The Debut of the Stem Cell-Derived Hamburger

A new Cultured Beef Burger made from cultured beef grown in a laboratory from stem cells of cattle, is held by the man who developed the burger, Professor Mark Post of Netherland's Maastricht University, during a the world's first public tasting event for the food product in London, Monday Aug. 5, 2013. The Cultured Beef could help solve the coming food crisis and combat climate change according to the producers of the burger which cost some 250,000 euros (US dlrs 332,000) to produce. (AP Photo / David Parry, PA)
A new Cultured Beef Burger made from cultured beef grown in a laboratory from stem cells of cattle, is held by the man who developed the burger, Professor Mark Post of Netherland’s Maastricht University, during a the world’s first public tasting event for the food product in London, Monday Aug. 5, 2013. The Cultured Beef could help solve the coming food crisis and combat climate change according to the producers of the burger which cost some 250,000 euros (US dollars 332,000) to produce. (AP Photo / David Parry, PA)

This might seem like an odd use of stem cells, but this could potentially feed people without the need of large herds of cows. Our food in the future could use a pinch of seasoning, and maybe some cheese. Laboratory grown stem cells have been used to generate bovine muscle that, when ground, looks like real beef.

Two volunteers took the first public bites of hamburger that was grown in a laboratory. While they thought that had excellent texture, there was much to be desired when it came to its taste.

“I miss the salt and pepper,” said Austrian nutritionist Hanni Ruetzler. U.S. journalist Josh Schonwald confessed that he had difficulty judging a burger “without ketchup or onions or jalapenos or bacon.” Both tasters ate the burger without a hamburger bun or lettuce and sliced tomatoes even those these were offered to them. Both tasters really wanted to concentrate their gustatory sensations on the meat itself.

Mark Post, the Dutch scientist who led the team that grew the meat from cattle stem cells deeply regretted having served the patty without aged gouda cheese: his favorite topping.
“That would have enhanced the whole experience tremendously,” he told The Associated Press. He said he was pleased with the reviews: “It’s not perfect, but it’s a good start.”

Post is a professor at Maastricht University in the Netherlands, and he and his research team developed the burger over five years. Post hopes that making meat in labs could eventually help feed the world and fight climate change even though this goal is certainly a decade or two away.

“The first (lab-made) meat products are going to be very exclusive,” said Isha Datar, director of New Harvest, an international nonprofit that promotes meat alternatives. “These burgers won’t be in Happy Meals before someone rich and famous is eating them.”

Sergey Brin, a co-founder of Google, announced that he funded the 250,000-euro ($330,000) project, saying he was motivated by a concern for animal welfare. “We’re trying to create the first cultured beef hamburger,” he said in a videotaped message. “From there, I’m optimistic we can really scale up by leaps and bounds.”

Scientists largely agree that improving the flavor probably won’t be difficult. “Taste is the least (important) problem since this could be controlled by letting some of the stem cells develop into fat cells,” said Stig Omholt, director of biotechnology at the Norwegian University of Life Sciences.

According to Omholt, adding fat to the burgers this way would probably be healthier than getting it from naturally fat cows. He called Monday’s tasting a publicity stunt, but he was not speaking detrimentally about it. Instead, Omholt said that it was a smart way to draw public attention, and possibly investor funds, to research efforts to develop lab-grown meat.

Post’s research team made their meat from shoulder muscle cells of two organically raised cows. These cells were put into a nutrient solution to help them develop into muscle tissue, and they grew into small strands of meat. Post and his colleagues had to grow some 20,000 strands of muscle tissue to make a single 140-gram (5-ounce) patty. Post said the lab-made patty had a yellowish tinge.

“I’m a vegetarian, but I would be first in line to try this,” said Jonathan Garlick, a stem cell researcher at Tufts University School of Dental Medicine in Boston. He has used similar techniques to make human skin but wasn’t involved in the burger research.

Experts say new ways of producing meat are needed to satisfy growing carnivorous appetites without exhausting resources. By 2050, the Food and Agriculture Organization predicts global meat consumption will double as more people in developing countries are able to afford it. Raising animals destined for the dinner table takes up about 70 percent of all agricultural land. Interestingly, the animal rights group PETA has thrown its support behind the lab-meat initiative.

