Scientists identify brain molecule that triggers schizophrenia-like behaviors, brain changes


Scientists at The Scripps Research Institute (TSRI) have identified a molecule in the brain that triggers schizophrenia-like behaviors, brain changes and global gene expression in an animal model. The research gives scientists new tools for someday preventing or treating psychiatric disorders such as schizophrenia, bipolar disorder and autism.

“This new model speaks to how schizophrenia could arise before birth and identifies possible novel drug targets,” said Jerold Chun, a professor and member of the Dorris Neuroscience Center at TSRI who was senior author of the new study.

The findings were published April 7, 2014, in the journal Translational Psychiatry.

What Causes Schizophrenia?

According to the World Health Organization, more than 21 million people worldwide suffer from schizophrenia, a severe psychiatric disorder that can cause delusions and hallucinations and lead to increased risk of suicide.

Although psychiatric disorders have a genetic component, it is known that environmental factors also contribute to disease risk. There is an especially strong link between psychiatric disorders and complications during gestation or birth, such as prenatal bleeding, low oxygen or malnutrition of the mother during pregnancy.

In the new study, the researchers studied one particular known risk factor: bleeding in the brain, called fetal cerebral hemorrhage, which can occur in utero and in premature babies and can be detected via ultrasound.

In particular, the researchers wanted to examine the role of a lipid called lysophosphatidic acid (LPA), which is produced during hemorrhaging. Previous studies had linked increased LPA signaling to alterations in architecture of the fetal brain and the initiation of hydrocephalus (an accumulation of brain fluid that distorts the brain). Both types of events can also increase the risk of psychiatric disorders.

“LPA may be the common factor,” said Beth Thomas, an associate professor at TSRI and co-author of the new study.

Mouse Models Show Symptoms

To test this theory, the research team designed an experiment to see if increased LPA signaling led to schizophrenia-like symptoms in animal models.

Hope Mirendil, an alumna of the TSRI graduate program and first author of the new study, spearheaded the effort to develop the first-ever animal model of fetal cerebral hemorrhage. In a clever experimental paradigm, fetal mice received an injection of a non-reactive saline solution, blood serum (which naturally contains LPA in addition to other molecules) or pure LPA.

The real litmus test to show if these symptoms were specific to psychiatric disorders, according to Mirendil, was “prepulse inhibition test,” which measures the “startle” response to loud noises. Most mice—and humans—startle when they hear a loud noise. However, if a softer noise (known as a prepulse) is played before the loud tone, mice and humans are “primed” and startle less at the second, louder noise. Yet mice and humans with symptoms of schizophrenia startle just as much at loud noises even with a prepulse, perhaps because they lack the ability to filter sensory information.

Indeed, the female mice injected with serum or LPA alone startled regardless of whether a prepulse was placed before the loud tone.

Next, the researchers analyzed brain changes, revealing schizophrenia-like changes in neurotransmitter-expressing cells. Global gene expression studies found that the LPA-treated mice shared many similar molecular markers as those found in humans with schizophrenia. To further test the role of LPA, the researchers used a molecule to block only LPA signaling in the brain.

This treatment prevented schizophrenia-like symptoms.

Implications for Human Health

This research provides new insights, but also new questions, into the developmental origins of psychiatric disorders.

For example, the researchers only saw symptoms in female mice. Could schizophrenia be triggered by different factors in men and women as well?

“Hopefully this animal model can be further explored to tease out potential differences in the pathological triggers that lead to disease symptoms in males versus females,” said Thomas.

In addition to Chun, Thomas and Mirendil, authors of the study, “LPA signaling initiates schizophrenia-like brain and behavioral changes in a mouse model of prenatal brain hemorrhage,” were Candy De Loera of TSRI; and Kinya Okada and Yuji Inomata of the Mitsubishi Tanabe Pharma Corporation.

Scientists manipulate molecules inside living cells with temperature gradients


The ability to make measurements of the biomolecular interactions that occur inside living cells is essential for understanding complex biological processes. But probing the inside of living cells without damaging them is a challenge. The cell membrane shields electrical fields, prohibiting the use of electrophoresis, a technique that is commonly used to analyze biological samples in a variety of areas outside living cells.
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Now in a new paper, researchers have demonstrated for the first time that thermophoresis—the movement of molecules due to a rather than an electric field—can be used to measure the movement of DNA and other molecules inside living cells. The paper, by Maren R. Reichl and Dieter Braun at the Ludwig Maximilian University of Munich, is published in a recent issue of The Journal of the American Chemical Society.

