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A new breakthrough in stem cell research has occurred, thanks to scientists at the Children's Medical Center Research Institute at UT Southwestern Medical Center in Dallas, Texas.

The researchers claim that protein synthesis - an essential biological process - can be studied in adult stem cells. This is something that scientists have been previously unable to accomplish.

It is believed that many degenerative diseases and some cancers are linked with mutations that affect the process of protein synthesis. But experts have been unable to pinpoint why this happens.

Therefore, the team's discovery is important in improving understanding of protein synthesis and why changes in the process are linked with the development of disease.

The research built on previous work that used a modified antibiotic, called puromycin, to make it possible to see and measure the amount of protein that is being synthesized in the body.

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Protein synthesis studied in stem cells for the first time

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This is a game changer, folks. Whereas mining stem cells has been either an ethical quandary or a months-long affair, scientist can now turn any old blood cells into stem cells in just 30 minutesby dipping them in acid.

That's right. Take blood cells, add acid, get stem cells. It's as simple as it sounds.

A team of Japanese scientists stumbled upon the method after observing a similar phenomenon in plants, where environmental stress can morph an ordinary cell into an immature one. New plants could then grow from the immature cell. This has also been known to happen in birds and reptiles, so the team from the Riken Center for Developmental Biology set out to see if something similar could happen with mammals.

They started with mice, of course. Sure enough, when they exposed blood cells from mice to acid, a transformation began. While some of the blood cells died, many became stem cells within a couple of days. "It looks a bit too good to be true, but the number of experts who have reviewed and checked this, I'm sure that it is," Chris Mason, professor of regenerative medicine at University College London, told the BBC. "If this works in people as well as it does in mice, it looks faster, cheaper and possibly safer than other cell reprogramming technologiespersonalized reprogrammed cell therapies may now be viable."

The breakthrough was described by other scientists as "remarkable," "revolutionary," and "a game changer." Why? Well, if you've been following the promise and perils of stem cell research, then you know that the issue is both controversial and complicated. At first, scientists mined stem cells directly from embryos, but that involved destroying the embryos. In 2006, teams from Japan and the United Kingdom developed a new method, whereby they introduced certain genes that caused cells to reprogram themselves, becoming stem cells. That discovery won them the Nobel Prize in 2012, but it's also expensive and time-consuming. Other experimental methods are in the works.

This new discovery not only means that we can produce stem cells cheaply and quickly but also potentially cut through the ethical debate, because no embryos would be harmed. If it works in humans, that is. Of course, there's plenty more research to be done before scientists can fully understand the process and develop methods for stem cell research. But hot damn, this is good news. [New Scientist, BBC]

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Retracted: Study That Found Acid Converts Blood Cells Into Stem Cells

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Newswise DALLAS March 9, 2014 For the first time, researchers have shown that an essential biological process known as protein synthesis can be studied in adult stem cells something scientists have long struggled to accomplish. The groundbreaking findings from the Childrens Medical Center Research Institute at UTSouthwestern (CRI) also demonstrate that the precise amount of protein produced by blood-forming stem cells is crucial to their function.

The discovery, published online today in Nature, measures protein production, a process known as translation, and shows that protein synthesis is not only fundamental to how stem cells are regulated, but also is critical to their regenerative potential.

We unveiled new areas of cellular biology that no one has seen before, said Dr. Sean Morrison, Director of the Childrens Research Institute, Professor of Pediatrics, and the Mary McDermott Cook Chair in Pediatric Genetics at UTSouthwestern Medical Center. No one has ever studied protein synthesis in somatic stem cells. This finding not only tells us something new about stem cell regulation, but opens up the ability to study differences in protein synthesis between many kinds of cells in the body. We believe there is an undiscovered world of biology that allows different kinds of cells to synthesize protein at different rates and in different ways, and that those differences are important for cellular survival.

