://www.vistagen.com and connect with VistaGen on Twitter, LinkedIn and Facebook.

Forward-Looking Statements

The statements in this press release that are not historical facts may constitute forward-looking statements that are based on current expectations and are subject to risks and uncertainties that could cause actual future results to differ materially from those expressed or implied by such statements. Those risks and uncertainties include, but are not limited to, risks related to the successful launch, continuation and results of the NIMH's Phase 2 (monotherapy) and/or the Company's planned Phase 2 (adjunctive therapy) clinical studies of AV-101 in MDD, and other CNS diseases and disorders, including neuropathic pain and levodopa (L-DOPA)-induced dyskinesia associated with Parkinson's disease, the potential for the Company's stem cell technology to produce NCEs, cellular therapies, regenerative medicine or bone marrow stem cells to treat any medical condition, including autoimmune disorders and cancer, protection of its intellectual property, and the availability of substantial additional capital to support its operations, including the AV-101 clinical development activities described above. These and other risks and uncertainties are identified and described in more detail in VistaGen's filings with the Securities and Exchange Commission (SEC). These filings are available on the SEC's website at http://www.sec.gov. VistaGen undertakes no obligation to publicly update or revise any forward-looking statements.

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VistaGen Therapeutics Reports First Fiscal Quarter 2018 Financial Results and Provides Business Update - Marketwired (press release)

Keeping a check on how many calories we consume helps to keep us looking trim from the outside. New research by collaborating scientists in the U.S. and Spain suggests that restricting calorie intake can also help to keep us more youthful on the inside by preventing age-related changes in how the natural rhythmical biological clocks within our cells work to control essential functions.

The two sets of studies in mice, by the team of Paolo Sassone-Corsi, Ph.D., at the University of California, Irvine (UCI), and by a research group headed by Salvador Aznar Benitah, Ph.D., at the Barcelona Institute of Science and Technology, have found that a low-calorie diet prevents age-related changes in the normal daily rhythmic oscillations in liver cell metabolism and adult stem cell functioning. They report their work in separate papers in the journal Cell that are entitled, Circadian Reprogramming in the Liver Identifies Metabolic Pathways of Aging and Aged Stem Cells Reprogram Their Daily Rhythmic Functions to Adapt to Stress.

Its already known that the process of aging and circadian rhythms are linked, while restricting calorie intake in fruit flies extends the insects lifespan. Work by the UCI and Barcelona Institute of Science and Technology researchers has now demonstrated that calorie restriction (CR) can influence the interplay between circadian rhythms and aging processes in cells.

The liver operates at the interface between nutrition and energy distribution in the body, and metabolism is controlled within cells under circadian control, explains the UCI team, led by Dr. Sassone-Corsi, director of the Center for Epigenetics & Metabolism. To investigate the effects of aging on circadian control of metabolism at the cellular level, the team first looked at the effects of aging on rhythmic function and circadian gene expression in the liver cells of both young mice (aged 6 months) and older mice (aged 18 months) that were an unrestricted diet. They found that although both young and old mice demonstrated a circadian-controlled metabolic system, the mechanisms that control gene expression according to the cells usage of energy was altered in the old mice. In effect, their liver cells processed energy less efficiently.

However, when these older mice were fed a diet with 30% fewer calories for six months, the biological clock was reset, and circadian functions were restored to those of younger mice. caloric restriction works by rejuvenating the biological clock in a most powerful way, Sassone-Corsi said in a statement. In this context, a good clock meant good aging.

For the companion study, the Barcelona Institute of Science and Technology team worked with professor Sassone-Corsis team and with colleagues at the Catalan Institution for Research and Advanced Studies, the Universitat Pompeu Fabra, and the Spanish National Center for Cardiovascular Research to compare circadian rhythm functionality in skin stem cells in both young and old mice. Again, stem cells in older mice did retain a circadian rhythm, but exhibited significant reprogramming away from the expression of genes involved in homeostasis to those involved with tissue-specific stresses, such as DNA damage. The stem cells were effectively rewired to match tissue-specific age-related traits.This age-related rewiring of circadian functionality was again prevented by long-term CR in older mice.