“Our work shows that the measurement of thermophoresis in living cells is possible—moreover, in parallel across the cell and not at one single point,” Braun told Phys.org.

In the new technique, a temperature gradient is applied across a cell by an infrared laser. Fluorescently marked molecules inside the cell move along this temperature gradient from hotter to colder regions. A camera can record this thermophoretic movement, with every camera pixel measuring thermophoresis simultaneously and independently. The technique can be performed in the natural environment of cells in vivo.

The researchers demonstrated the use of thermophoresis measurements of DNA in the cytoplasm of living cells. Interestingly, the results revealed that DNA movement in the cytoplasm is slowed down, probably due to molecular crowding. In addition to measuring the movement of DNA, the thermophoresis technique could also measure the movement of proteins, pharmaceutical components, and other molecules in cells as long as they can move through the cytoplasm. Ribosomes, for example, are so large and bound to the endoplasmic reticulum that they cannot easily diffuse through the cytoplasm, making them poor candidates for thermophoresis.

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Thermophoresis measurements of DNA and the dye molecule BCECF in the cytoplasm of living cells. Credit: Reichl and Braun. ©2014 American Chemical Society

One way that thermophoresis inside living cells can be used is to measure the binding affinities of molecules. As the scientists explain, the binding of a fluorescently marked molecule such as DNA or a protein leads to a change in the thermophoretic depletion strength. Binding affinities can reveal more detailed information about the interactions of these molecules.

“The dream would be to record binding affinities in living , i.e., translating the award-winning microscale thermophoresis (MST) technique of our startup company Nanotemper into ,” Braun said. “However, the measurement protocol is not yet robust against the shape of the cell, so some more tricks to make it work will be necessary. But we are optimistic—experimental tricks are our specialty.”

Gene Used In Embryogenesis Can Repair Adult Tissue.


There are some amazing genes and cellular processes active during embryonic development that are never seen again later in life. Though some insects and amphibians are able to carry those traits into adulthood, mammals have a dramatic decrease in the ability to regenerate tissue after birth. A new study has shown that one embryonic protein can be used to help regenerate adult tissue in a living organism, not just in a dish.

The protein Lin28a typically only contributes to processes during embryogenesis, affecting things like metabolism and the pluripotency of stem cells. A study published Nov. 7 in Cell has shown that these proteins can actually be used in adult tissue and help in the regeneration of cartilage, hair follicles, bone, and mesenchyme, a type of undifferentiated connective tissue. It works by binding microRNA in the cell’s nucleus to inhibit let7. Let7 encourages cells to mature and lose the regenerative abilities.

Mice that had been genetically altered to produce Lin28a throughout life had outstanding regenerative power. Though regular mice typically stop producing new hair at around 10 weeks, those with a continued presence of Lin28a kept growing fur throughout their lives. Lin28a also boosted regeneration of limbs. During development, Lin28a is commonly found in the limb buds, but is hardly expressed in those regions after birth. For the mice over expressing Lin28a, some digits that were amputated early in life grew back nearly completely. This ability was diminished as the mouse approached adulthood. Because cardiac tissue also wasn’t regenerated by the presence of Lin28a, there could be other unknown proteins that regulate body aging.

Lin28a was also shown to promote prompt healing of damaged ears, increase metabolism, and contribute to cell proliferation and migration, which are necessary for tissue repair. Unfortunately, some of these attributes can also lead to tumorigenesis, which has been the focus of a great deal of recent cancer research.

This discovery is a long way off from having clinical significance as a miracle “fountain of youth” treatment. Because Lin28a binds to RNA, not the surface of the cell, current drug delivery systems would be very ineffective. Also, because the protein affects so many different tissues in the body, it would be incredibly difficult to target only the desired area. In the future, however, this could be used as a treatment for diseases like alopecia and for tissues that have been injured or are degenerating.