“As long as there’s anybody who’s willing to kill a chicken, a cow or a pig to make their meal, we are all for this,” said Ingrid Newkirk, PETA’s president and co-founder. “Instead of the millions and billions (of animals) being slaughtered now, we could just clone a few cells to make burgers or chops,” she said.

If the product is ever ready for market, national food authorities will likely require extensive data that proves that the lab meat is safe. Unfortunately, when it comes to lab-grown meat, there is no precedent. Some experts said officials might regulate the process used to make such meat, similar to how they monitor beer and wine production.

Only one patty was cooked Monday, and the testers each took less than half of it. Post said he would take the leftovers home so his kids can have a taste.

Using Stem Cells to Model the Blood-Brain Barrier

Our central nervous system include the brain and spinal cord. The central nervous system (CNS) is surrounded by a series of tough coverings called meninges that protect it and is bathed and fed by a circulating fluid called cerebrospinal fluid (CSF). The blood vessels that circulate blood through the CNS are composed of specialized cells that are very tightly apposed. These specialized blood vessels prevent molecules from spreading from the body to the CNS. In order for something to enter the CNS, the blood vessel-making cells (endothelia) must possess specific receptors that bind the desired molecule and allow it to pass into the CNS. Over 100 years ago, scientists found that if dye was injected into the bloodstream of a laboratory animal, the dye would enter everywhere except the CNS. This shows that there is a barrier that prevents the passage of all but a select set of molecules into the CNS and this barrier is called the blood-brain barrier (BBB).

The BBB is selectively permeable, which means that it allows some materials to cross into the CNS, but prevents others from doing so. In most parts of the body, the smallest blood vessels, called capillaries, are lined with endothelial cells. Endothelial tissue has small spaces between each individual cell so substances can move readily between the inside and the outside of the vessel. However, in the brain, the endothelial cells fit tightly together and substances cannot pass out of the bloodstream into the CNS. Some molecules, such as glucose, are transported out of the blood by special mechanisms.

Generally speaking. the BBB does not allow passage of large molecules, and non-fat soluble molecules also do not enter the brain. However, fat soluble molecules, such as barbituate drugs, can rapidly enter the brain. Also molecules that have a high electrical charge, if they enter the CNS at all, only do so rather slowly.

The BBB also prevents cancer drugs from entering the CNS, and this is one of the main reasons cancers of the CNS are difficult to treat. Designing cancer drugs that can enter the CNS and bypass the BBB is also challenging.

Fortunately, a new study from the University of Wisconsin, Madison, has shown that embryonic stem cells can be coaxed into differentiating into structures that greatly resemble the BBB. This might provide drug companies with a new model system to study the movement of experimental drugs into the CNS.

Eric Shusta is professor of chemical and biological engineering, is one of he senior authors of this new study. Since his laboratory has succeeded in differentiating embryonic stem cells into endothelial cells with BBB characteristics, he thinks that this “has the potential to streamline drug discovery for neurological disease. You can look at tens of thousands of drug candidates and just ask the question if they have a chance to get into the brain. There is a broad interest from the pharmaceutical industry.”

The endothelial cells generated in Shusta’s lab exhibit the active and passive regulatory characteristics of endothelial cells from the brains of a living animal.

Shusta and his team were able to induce embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) into forming BBB-like structures. The ability to drive iPSCs to form BBB-like structures is significant, since scientists could use cells from patients with particular neurological diseases to make BBB-like structures and then tailor drug treatments that will take into account the capacity of the patient’s BBB to admit or exclude particular drugs.

From an industrial standpoint, because these cells can be grown in culture and mass-produced, the can be used for diverse high-throughput screens for molecules that may have therapeutic value for neurological conditions or to identify neurotoxic properties of existing drugs.

According to Shusta: “The nice thing about deriving endothelial cells from induced pluripotent stem cells is that you can make disease-specific models of brain disease that incorporate the BBB. The cells you create will carry the genetic information of the condition you want to study.”