The low-calorie diet greatly contributes to preventing the effects of physiological aging," commented Benitah. "Keeping the rhythm of stem cells 'young' is important because in the end these cells serve to renew and preserve very pronounced daynight cycles in tissue. Eating less appears to prevent tissue aging and, therefore, prevent stem cells from reprogramming their circadian activities."

Future studies will be needed to identify which components are responsible for the aging-related rewiring of the daily fluctuating functions of stem cells and to find out whether they could be targeted therapeutically to maintain the proper timing of stem cell function during aging in humans, the Spanish team suggests in their published paper.

"These studies also present something like a molecular holy grail, revealing the cellular pathway through which aging is controlled," Sassone-Corsi added. "The findings provide a clear introduction on how to go about controlling these elements of aging in a pharmacological perspective."

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Calorie-Controlled Diet Restores Youthful Rhythmic Control of Metabolism in Old Mice - Genetic Engineering & Biotechnology News (blog)

Skin transplantation could be an effective way to deliver gene therapy to treat type 2 diabetes and obesity, new research in mice suggests.

The technique could enable a wide range of gene-based therapies to treat many human diseases.

We think this can provide a long-term safe option for the treatment of many diseases

We resolved some technical hurdles and designed a mouse-to-mouse skin transplantation model in animals with intact immune systems, says study author Xiaoyang Wu, assistant professor in the cancer research department at the University of Chicago.

We think this platform has the potential to lead to safe and durable gene therapy in mice and, we hope, in humans, using selected and modified cells from skin.

Beginning in the 1970s, physicians learned how to harvest skin stem cells from a patient with extensive burn wounds, grow them in the laboratory, then apply the lab-grown tissue to close and protect a patients wounds. This approach is now standard. However, the application of skin transplants is better developed in humans than in mice.

The mouse system is less mature, Wu says. It took us a few years to optimize our 3D skin organoid culture system.

This study is the first to show that an engineered skin graft can survive long term in wild-type mice with intact immune systems.

We have a better than 80 percent success rate with skin transplantation, Wu says. This is exciting for us.

The researchers focused on diabetes because it is a common non-skin disease that can be treated by the strategic delivery of specific proteins.

They inserted the gene for glucagon-like peptide 1 (GLP1), a hormone that stimulates the pancreas to secrete insulin. This extra insulin removes excessive glucose from the bloodstream, preventing the complications of diabetes. GLP1 can also delay gastric emptying and reduce appetite.

Using CRISPR, a tool for precise genetic engineering, they modified the GLP1 gene. They inserted one mutation, designed to extend the hormones half-life in the blood stream, and fused the modified gene to an antibody fragment so that it would circulate in the blood stream longer. They also attached an inducible promoter, which enabled them to turn on the gene to make more GLP1, as needed, by exposing it to the antibiotic doxycycline. Then they inserted the gene into skin cells and grew those cells in culture.

When these cultured cells were exposed to an air/liquid interface in the laboratory, they stratified, generating what the authors referred to as a multi-layered, skin-like organoid.

Next, they grafted this lab-grown gene-altered skin onto mice with intact immune systems. There was no significant rejection of the transplanted skin grafts.

When the mice ate food containing minute amounts of doxycycline, they released dose-dependent levels of GLP1 into the blood. This promptly increased blood-insulin levels and reduced blood-glucose levels.

When the researchers fed normal or gene-altered mice a high-fat diet, both groups rapidly gained weight. They became obese. When normal and gene-altered mice got the high-fat diet along with varying levels of doxycycline, to induce GLP1 release, the normal mice grew fat and mice expressing GLP1 showed less weight gain.

Expression of GLP1 also lowered glucose levels and reduced insulin resistance.

Together, our data strongly suggest that cutaneous gene therapy with inducible expression of GLP1 can be used for the treatment and prevention of diet-induced obesity and pathologies, the authors write.