Fountain of youth? Scientists discover why wounds heal quicker for young people


Fountain of youth? Scientists discover why wounds heal quicker for young people .

The mystery of why wounds heal more quickly in the young compared to the elderly may soon be solved following the discovery of two of the genes involved in tissue regeneration.

Scientists believe that the findings will help to develop new drugs and treatments for faster wound-healing as well as shedding light on the ageing process itself, and what could amount to a genetic “fountain of youth”.

Two teams of researchers found separate genes that accelerate tissue regeneration in laboratory mice. Both genes, which are also present in the human genome, are more active in young mice compared to older mice.

The scientists believe that the genes, called Lin28a and IMP1, are designed to be especially active during the foetal stages of development and are gradually turned off as an animal ages – which could explain why wounds take longer to heal in the elderly and how ageing occurs.

One of the teams, led by George Daley of the Boston Children’s Hospital and Harvard Medical School, activated the Lin28a gene in adult mice and found that shaved fur on their backs grew back much faster than in ordinary adult mice where the gene had not be artificially boosted.

“It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals,” said Dr Daley, whose study is published in the journal Cell.

Asked what the implications are for human health, Dr Daley said: “My strongest conclusion is that Lin28a, or drug manipulations that mimic the metabolic effects of Lin28a, enhances wound healing and tissue repair, and thus in the future might translate into improved healing of wounds after surgery or trauma in patients.”

The study revealed that the Lin28a gene is responsible for a protein that binds to the key molecules of RNA involved in the metabolism of energy within the mitochondria, the “power packs” of the cells. The result is that when the gene is active, the cells are better and more efficient at repairing themselves – the activated genes also accelerated the repair of injuries.

Tissue regeneration is important in early foetal development and when damaged tissues need to be healed. A gradual loss of tissue regeneration and repair is one of the hallmarks of ageing so anything that could improve it could lead to anti-ageing treatments

“We were surprised that what was previously believed to be a mundane cellular ‘housekeeping’ function would be so important for tissue repair,” said Shyh-Chang Ng of Harvard Medical School, the lead author of the Cell study.

“One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans.”

The second gene, IMP1, also produces a protein that binds to the RNA molecules, but this time it promotes the self-renewal of key stem cells during foetal development, and also during tissue repair in later life, said Hao Zhu of the University of Texas in Dallas.

“This finding opens up an exciting possibility that metabolism could be modulated to improve tissue repair, whereby metabolic drugs could be employed to promote regeneration,” Dr Zhu said.

Scientists believe that the findings will help to develop new drugs and treatments for faster wound-healing as well as shedding light on the ageing process itself, and what could amount to a genetic “fountain of youth”.

Two teams of researchers found separate genes that accelerate tissue regeneration in laboratory mice. Both genes, which are also present in the human genome, are more active in young mice compared to older mice.

The scientists believe that the genes, called Lin28a and IMP1, are designed to be especially active during the foetal stages of development and are gradually turned off as an animal ages – which could explain why wounds take longer to heal in the elderly and how ageing occurs.

One of the teams, led by George Daley of the Boston Children’s Hospital and Harvard Medical School, activated the Lin28a gene in adult mice and found that shaved fur on their backs grew back much faster than in ordinary adult mice where the gene had not be artificially boosted.

“It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals,” said Dr Daley, whose study is published in the journal Cell.

Asked what the implications are for human health, Dr Daley said: “My strongest conclusion is that Lin28a, or drug manipulations that mimic the metabolic effects of Lin28a, enhances wound healing and tissue repair, and thus in the future might translate into improved healing of wounds after surgery or trauma in patients.”

The study revealed that the Lin28a gene is responsible for a protein that binds to the key molecules of RNA involved in the metabolism of energy within the mitochondria, the “power packs” of the cells. The result is that when the gene is active, the cells are better and more efficient at repairing themselves – the activated genes also accelerated the repair of injuries.

Tissue regeneration is important in early foetal development and when damaged tissues need to be healed. A gradual loss of tissue regeneration and repair is one of the hallmarks of ageing so anything that could improve it could lead to anti-ageing treatments

“We were surprised that what was previously believed to be a mundane cellular ‘housekeeping’ function would be so important for tissue repair,” said Shyh-Chang Ng of Harvard Medical School, the lead author of the Cell study.