The BBB is also complete at birth but fragile. Former experiments led scientist to believe that the BBB was immature at birth, but these experiments used conditions that were destructive for the BBB. Therefore, high levels of particular molecules that are not a problem for an adult, such as bilirubin, can cause profound problems in a baby. Kernicterus is a form of mental retardation that results from high blood bilirubin levels in a newborn. The bilirubin accumulates in the brain and causes brain damage. This is a phenomenon that results from the BBB in neonates being overloaded with bilirubin. Certain medical conditions increase the risk of kernicterus. For example, premature birth, Rh incompatibility, polycythemia (too many red blood cells), certain drugs such as sulphonamides, which displace bilirubin from serum albumin, Crigler-Najjar syndrome, Gilbert’s syndrome or G6PD deficiency all predispose babies to kernicterus. A model system in which BBB cells from patients with these diseases are cultured and grown in the lab to provide profound and potentially life-saving insights into these diseases and how they affect the BBBs of newborn babies.

Making the BBB in culture also led to another important insight, The formation of the BBB requires the activity of brain-specific cells such as neurons. Shusta explained that neurons develop at the same time as the endothelial cells. Therefore, the developing neurons seem to secrete chemical cues that help determine functional specificity to the growing endothelial cells. Presently, Shusta and his group do not know what those chemicals are, but with this in the dish model, it will be relatively easy to go back and look.

Finally, in quoting from the abstract of this paper, “The resulting endothelial cells have many BBB attributes, including well-organized tight junctions, appropriate expression of nutrient transporters and polarized efflux transporter activity. Notably, they respond to astrocytes, acquiring substantial barrier properties as measured by transendothelial electrical resistance (1,450 ± 140 Ω cm2), and they possess molecular permeability that correlates well with in vivo rodent blood-brain transfer coefficients.” In other words their model BBB looks like a BBB and functionally acts like one. The possibilities for this model system are truly tremendous.

Obamacare: The Aftermath

Since many have asked my what I think about Obamacare and the recent Supreme Court ruling, I thought that I might provide my views on the topic.

In the first place, the law is obviously unconstitutional. The federal government cannot compel you to buy something. There is simply no universe in which someone can read our Constitution and come to the conclusion that the Constitution gives the government that power over its citizens.

Secondly, if Obamacare is a tax, then the lawsuit before the Supreme Court would have been dismissed, because according to the Anti-Injunction Act Donald Verrilli argued before the Supreme Court that the individual mandate is NOT a tax. However, in order to find the bill constitutional, Roberts had to treat it as though it was a tax. But wait a minute. The Anti-Injunction Act says that you cannot contest a tax bill until the tax is paid. Therefore, if Obamacare was a tax, then the case should have been dismissed til the tax was collected. Thus for the sake constitutionality, Obamacare is a tax, but for the sake of litigating it, it is not a tax. Roberts tried to have it both ways, but he can’t. This is the reason why legal pundits all over the US are troubled by Robert’s garbled, self-contradictory opinion. If this was a principled ruling then why did it make no internal sense.

Third, Obamacare is unworkable. In the words of Holman Jenkins of the Wall Street Journal, Obamacare is “upheld and doomed.” The problems with Obamacare are four-fold and they are :

1. Taxes

Besides being a massive federal power grab, Obamacare contains one of the largest tax increases ever imposed on the American economy. These tax increases come at a time when job growth should be the nation’s number one priority.. The tax sections of Obamacare begins with an increase in the Medicare payroll tax of 0.9 percent for individuals with incomes above $200,000 ($250,000 for couples) in 2013. Needless to say, this tax will depress the demand for labor at a time when job creation is critical in order to for jump-start the economy. Some might think that this tax will not hit the middle class because of the relatively high initial income thresholds, but they are wrong. These income thresholds were purposely not indexed to inflation. Therefore, as the years pass, more and more middle-income families will cross the thresholds because of normal wage growth.

Obamacare also includes an additional 3.8 percent tax on investment income; a new 2.3 percent excise tax on medical devices that will reduce the size of the industry. It also includes taxes on the drug and insurance industry that will be passed on to consumers in the form of higher premiums; and a tax on high-premium insurance plans that will also be passed on to consumers.