When they transplanted gene-altered human cells to mice with a limited immune system, they saw the same effect. These results, the authors wrote, suggest that cutaneous gene therapy for GLP1 secretion could be practical and clinically relevant.

This approach, combining precise genome editing in vitro with effective application of engineered cells in vivo, could provide significant benefits for the treatment of many human diseases, the authors note.

We think this can provide a long-term safe option for the treatment of many diseases, Wu says. It could be used to deliver therapeutic proteins, replacing missing proteins for people with a genetic defect, such as hemophilia. Or it could function as a metabolic sink, removing various toxins.

Skin progenitor cells have several unique advantages that are a perfect fit for gene therapy. Human skin is the largest and most accessible organ in the body. It is easy to monitor. Transplanted skin can be quickly removed if necessary. Skins cells rapidly proliferate in culture and can be easily transplanted. The procedure is safe, minimally invasive, and inexpensive.

There is also a need. More than 100 million US adults have either diabetes (30.3 million) or prediabetes (84.1 million), according the Centers for Disease Control and Prevention. More than two out of three adults are overweight. More than one out of three are considered obese.

Additional authors of the study are from the University of Chicago and the University of Illinois at Chicago. The National Institutes of Health, the American Cancer Society, and the V Foundation funded the study.

Source: University of Chicago

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Skin transplants could treat diabetes and obesity - Futurity - Futurity: Research News

With a jolt from a tiny chip, humdrum skin cells may transform into medical mavericks.

A small electrical pulse blasts open tiny pores in cells and zaps in fragments of DNA or RNA loaded in the chips nanochannels. Those genetic deliveries then effectively reprogram the skin cells to act like other types of cells and repair damaged tissue. In early experiments on mice, researchers coaxed skin cells to act like brain cells. They also restored blood flow to a rodents injured limb by prompting skin cells to grow into new blood vessels.

The technology, published this week in Nature Nanotechnology, is still a long way from confirmed clinical applications in humans. But, the Ohio State researchers behind the chip are optimistic that it may one day perform myriad medical featsincluding healing severe injuries, restoring diseased organs, erasing brain damage, and even turning back the clock on aging tissues.

The researchers, led by regenerative medicine expert Chandan Sen and biomolecular engineer L. James Lee, expect to begin clinical trials next year.

The concept is very simple, Lee said in a press statement. As a matter of fact, we were even surprised how it worked so well. In my lab, we have ongoing research trying to understand the mechanism and do even better. So, this is the beginning, more to come.

Their concept is similar to other cell-based regenerative therapies under development, but it skips some pesky steps. Some other methods explored by researchersand dubious clinicsinvolve harvesting adult cells from patients, reprograming them to revert to stem cells, then injecting those cells back into patients, where they develop into a needed cell type.

But this setup has snags. Researchers often use viruses to deliver the genetic elements that reprogram the cells, which have caused cancer in some animal studies. The method also requires a lot of manipulation of cells in lab, adding complications. Its unclear if the suspect stem cell clinics are even successful at reprogramming cells.

The method used by Lee, Sen, and colleagues ditches the need for a virus and for any cellular handling. The electrical pulse opens pores in cells that allow for direct genetic deliverya process called electroporation. The researchers skipped the need to make stem cells by using preexisting methods of converting one cell type directly into a different one. Generally, this works by introducing bits of genetic material that code for gene regulators key to a specific cell type. Once delivered, these regulators can switch genes on or off so cells can start acting like the different cell type. Such a method has been worked out for creatingliver, brain, and vascular cellsfrom other cell types.

Finally, the researchers method also all takes place on a patch of skin on a living subject, potentially directly where its neededno cell harvesting or lab manipulations are required. (That said, the researchers note that future therapies could use skin patches to generate specific cell types that can then be transferred to other locations in the body if needed.)

So far, the researchers have dabbled with making brain cells and vasculature cells from skin cells. In early experiments, their direct delivery proved effective at converting the cells. The researcher verified that the converted cells mirrored normal brain and vasculature cells' gene expression profilesthe pattern of genes they have turned on and off.