Dr. Adrian Salics laboratory at Harvard Medical School chemically modified the antibiotic puromycin in a way that made it possible to visualize and quantify the amount of protein synthesized by individual cells within the body. Dr. Robert A.J. Signer, a postdoctoral research fellow in Dr. Morrisons laboratory and first author of the study, realized that this reagent could be adapted to measure new protein synthesis by stem cells and other cells in the blood-forming system.

What they came across was astonishing, Dr. Morrison said. The findings suggested that different types of blood cells produce vastly different amounts of protein per hour, and stem cells in particular synthesize much less protein than any other blood-forming cells.

This result suggests that blood-forming stem cells require a lower rate of protein synthesis as compared to other blood-forming cells, said Dr. Morrison, the papers senior author.

Researchers applied the findings to a mouse model with a genetic mutation in a component of the ribosome the machinery that makes proteins and the rate of protein production was reduced in stem cells by 30 percent. The scientists also increased the rate of protein synthesis by deleting the tumor suppressor gene Pten in blood-forming stem cells. In both instances, stem cell function was noticeably impaired.

Together, these observations demonstrate that blood-forming stem cells require a highly regulated rate of protein synthesis, such that increases or decreases in that rate impair stem cell function.

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Stem Cell Study Opens Door to Undiscovered World of Biology

Scientists from the Harvard School of Engineering and Applied Sciences (SEAS) have developed a new gel-based material that could allow stem cells to fill in the gaps in teeth and bones. This advance in tissue engineering comes from an examination of embryonic development. The researchers have essentially created a material that mimics the physical conditions under which tissue forms naturally specifically, the gel shrinks.

Tissue engineers have been wrestling with the difficulties of coaxing human cells to form three-dimensional structures in the lab, but the combination of growth factors and artificial gene activation cant quite get us there. The bio-inspired gel developed at SEAS could be the first step in solving those problems. This is the first approach that has taken a process called mesenchymal condensation into account.

Mesenchymal condensation is a process involving two tissue layers in embryos where organ formation takes place. A layer of undifferentiated connective tissue cells (mesenchyme) and an epithelium exchange biochemical signals, which causes the mesenchymal cells to contract and form a small knot right where the new organ tissue is supposed to develop (see the image at the top). Mesenchymal cells are a type of stem cell that can develop into bone, enamel, fat, and other mature cells.

The gel developed at SEAS simulates the compressionthat mesenchymal cells would experience naturally in mesenchymal condensation. A modified form of PNIPAAm polymer forms the base of the gel. It normally contracts when warmed slightly, but was tweaked in this experiment to activate at body temperature. The loose matrix of the gel is impregnated with mesenchymal cells, which are compressed as it warms. Thats how theyre encouraged to start differentiating into the appropriate types of cells and lay down new tissues, in this case teeth composed of dentin and enamel.

In embryonic development, mesenchymal cells cant form complete teeth without that extra epithelial layer. The team hopes to test its shrinking gel with both tissue layers to see if it can form a full tooth all on its own. Other tissue types could follow if the team finds that its shrinking gel works.

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New shrinking gel could help repair damaged teeth or bones

By Marcus Johnson

Stem cell researchers from Harvard have been able to turn patients skin cells into neurons that can be affected by early-onset Alzheimers. Experts believe that this will make it easier to gather the results of cells affected by the disease. It is also believed that the research will make the development of new treatments a faster process.

The research was published in the Human Molecular Genetics journal and headed by Tracy Young-Pearse. The data showed that peopl suffering from Alzheimers had cell mutations t similar to mutations occurring in mice. We see this mild increase in A42 in cells from patients with Alzheimer's disease, which seems to be enough to trigger disease processes, said Young-Pearse. We also see increases of a smaller species of amyloid-beta called A38, which was unexpected as it should not be very aggregation prone. We don't fully understand what it means, but it may combine with other forms of amyloid-beta to stimulate plaque formation.

The researchers hope that their work can lead to new drugs that are more effective against the disease. Alzheimers drugs have had a high rate of failure during clinical trials because much of the drug development was based on non-human models. Young-Pearse hopes that their research can make it easier to treat the disease and develop new drugs. Because of the Harvard Stem Cell Institute, we were able to work with other researchers to make patient cells into any type of neuron," said Young-Pearse. "The environment provides a really nice system for testing many kinds of hypotheses.