2. Deficits and Debt

Obamacare will exacerbate our nation’s already alarming entitlement spending and debt crises. The dramatic rise in spending on Medicare and Medicaid already is pushing the federal budget to the breaking point. Obamacare makes the problem much worse since it adds two new additional entitlement programs in the form of a massive Medicaid expansion and a new premium credit entitlement for households with incomes between 138 percent and 400 percent of the federal poverty level. These two entitlement expansions are expected to add a minimum of 35 million Americans to the entitlement rolls when phased in, at an expense of more than $200 billion annually by the end of the decade (CBO, Letter to House Speaker Nancy Pelosi, March 20, 2010, Table 4.).

Obamacare was sold by means of offsetting cuts in Medicare that supposedly would pay for it. Unfortunately, the Medicare cuts have been exposed as unrealistic because they would result in Medicare paying even less for medical services than Medicaid does today. (John D. Shatto and M. Kent Clemens, “Projected Medicare Expenditures Under Illustrative Scenarios with Alternative Payment Updates to Medicare Providers,” Office of the Actuary, Centers for Medicare and Medicaid Services, May 18, 201). This would severely jeopardize seniors’ access to care. Even worse, the offsetting cuts were made, the savings are double-counted under Obamacare, and are used once to pay for future Medicare commitments that are today counted as unfunded governmental liabilities, and then a second time to supposedly cover the costs of Obamacare’s entitlement expansions (Charles Blahous, “The Fiscal Consequences of the Affordable Care Act,” The Mercatus Center of George Mason University, 2012). Since money cannot be used twice, Obamacare will add hundreds of billions of dollars in new debts this decade, and trillions over the longer term (James C. Capretta, “The Medicare Trustees’ Report and the $8.1 Trillion Double-Count,” The Weekly Standard Blog, April 24, 2012).

3. Individual Mandate

The individual mandate hands immense regulatory power to the Department of Health and Human Services (HHS). According to Obamacare, HHS controls just about every aspect of the nation’s health system. In January 2012, the Administration announced that it planned to use that power to impose new benefit requirements on all employer-sponsored insurance in the name of “preventive health services” (now frequently termed the “HHS mandate”).

Additionally, the regulations issued by the Administration in this regard would require all employers, including religious employers such as Catholic hospitals and universities, to cover abortifacient products, contraceptives, and sterilization procedures in the health plans they offer to workers. By requiring all employers to offer these products and services in their health insurance policies, they would directly violate the religious liberty rights of thousands of religious institutions around the country.

4. The Bureaucratic Micromanagement of American Health Care

The bulk of Obamacare is based on the theory that the federal government has the capacity and know-how to micromanage American health care. This is the basis for the provisions that establish an unaccountable and unelected board—the Independent Payment Advisory Board (IPAB)—to oversee all aspects of how Medicare is run. It is also the theory behind Accountable Care Organizations (ACOs), which are authorized in Obamacare to give the federal government a new role in influencing how doctors and hospitals are organized to deliver care to seniors.

Unfortunately and contrary to socialistic preconceptions, the government is NOT adept at micromanaging how health care or any other aspect of people’s lives. When the government is given this much authority and discretion, it does not result in higher-quality care for patients. Instead, it leads to price controls and one-size-fits-all regulations that misallocate resources and lead to access problems. Obamacare compounds the problem since it creates massive new and costly bureaucracies at the federal and state levels of government that will become permanent and unresponsive centers of power. The IRS and HHS will grow. A new agency in HHS is slated to spend $10 billion supposedly testing new ideas, but already there is indication that the money is being wasted on projects driven more by politics than substance.

Obamacare is also pours hundreds of millions of dollars into the states to coax them into building the “exchanges” that will become the foundation of the Obamacare edifice. These exchanges, far from fulfilling the supposed mission of fostering a dynamic marketplace, will be the means by which the federal government will extend its reach to every corner of the health sector. Every American who does not obtain his or her insurance through an employer will have little choice but to go through Obamacare’s exchanges.   It will only be a matter of time before the federal government uses its new powers to impose even more top-down cost controls on the health system, to the detriment of the quality of American health care.