In their ultimate test, the researchers severed leg arteries in ahandful of mice. Then a researcher placed over the injuries nanochips loaded with genetic ingredients for converting skin cells to vasculature cells. The conversion reached cells deep within the skin layers. After a week, the researchers saw more blood flow and less tissue death in the treated mice compared withcontrol animals that werent treated.

Much work still needs to be done to test the idea and prove it's effective for certain treatments. But the researchers are optimistic. They conclude in the study that the technology has the potential to ultimately enable the use of a patients own tissue as a prolific immunosurveilled bioreactor.

Nature Nanotechnology, 2017. DOI: 10.1038/nnano.2017.134 (About DOIs).

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Heal thyself: Skin-zapping chip aims to reprogram cells for tissue repair - Ars Technica

A med-tech startup has developed a fast and easy way to treat certain burn wounds with stem cells. This technology is developed by German researcher Dr. Jrg Gerlach. He is the worlds first ever person who use a patients stem cells to directly heal the skin. The technique is meant to reduce the healing time and minimize complications, with aesthetically and functionally satisfying outcomes. There are no scars, no residual pain and its like there wasnt any burn to start with. Its not less than a miracle.

The medical technology startup has now transformed the proof-of-concept device from a complicated prototype into a user-friendly product called a SkinGun, which it hopes doctors will be able to use outside of an experimental setting. RenovaCare CEO Thomas Bold believes, the SkinGun can compete with, or even replace, todays standard of care. The sprayer allows us to have a generous distribution of cells on the wound, explained Roger Esteban-Vives, director of cell sciences at RenovaCare.

RenovaCares SkinGun sprays a liquid suspension of a patients stem cells onto a burn or wound in order to re-grow the skin without scars. Stem-cell methods helped cut this risk by quickening healing and providing a source of new skin from a very small area. Cell Mist method gets a greater yield from its harvest than mesh grafting, a more common way to treat burns. At a maximum, grafting can treat six times the size of its harvest area. Cell Mist can cover 100 times its harvest area.

When dispensing cells over a wound, its important that they make the transition without any damage. Damaged cells reduce the effectiveness of the treatment.

High cell viability also contributes to faster healing. When a wound heals naturally, cells migrate to it to build up the skin. That process can take weeks.

Stem cells have tremendous promise to help us understand and treat a range of diseases, injuries and other health-related conditions.

There is still a lot to learn about stem cells, however, and their current applications as treatments are sometimes exaggerated by the media and other parties who do not fully understand the science and current limitations

Beyond regulatory matters, there are also limitations to the technology that make it unsuitable for competing with treatments of third-degree burns, which involve damage to muscle and other tissue below the skin.

When burn victims need a skin graft they typically have to grow skin on other parts of their bodies. This is a process that can take weeks. A new technique uses stem cells derived from the umbilical cord to generate new skin much more quickly.The umbilical cord consists of a gelatinous tissue that contains uncommitted mesenchymal stemcells (MSC)

Research is underway to develop various sources for stem cells, and to apply stem-cell treatments for neurodegenertive diseasesand conditions such as diabetes, heart disease, and other conditions.

Tens of thousands of grafts are performed each year for burn victims, cosmetic surgery patients, and for people with large wounds having difficulty healing. Traditionally, this involves taking a large patch of skin (typically from the thigh) and removing the dermis and epidermis to transplant elsewhere on the body. Burns victims are making incredible recoveries thanks to a revolutionary gun that sprays stem cells on to their wounds, enabling them to rapidly grow new skin. Patients who have benefited say their new skin is virtually indistinguishable from that on the rest of the body.

Thomas Bold, chief executive of RenovaCare, the company behind SkinGun, said: The procedure is gentler and the skin that regrows looks, feels and functions like the original skin.