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Stem Cells Driving Alzheimer's Research

The breakthrough might set up another showdown about cloning for therapeutic purposes

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From Nature magazine

It was hailed some 15 years ago as the great hope for a biomedical revolution: the use of cloning techniques to create perfectly matched tissues that would someday cure ailments ranging from diabetes to Parkinsons disease. Since then, the approach has been enveloped in ethical debate, tainted by fraud and, in recent years, overshadowed by a competing technology. Most groups gave up long ago on the finicky core method production of patient-specific embryonic stem cells (ESCs) from cloning. A quieter debate followed: do we still need therapeutic cloning?

A paper published this week by Shoukhrat Mitalipov, a reproductive biology specialist at the Oregon Health and Science University in Beaverton, and his colleagues is sure to rekindle that debate. Mitalipov and his team have finally created patient-specific ESCs through cloning, and they are keen to prove that the technology is worth pursuing.

Therapeutic cloning, or somatic-cell nuclear transfer (SCNT), begins with the same process used to create Dolly, the famous cloned sheep, in 1996. A donor cell from a body tissue such as skin is fused with an unfertilized egg from which the nucleus has been removed. The egg reprograms the DNA in the donor cell to an embryonic state and divides until it has reached the early, blastocyst stage. The cells are then harvested and cultured to create a stable cell line that is genetically matched to the donor and that can become almost any cell type in the human body.

Many scientists have tried to create human SCNT cell lines; none had succeeded until now. Most infamously, Woo Suk Hwang of Seoul National University in South Korea used hundreds of human eggs to report two successes, in 2004 and 2005. Both turned out to be fabricated. Other researchers made some headway. Mitalipov created SCNT lines in monkeys in 2007. And Dieter Egli, a regenerative medicine specialist at the New York Stem Cell Foundation, successfully produced human SCNT lines, but only when the eggs nucleus was left in the cell. As a result, the cells had abnormal numbers of chromosomes, limiting their use.

Monkeying around Mitalipov and his group began work on their new study last September, using eggs from young donors recruited through a university advertising campaign. In December, after some false starts, cells from four cloned embryos that Mitalipov had engineered began to grow. It looks like colonies, it looks like colonies, he kept thinking. Masahito Tachibana, a fertility specialist from Sendai, Japan, who is finishing a 5-year stint in Mitalipovs laboratory, nervously sectioned the 1-millimetre-wide clumps of cells and transferred them to new culture plates, where they continued to grow evidence of success. Mitalipov cancelled his holiday plans. I was happy to spend Christmas culturing cells, he says. My family understood.

The success came through minor technical tweaks. The researchers used inactivated Sendai virus (known to induce fusion of cells) to unite the egg and body cells, and an electric jolt to activate embryo development. When their first attempts produced six blastocysts but no stable cell lines, they added caffeine, which protects the egg from premature activation.

None of these techniques is new, but the researchers tested them in various combinations in more than 1,000 monkey eggs before moving on to human cells. They made the right improvements to the protocol, says Egli. Its big news. Its convincing. I believe it.

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Patient-Specific Human Embryonic Stem Cells Created by Cloning

Sir Ian Wilmut proposes an alternative method as a possible means of creating a mammoth--or a hybrid. Such research could lead to major biological discoveries and advances

Wikimedia Commons/Mammut

Editor's note: The following essay is reprinted with permission from The Conversation UK, an online publication covering the latest research.

By Ian Wilmut, University of Edinburgh

It is unlikely that a mammoth could be cloned in the way we created Dolly the sheep, as has been proposed following the discovery of mammoth bones in northern Siberia. However, the idea prompts us to consider the feasibility of other avenues. Even if the Dolly method is not possible, there are other ways in which it would be biologically interesting to work with viable mammoth cells if they can be found.