“One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans.”

The second gene, IMP1, also produces a protein that binds to the RNA molecules, but this time it promotes the self-renewal of key stem cells during foetal development, and also during tissue repair in later life, said Hao Zhu of the University of Texas in Dallas.

“This finding opens up an exciting possibility that metabolism could be modulated to improve tissue repair, whereby metabolic drugs could be employed to promote regeneration,” Dr Zhu said.

Scientists believe that the findings will help to develop new drugs and treatments for faster wound-healing as well as shedding light on the ageing process itself, and what could amount to a genetic “fountain of youth”.

Two teams of researchers found separate genes that accelerate tissue regeneration in laboratory mice. Both genes, which are also present in the human genome, are more active in young mice compared to older mice.

The scientists believe that the genes, called Lin28a and IMP1, are designed to be especially active during the foetal stages of development and are gradually turned off as an animal ages – which could explain why wounds take longer to heal in the elderly and how ageing occurs.

One of the teams, led by George Daley of the Boston Children’s Hospital and Harvard Medical School, activated the Lin28a gene in adult mice and found that shaved fur on their backs grew back much faster than in ordinary adult mice where the gene had not be artificially boosted.

“It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals,” said Dr Daley, whose study is published in the journal Cell.

Asked what the implications are for human health, Dr Daley said: “My strongest conclusion is that Lin28a, or drug manipulations that mimic the metabolic effects of Lin28a, enhances wound healing and tissue repair, and thus in the future might translate into improved healing of wounds after surgery or trauma in patients.”

The study revealed that the Lin28a gene is responsible for a protein that binds to the key molecules of RNA involved in the metabolism of energy within the mitochondria, the “power packs” of the cells. The result is that when the gene is active, the cells are better and more efficient at repairing themselves – the activated genes also accelerated the repair of injuries.

Tissue regeneration is important in early foetal development and when damaged tissues need to be healed. A gradual loss of tissue regeneration and repair is one of the hallmarks of ageing so anything that could improve it could lead to anti-ageing treatments

“We were surprised that what was previously believed to be a mundane cellular ‘housekeeping’ function would be so important for tissue repair,” said Shyh-Chang Ng of Harvard Medical School, the lead author of the Cell study.

“One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans.”

The second gene, IMP1, also produces a protein that binds to the RNA molecules, but this time it promotes the self-renewal of key stem cells during foetal development, and also during tissue repair in later life, said Hao Zhu of the University of Texas in Dallas.

“This finding opens up an exciting possibility that metabolism could be modulated to improve tissue repair, whereby metabolic drugs could be employed to promote regeneration,” Dr Zhu said.

The 2013 Nobel Prize in Physiology or Medicine.


The 2013 Nobel Prize honours three scientists who have solved the mystery of how the cell organizes its transport system. Each cell is a factory that produces and exports molecules. For instance, insulin is manufactured and released into the blood and chemical signals called neurotransmitters are sent from one nerve cell to another. These molecules are transported around the cell in small packages called vesicles. The three Nobel Laureates have discovered the molecular principles that govern how this cargo is delivered to the right place at the right time in the cell.

Randy Schekman discovered a set of genes that were required for vesicle traffic. James Rothman  unravelled protein machinery that allows vesicles to fuse with their targets to permit transfer of cargo. Thomas Südhof revealed how signals instruct vesicles to release their cargo with precision.

Through their discoveries, Rothman, Schekman and Südhof have revealed the exquisitely precise control system for the transport and delivery of cellular cargo. Disturbances in this system have deleterious effects and contribute to conditions such as neurological diseases, diabetes, and immunological disorders.

How cargo is transported in the cell

In a large and busy port, systems are required to ensure that the correct cargo is shipped to the correct destination at the right time. The cell, with its different compartments called organelles, faces a similar problem: cells produce molecules such as hormones, neurotransmitters, cytokines and enzymes that have to be delivered to other places inside the cell, or exported out of the cell, at exactly the right moment. Timing and location are everything. Miniature bubble-like vesicles, surrounded by membranes, shuttle the cargo between organelles or fuse with the outer membrane of the cell and release their cargo to the outside. This is of major importance, as it triggers nerve activation in the case of transmitter substances, or controls metabolism in the case of hormones. How do these vesicles know where and when to deliver their cargo?