If you are planning to have stem cell treatments dont forget to remember these points

Stem cell researchers are making great advances in understanding normal development. They are trying to figure out what goes wrong in disease and developing and testing potential treatments to help patients. They still have much to learn. However, about how stem cells work in the body and their capacity for healing. Safe and effective treatments for most diseases, conditions and injuries are in the future.

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Dramatic Burn-Healing Through Stem Cell Treatment - Fox Weekly

The chip has not been tested in humans, but it has been used to heal wounds in mice. Wexner Medical Center/The Ohio State University hide caption

The chip has not been tested in humans, but it has been used to heal wounds in mice.

Scientists have created an electronic wafer that reprogrammed damaged skin cells on a mouse's leg to grow new blood vessels and help a wound heal.

One day, creator Chandan Sen hopes, it could be used to be used to treat wounds on humans. But that day is a long way off as are many other regeneration technologies in the works. Like Sen, some scientists have begun trying to directly reprogram one cell type into another for healing, while others are attempting to build organs or tissues from stem cells and organ-shaped scaffolding.

But other scientists have greeted Sen's mouse experiment, published in Nature Nanotechnology on Monday, with extreme skepticism. "My impression is that there's a lot of hyperbole here," says Sean Morrison, a stem cell researcher at the University of Texas Southwestern Medical Center. "The idea you can [reprogram] a limited number of cells in the skin and improve blood flow to an entire limb I think it's a pretty fantastic claim. I find it hard to believe."

When the device is placed on live skin and activated, it sends a small electrical pulse onto the skin cells' membrane, which opens a tiny window on the cell surface. "It's about 2 percent of the cell membrane," says Sen, who is a researcher in regenerative medicine at Ohio State University. Then, using a microscopic chute, the chip shoots new genetic code through that window and into the cell where it can begin reprogramming the cell for a new fate.

Sen says the whole process takes less than 0.1 seconds and can reprogram the cells resting underneath the device, which is about the size of a big toenail. The best part is that it's able to successfully deliver its genetic payload almost 100 percent of the time, he says. "No other gene delivery technique can deliver over 98 percent efficiency. That is our triumph."

Chandan Sen, a researcher at Ohio State University, holds a chip his lab created that has reprogrammed cells in mice. Wexner Medical Center/The Ohio State University hide caption

Chandan Sen, a researcher at Ohio State University, holds a chip his lab created that has reprogrammed cells in mice.

To test the device's healing capabilities, Sen and his colleagues took a few mice with damaged leg arteries and placed the chip on the skin near the damaged artery. That reprogrammed a centimeter or two of skin to turn into blood vessel cells. Sen says the cells that received the reprogramming genes actually started replicating the reprogramming code that the researchers originally inserted in the chip, repackaging it and sending it out to other nearby cells. And that initiated the growth of a new network of blood vessels in the leg that replaced the function of the original, damaged artery, the researchers say. "Not only did we make new cells, but those cells reorganized to make functional blood vessels that plumb with the existing vasculature and carry blood," Sen says. That was enough for the leg to fully recover. Injured mice that didn't get the chip never healed.

When the researchers used the chip on healthy legs, no new blood vessels formed. Sen says because injured mouse legs were was able to incorporate the chip's reprogramming code into the ongoing attempt to heal.

That idea hasn't quite been accepted by other researchers, however. "It's just a hand waving argument," Morrison says. "It could be true, but there's no evidence that reprogramming works differently in an injured tissue versus a non-injured tissue."

What's more, the role of exosomes, the vesicles that supposedly transmit the reprogramming command to other cells, has been contentious in medical science. "There are all manners of claims of these vesicles. It's not clear what these things are, and if it's a real biological process or if it's debris," Morrison says. "In my lab, we would want to do a lot more characterization of these exosomes before we make any claims like this."

Sen says that the theory that introduced reprogramming code from the chip or any other gene delivery method does need more work, but he isn't deterred by the criticism. "This clearly is a new conceptual development, and skepticism is understandable," he says. But he is steadfast in his confidence about the role of reprogrammed exosomes. When the researchers extracted the vesicles and injected them into skin cells in the lab, Sen says those cells converted into blood vessel cells in the petri dish. "I believe this is definitive evidence supporting that [these exosomes] may induce cell conversion."