Obamacare is a disaster. Had the Supreme Court ruled properly, we would be out of this mess, but as it sits now, repeal – complete and total repeal – is the only answer.

Human-Eye Precursors are Grown from Embryonic Stem Cells

Yoshiki Sasai of the RIKEN Center for Developmental Biology (CBD) in Kobe, Japan has managed to grow eye precursors in the laboratory from embryonic stem cells.  Such an achievement provides a remarkable opportunity to investigate early eye development and the pathology of eye abnormalities.

Eye development is a complex process, since mammalian eyes develop as an extension of the central nervous system.  The development of the central nervous system begins at about 18 days after fertilization with the formation of a thickened layer of cells on the surface of the embryo called the neural plate.  The neural plate is induced by a cluster of cells that clumps together to form a hollow tube called the “notochordal plate.”  The neural plate rolls into a tube called the neural tube and this neural tube is the beginnings of the central nervous system.  The front of the neural tube will inflate to form the brain and the portion of the tube behind the brain forms the spinal cord.  The neural tube forms as a result of high points that form in the neural plate called the neural folds.  These neural folds fuse to form a tube that is below the outermost layer of the embryo (ectoderm).

About 22 days after fertilization, inflations on either side of the developing brain extend from the brain, and these are the beginnings of the eye.  These “optic vesicles” as they are called continue to grow until their connection to the brain becomes narrower and narrower.  The narrow connections between the optic vesicles and the brain are called the optic stalks and they will become the rudiments of the optic nerves.

The optic vesicles make contact with the surface of the embryo and this does two things.  The vesicle collapses into a two-layered structure called the optic cup and the embryonic ectoderm pinches in and forms a vesicle that will form the lens of the eye (lens vesicle).  The optic cup is about 550 micrometers in diameter and initially contains two layers of cells.  These cells divide quickly to form an inner neural retina and an outer retinal pigment epithelium.  The neural retina divides to form multiple layers of cells, including photoreceptor cells, which respond to light.  Austin Smith, director of the Centre for Stem Cell Research at the University of Cambridge, UK said of the developing eye: “The morphology is the truly extraordinary thing.”

Previously, stem-cell biologists were able to grow embryonic stem-cells into two-dimensional sheets, but over the past four years, Sasai and his colleagues have used mouse embryonic stem cells to grow well-organized, three-dimensional cerebral-cortex tissue (Eiraku, M., et al. Cell Stem Cell 3, 519–532, 2008)., pituitary-gland (Suga, H., et al. Nature 480, 57–62, 2011)., and optic-cup tissue (Eiraku, M., et al. Nature 472, 51–56, 2011).  His present successes represent the first time that anyone has managed a similar feat using human cells.

The fact that Sasai’s laboratory was able to grow the optic cup in the laboratory, and that it recapitulated the same developmental events in the same order shows that the cues for this the formation of the eye rely, primarily, on cue from inside the cell, rather than relying on external triggers.  “This resolves a long debate,” says Sasai, over whether the development of the optic cup is driven by internal or external cues.

This achievement could make a big difference in the clinic.  There have been increasing successes cell transplantations in the last few years.  For example, a last month, a group at University College London showed that a transplantation of stem-cell derived photoreceptors could rescue vision in mice (Pearson, R. A., et al. Nature 485, 99–103, 2012).  The transplant involved only rod-shaped receptors, not cone-shaped ones, which would leave the recipient seeing fuzzy images. Sasai’s organically-layered structure provides hope that integrated photoreceptor tissue might be transplantable someday.   The developmental process could also be adapted to treat a particular disease, and stocks of tissue could be created for transplant and frozen.

Sasai emphasized that the cells in the optic cup are differentiating and there are no embryonic stem cells in them.  This reduces concerns that transplants of these optic cups or structures derived from them might develop cancerous growths or fragments of unrelated tissues. “It’s like pulling an apple from a tree. You wouldn’t expect iron to be growing inside,” says Sasai. “You’d have no more reason to expect bone to be growing in these eyes.”

Masayo Takahashi, an ophthalmologist at the CBD, has already started transferring sheets of the retina from such optic cups into mice, and she would like to do the same with monkeys sometime this year.  The big question is whether transplanted tissue will integrate into native tissue.