Traffic congestion reveals genetic controllers

Randy Schekman was fascinated by how the cell organizes its transport system and in the 1970s decided to study its genetic basis by using yeast as a model system. In a genetic screen, he identified yeast cells with defective transport machinery, giving rise to a situation resembling a poorly planned public transport system. Vesicles piled up in certain parts of the cell. He found that the cause of this congestion was genetic and went on to identify the mutated genes. Schekman identified three classes of genes that control different facets of the cell´s transport system, thereby providing new insights into the tightly regulated machinery that mediates vesicle transport in the cell.

Docking with precision

James Rothman was also intrigued by the nature of the cell´s transport system. When studying vesicle transport in mammalian cells in the 1980s and 1990s, Rothman discovered that a protein complex enables vesicles to dock and fuse with their target membranes. In the fusion process, proteins on the vesicles and target membranes bind to each other like the two sides of a zipper. The fact that there are many such proteins and that they bind only in specific combinations ensures that cargo is delivered to a precise location. The same principle operates inside the cell and when a vesicle binds to the cell´s outer membrane to release its contents.

It turned out that some of the genes Schekman had discovered in yeast coded for proteins corresponding to those Rothman identified in mammals, revealing an ancient evolutionary origin of the transport system. Collectively, they mapped critical components of the cell´s transport machinery.

Timing is everything

Thomas Südhof was interested in how nerve cells communicate with one another in the brain. The signalling molecules, neurotransmitters, are released from vesicles that fuse with the outer membrane of nerve cells by using the machinery discovered by Rothman and Schekman. But these vesicles are only allowed to release their contents when the nerve cell signals to its neighbours. How is this release controlled in such a precise manner? Calcium ions were known to be involved in this process and in the 1990s, Südhof searched for calcium sensitive proteins in nerve cells. He identified molecular machinery that responds to an influx of calcium ions and directs neighbour proteins rapidly to bind vesicles to the outer membrane of the nerve cell. The zipper opens up and signal substances are released. Südhof´s discovery explained how temporal precision is achieved and how vesicles´ contents can be released on command.

Vesicle transport gives insight into disease processes

The three Nobel Laureates have discovered a fundamental process in cell physiology. These discoveries have had a major impact on our understanding of how cargo is delivered with timing and precision within and outside the cell.  Vesicle transport and fusion operate, with the same general principles, in organisms as different as yeast and man. The system is critical for a variety of physiological processes in which vesicle fusion must be controlled, ranging from signalling in the brain to release of hormones and immune cytokines. Defective vesicle transport occurs in a variety of diseases including a number of neurological and immunological disorders, as well as in diabetes. Without this wonderfully precise organization, the cell would lapse into chaos.

James E. Rothman was born 1950 in Haverhill, Massachusetts, USA. He received his PhD from Harvard Medical School in 1976, was a postdoctoral fellow at Massachusetts Institute of Technology, and moved in 1978 to Stanford University in California, where he started his research on the vesicles of the cell. Rothman has also worked at Princeton University, Memorial Sloan-Kettering Cancer Institute and Columbia University. In 2008, he joined the faculty of Yale University in New Haven, Connecticut, USA, where he is currently Professor and Chairman in the Department of Cell Biology.

Randy W. Schekman was born 1948 in St Paul, Minnesota, USA, studied at the University of California in Los Angeles and at Stanford University, where he obtained his PhD in 1974 under the supervision of Arthur Kornberg (Nobel Prize 1959) and in the same department that Rothman joined a few years later. In 1976, Schekman joined the faculty of the University of California at Berkeley, where he is currently Professor in the Department of Molecular and Cell biology. Schekman is also an investigator of Howard Hughes Medical Institute.