Even if the device works as well as Sen and his colleagues hope it does, they only tested it on mice. Repairing deeper injuries, like vital organ damage, would also require inserting the chip into the body to reach the wound site. It has a long way to go before it can ever be considered for use on humans. Right now, scientists can only directly reprogram adult cells into a limited selection of other cell types like muscle, neurons and blood vessel cells. It'll be many years before scientists understand how to reprogram one cell type to become part of any of our other, many tissues.

Still, Morrison says the chip is an interesting bit of technology. "It's a cool idea, being able to release [genetic code] through nano channels," he says. "There may be applications where that's advantageous in some way in the future."

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A Chip That Reprograms Cells Helps Healing, At Least In Mice - NPR

Marrow Drives

The Office of Management and Budget has withdrawn a proposed rule banning compensation for hematopoietic stem cells. In other words, you can get paid when someone harvests stem cells from your bone marrow.

Bone marrow transplantation is used to treat a variety of ailments, including aplastic anemia, sickle cell anemia, bone marrow damage during chemotherapy, and blood cancers such as leukemia, lymphoma, and multiple myeloma. In 1984, Congress passed the National Organ and Transplant Act, which outlawed compensation to the donors of solid organs like kidneys and livers. Oddly, the act also defined renewable bone marrow as a solid organ.

Originally, hematopoietic stem cells were obtained from bone marrow obtained by inserting a needle into donors' hip bones. Researchers later developed a technique in which donors are treated with substance that overstimulates the production of hematopoietic stem cells, which then circulate in their bloodstreams. In a process similar to blood donation, the hematopoietic stem cells are then filtered from the donors' blood. The red blood cells and plasma are returned to the donors.

More Marrow Donors, a California-based nonprofit, wanted to set up a system to encourage hematopoietic stem cell donations with $3,000 awards, in the form of scholarships, housing allowances, or gifts to charity. The Institute for Justice, a libertarian law firm, brought suit on their behalf, and in 2012 a federal appeals court sensibly ruled that the law's ban on compensation for solid organ donations did not apply to stem cells obtained from donors' bloodstreams. The Obama administration reacted by proposing a regulation defining stem cells obtained from blood as the equivalent of a solid organ.

Now the new administration has withdrawn the proposal.

"Banning compensation for donors would have eliminated the best incentive we havemoneyfor persuading strangers to work for each other," Jeff Rowes, a senior attorney with the Institute for Justice, says in a press release. "Predictably, the ban on compensation for blood stem cell donors created chronic shortages and waiting lists. During the past four years, thousands of Americans needlessly died because compensation for bone marrow donors was unavailable."

The system of uncompensated donation is falling far short of meeting patient needs. As the Institute for Justice notes:

At any given time, more than 11,000 Americans are actively searching for a bone marrow donor. According to the New England Journal of Medicine, Caucasian potential donors are available and willing to donate about 51 percent of the time; Hispanic and Asian about 29 percent; and African-American about 23 percent. Caucasian patients can find a matching, available and willing donor about 75 percent of the time; Hispanic about 37 percent; Asian-American about 35 percent; and African-American patients only about 19 percent of the time. This demonstrates the huge gap between the need for compatible donors and the supply.

This is even more true in the case of solid organs from live and brain-dead donors. Right now there are more than 116,000 Americans waiting for a life-saving transplant organ. My colleagues and I at Reason have been arguing for decades in favor of compensating live donors for kidneys and pieces of their livers and the next-of-kin of brain-dead donors for other solid organs. If researchers and entrepreneurs succeed in boosting bone marrow donations by implementing various compensation schemes, perhaps that will prompt Congress to repeal its ill-conceived ban on compensation for organs donated for transplant.

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Trump Administration Withdraws Proposed Obama Ban on Compensation for Bone Marrow - Reason (blog)