The big question is whether or not clinicians and stem-cell biologists can easily repeat Sasai’s results?  Some, in fact, have already tried and failed to reproduce Sasai’s mouse experiment using human cells. “We need to know how robust, how reproducible it is,” says Smith.

Mifepristone – Not as Safe a Drug as you Might Think

According to data released by the US Food and Drug Administration (FDA) on the abortion pill, mifepristone, more than 1.2 million unborn children have lost their lives because of it, but even more stunningly, thousands of women have been injured and this includes more than a dozen who have died in the United States alone.

Just after the approval of mifepristone during the Clinton administration, the FDA released a report in 2006 that showed that more than 1,100 women had been subjected to “adverse effects” after taking mifepristone.  Pro-life advocates have waited five years for the FDA to come out with a new report of the adverse effects associated with this drug.  This drug seems to continue to kill and injure women all across the globe.

Mifespristone, which is marketed under the trade names Mifeprex and Korlyn, is still known by the name given to it when it was an experimental drug, RU486.  Mifepristone is a synthetic steroid drug that binds to the progesterone receptors in cells in the endometrium and prevents the progesterone receptor from receiving signals from progesterone.  Because the endometrium requires constant progesterone signaling to maintain itself, mifepristone causes the endometrium to breakdown.  It also causes the cervix to soften and induces the release of mo9lecules called prostaglandins.  These prostaglandins causes the smooth muscle of the uterus to contract, but mifepristone, also increases the sensitivity of the smooth muscle of the uterus to prostaglandins.  The breakdown of the endometrium and the contractions of the uterine smooth muscle cause the embryo to detach.  This eventually kills of all sources of progesterone production in the mother’s body, and the embryo dies.  Typically, mifepristone is followed by an oral prostaglandin (misoprostol) to increase uterine smooth muscle contraction and expulsion of the dead embryo.  Mifepristone is used to terminate pregnancies that are not older than 49 days.  The approval of mifepristone did include a Black Box Warning, as required under Subsection H.

There are several excellent articles about this FDA data.  Read about it here, here and here.  Mifepristone also has caused problems in women all around the world.  These data in this report is limited to adverse effects in the United States only.

Cardiophere-Derived Cells Embedded in Platelet Gel Increases Heart Function and Improves Heart Structure After a Heart Attack

Biomaterials are organic compounds that can be molded into the shape of a particular organ or tissue, and can be seeded with cells that will form the shape of the organ or tissue and degrade the it, while using the biomaterial as a scaffold for their growth and development.

One organ where biomaterials can make a great difference is the heart, since implanted cells tend to either die to move away from the heart. By implanting cells into the heart that are embedded in biomaterials, the implanted cells stay put, are protected from cell death induced by the inhospitable environment of the heart after a heart attack, and tend to differentiate into heart-specific cells at the site at which they were implanted.

Injectable biomaterials are preferable for the heart, since non-injectable biomaterials require that the surgeon crack the chest and implant the biomaterial, which is a much more invasive procedure. One of the most appealing injectable biomaterials is platelet gel (also known as platelet fibrin scaffold).

The body naturally generates platelet gel after injury, however, it can be engineered as a tissue substitute to speed healing. The scaffold for platelet gel consists of naturally occurring biomaterials composed of a cross-linked fibrin network.

Platelet gel polymerization requires the enzyme thrombin and its substrate fibrinogen. Thrombin degrades fibrinogen to fibrin, which self-assembles to form the fibrin meshwork that composes the ground substance for platelet gel.  This reaction is affected primarily by the concentration of thrombin and temperature. Platelet gels are composed of fibers whose thicknesses vary according to the reaction conditions, and can be enriched by addition of other molecules (fibronectin, vitronectin, laminin, and collagen). Linking these molecules to the fibrin scaffold greatly affects the properties of the platelet gel, and the gel can also serve as a reservoir for growth factors and other molecules that speed healing.

Injection of platelet gel into a heart that has just experienced a heart attack prevents remodeling. Can stem cells that have a documented ability to heal damaged hearts have their healing capacities increased by implanting them in platelet gel?