In order for a Dolly-like clone to be born it is necessary to have females of a closely related species to provide unfertilised eggs, and, if cloned embryos are produced, to carry the pregnancies. Cloning depends on having two cells. One is an egg recovered from an animal around the time when usually she would be mated.

In reality there would be a need for not just one, but several hundred or even several thousand eggs to allow an opportunity to optimise the cloning techniques. The cloning procedure is very inefficient. After all, after several years of research with sheep eggs, Dolly was the only one to develop from 277 cloned embryos. In species in which research has continued, the typical success rate is still only around 5% at best.

Elephant eggs

In this case the suggestion is to use eggs from elephants. Because there is a danger of elephants becoming extinct it is clearly not appropriate to try to obtain 500 eggs from elephants. But there is an alternative.

There is a considerable similarity in the mechanisms that regulate function of the ovaries in different mammals. It has been shown that maturation of elephant eggs is stimulated if ovarian tissue from elephants is transplanted into mice.

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Produce Woolly Mammoth Stem Cells, Says Creator of Dolly the Sheep

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6-Mar-2014

Contact: Jessica Maki jmaki3@partners.org 617-525-6373 Brigham and Women's Hospital

Boston, MA A team of Alzheimer's disease (AD) researchers at Brigham and Women's Hospital (BWH) has been able to study the underlying causes of AD and develop assays to test newer approaches to treatment by using stem cells derived from related family members with a genetic predisposition to (AD).

"In the past, research of human cells impacted by AD has been largely limited to postmortem tissue samples from patients who have already succumbed to the disease," said Dr. Tracy L. Young-Pearse, corresponding author of the study recently published in Human Molecular Genetics and an investigator in the Center for Neurologic Diseases at BWH. "In this study, we were able to generate stem cells from skin biopsies of living family members who carry a mutation associated with early-onset AD. We guided these stem cells to become brain cells, where we could then investigate mechanisms of the disease process and test the effects of newer antibody treatments for AD."

The skin biopsies for the study were provided by a 57-year-old father with AD and his 33 year-old- daughter, who is currently asymptomatic for AD. Both harbor the "London" familial AD Amyloid Precursor Protein (APP) mutation, V7171. More than 200 different mutations are associated with familial AD. Depending on the mutation, carriers can begin exhibiting symptoms as early as their 30s and 40s. APPV7171 was the first mutation linked to familial AD and is the most common APP mutation.

The BWH researchers submitted the skin biopsies to the Harvard Stem Cell Institute, where the cells were converted into induced pluripotent stem cells (or iPSCs). Dr. Young-Pearse's lab then directed the stem cells derived from these samples into neurons specifically related to a particular region of the brain which is responsible for memory and cognitive function. The scientists studying these neurons made several important discoveries. First, they showed that the APPV7171 mutation alters APP subcellular location, amyloid-beta protein generation, and then alters Tau protein expression and phosphorylation which impacts the Tau protein's function and activity. Next, the researchers tested multiple amyloid-beta antibodies on the affected neurons. Here, they demonstrated that the secondary increase in Tau can be rescued by treatment with the amyloid -protein antibodies, providing direct evidence linking disease-relevant changes in amyloid-beta to aberrant Tau metabolism in living cells obtained directly from an AD patient.

While AD is characterized by the presence of amyloid-beta protein plaques and Tau protein tangles, observing living cell behavior and understanding the mechanisms and relationship between these abnormal protein deposits and tangles has been challenging. Experimental treatments for AD are using antibodies to try to neutralize the toxic effects of amyloid-beta, because they can bind to and clear the amyoid-beta peptide from the brain.

This study is the first of its kind to examine the effects of antibody therapy on human neurons derived directly from patients with familial AD.

"Amyloid-beta immunotherapy is a promising therapeutic option in AD, if delivered early in the disease process," said Dr. Young-Pearse. "Our study suggests that this stem cell model from actual patients may be useful in testing and comparing amyloid-beta antibodies, as well as other emerging therapeutic strategies in treating AD."

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Alzheimer's research team employs stem cells to understand disease processes and study new treatment