Thomas C. Südhof was born in 1955 in Göttingen, Germany. He studied at the Georg-August-Universität in Göttingen, where he received an MD in 1982 and a Doctorate in neurochemistry the same year. In 1983, he moved to the University of Texas Southwestern Medical Center in Dallas, Texas, USA, as a postdoctoral fellow with Michael Brown and Joseph Goldstein (who shared the 1985 Nobel Prize in Physiology or Medicine). Südhof became an investigator of Howard Hughes Medical Institute in 1991 and was appointed Professor of Molecular and Cellular Physiology at Stanford University in 2008.

Silicon chips detect intracellular pressure changes in living cells.


The ability to measure pressure changes inside different components of a living cell is important, because it offers an alternative way to study fundamental processes that involve cell deformation1. Most current techniques such as pipette aspiration2, optical interferometry3 or external pressure probes4 use either indirect measurement methods or approaches that can damage the cell membrane.chip

Here we show that a silicon chip small enough to be internalized into a living cell can be used to detect pressure changes inside the cell. The chip, which consists of two membranes separated by a vacuum gap to form a Fabry–Pérot resonator, detects pressure changes that can be quantified from the intensity of the reflected light. Using this chip, we show that extracellular hydrostatic pressure is transmitted into HeLa cells and that these cells can endure hypo-osmotic stress without significantly increasing their intracellular hydrostatic pressure.

Scientists create replacement organs using body’s own cells.


One of the problems of organ transplants is the potential for the body to reject the foreign organ. For this reason, organ donor recipients have to take drugs that suppress the immune system.

Scientists are having preliminary success with a new way to get patients new organs that they may need: bioartificial organs made of plastic and the patient’s own cells.

So far, only a few such organs have been created and transplanted, and the they aren’t complex organs — just simples one like bladders and a windpipe. But, the New York Times reports, scientists are working on creating more complex organs such as kidneys and livers with these techniques.

A windpipe made to order

The Times article features the case of Andemariam Beyene, whose doctors discovered a golf ball-sized tumor growing in his windpipe two-and-a-half years ago. When he was nearly out of options for treatment, he went to see Dr. Paolo Macchiarini, at the Karolinska Institute in Stockholm, who suggested making Mr. Beyene a windpipe out of plastic and his own cells.

In order to make it, Dr. Macchiarini began by using a porous, fibrous plastic to make a copy of Mr. Beyene’s windpipe. He then seeded it with stem cells from Mr. Beyene’s bone marrow and placed the windpipe in an incubator that spun the windpipe “rotisserie-style,” says the Times, in a nutrient solution.

Then, he substituted that in for Mr. Beyene’s cancerous windpipe.

Fifteen months after surgery, Mr. Beyene is cancer-free.

The blueprint

Scientists are looking to nature to guidance on how to create these bioartificial organs.

In Dr. Macchiarini’s lab, a researcher named Philipp Jungebluth took a heart and lungs from a rat and put them in a glass jar. A detergent-like liquid connected via tube dripped into the jar and out, slowly stripping the organs of their living cells. After all the cells were gone (in three days), what was left of the organs was the scaffold, the basic shape of the organ, composed of a matrix of proteins and other compounds that keep the right cells in the right places.

Human scaffolds could be better for building new organs than synthetic scaffolds that just try to imitate nature. For example, donor lungs could be stripped of cells and re-seeded with a patient’s own cells before implantation.

Dr. Macchiarini has used scaffolds to successfully replace windpipes from cadavers in about a dozen patients who don’t have the major problem facing other organ donor recipients: the risk of organ rejection.

But scaffolds still have some problems of traditional organ transplants: They require donor organs, for which there is a long waiting list, and the patient has to wait for the organ to be stripped of cells. Also, when it comes to windpipes, a donated windpipe may not be the right size. For that reason, Mr. Beyene’s windpipe, made of the plastic replica of his own windpipe, fit perfectly.

Dr. Macchiarini is looking at future improvements on this still preliminary work: The Times reports that someday, re-seeding the cells of a new organ may not take place outside the body:

“Instead, he envisions developing even better scaffolds and implanting them without cells, relying on drugs to stimulate the body to send cells to the site. His ultimate dream is to eliminate even the synthetic scaffold. Instead, drugs would enable the body to rebuild its own scaffold.”

“Don’t touch the patient,” Dr. Macchiarini told The Times. “Just use his body to recreate his own organ. It would be fantastic.”

Source: The New York Times /Smart planet