A paper published workers in Eduardo Marban’s lab at Cedars-Sinai Medical Center in Los Angeles in the journal Biomaterials asks this very question, using rats as a model. In this article, Marban’s group used cardiosphere-derived cells (CDCs), which were successfully used in the CADUCEUS clinical trial to heal the hearts of human patients who have suffered a heart attack. The strategy used in these experiments was relatively simple (in principle): Induce heart attacks in the rats, treat once group with platelet gel alone, and the other group with CDCs embedded in platelet gel. Then compare the structural and functional integrity of the hearts in each group.

The results of these experiments come in several categories. First of all, the CDCs grown in platelet gel showed increased viability (reduced death) in comparison to CDCs grown on standard tissue culture plates. Furthermore, platelet gel-grown CDCs also differentiated into three-dimensional structures such as blood vessels. The CDCs also degraded the platelet gel and by two weeks of culture, two-thirds of the platelet gel was degraded. Furthermore, CDCs in platelet gel spread out and began to beat. Far more CDCs spread out and beat when grown in platelet gel than those grown in tissue culture plates. The contraction of the CDC-formed heart muscle cells was also much more robust in platelet gel than in tissue culture plates. Overall, the CDCs did much better in platelet gel than in standard tissue culture plates. They grew better, survived better, formed more heart-specific structures, and differentiated in more mature heart cell types when grown in platelet gel.

Another bonus to the platelet gel consists in its ability to trap growth factors. The CDCs in the platelet gel secrete a wide variety of growth factors, and these growth factors bind to the platelet gel and are concentrated by it. This recruits other cells to the platelet gel. That increases the ability of the platelet gel to facilitate stem cell-mediated healing.

Implanting platelet gel alone and platelet gel seeded with CDCs into damaged hearts caused increased heart wall thickness, decreased infarct size, and improved cardiac function. However in all cases, the CDC-seeded platelet gel causes even greater improvements than platelet gel alone.

These experiments show that stem cell-mediated healing is improved by the use of biomaterials. Furthermore, platelet gel is a very easily manufactured biomaterial that improves the growth and heart-specific differentiation of CDCs. Give the demonstrated healing capacities of CDCs, augmenting those capabilities with biomaterials such as platelet gel should be a priority for future clinical trials.

The First Limbal Stem Cell Transplant with Cultured Limbal Stem Cells from a Cadaver

A genetic condition called “aniridia” results from mutations in the PAX6 gene. Approximately 1/50,000-1/1000,000 babies have aniridia. Aniridia results in the complete absence of an iris, and aniridia patients are unable to adjust to light differences.

Because mutations in the PAX6 gene are dominant, aniridia patients half a 50% chance of passing the aniridia condition to their children.

Fortunately for aniridia patients, limbal stem cells can now be cultured in the laboratory and used in clinical settings (see Di Iorio E, et al., Ocul Surf. 2010;8(3):146-53). A Scottish woman with aniridia has just received on of the first limbal stem cell transplants from a cadaver. These cadaver limbal stem cells were cultured and then transplanted onto the surface of her eye.

This woman, Sylvia Paton, who is 50 years old and from the Scottish town of Corstorphine (a west suburb of Edinburgh), is the first person in the United Kingdom to experience this ground-breaking treatment in February of 2012. Her procedure will hopefully reduce her vision problems and ready her for another procedure whereby her lens will be replaced.

For this procedure, limbal stem cells from a dead donor were cultured in the laboratory. The cells were attached to a membrane and then transplanted onto the surface of the left eye. The operation took a total of three hours.

Before her operation, Mrs. Paton could previously only see dark and light through her eye, but this treatment should repair her cornea, and prepare her for another surgery one year later to remove her cataract.

Dr Ashish Agrawal, the National Health Service consultant ophthalmologist who performed the operation, said: “It is now 12 weeks since the transplant and I am delighted to report that Sylvia is recovering well. Her cornea is clear and I hope that it will continue to maintain clarity. However, this is the first and the major step in the complex visual rehabilitation process and she will require further surgical treatment to restore vision.”

We wish Mrs. Paton well and hope that her vision continues to improve.