Six million years ago, chimpanzees and humans diverged from a common ancestor and evolved into unique 1) ___. UCLA scientists have identified a new way to pinpoint the 2) ___ that separate us from our closest living relative — and make us uniquely human. We share more than 95% of our genetic blueprint with chimps. What sets us apart from chimps are our 3) ___: homo sapiens means ‘the knowing man. During evolution, changes in some genes alter how the human brain functions. Research has identified an entirely new way to identify these genes in the small portion of our DNA that differs from the chimpanzee’s. By evaluating the correlated activity of thousands of genes, a UCLA team identified not just individual genes, but entire networks of 4) ___ genes whose expression patterns, within the brains of humans, varied from those in the chimpanzee. Genes don’t operate in 5) ___ — each functions within a system of related genes. If we examine each gene individually, it would be similar to reading every fifth word in a paragraph — you don’t get to see how each word relates to the other. So instead we use a systems biology approach to study each gene within its context. The scientists identified networks of genes that correspond to specific brain regions. When they compared these 6) ___ between humans and chimps, they found that the gene networks differed the most widely in the cerebral cortex — the brain’s most highly evolved region, which is three times larger in humans than chimps. They also discovered that many of the genes that play a central role in cerebral cortex networks in humans, but not in the chimpanzee, also show significant changes at the 7) ___ level. When we see alterations in a gene network that correspond to functional changes in the genome, it implies that these differences are very meaningful. This finding supports the theory that variations in the DNA sequence contributed to human evolution. Relying on a new analytical approach the UCLA team used data from DNA microarrays — vast collections of tiny DNA spots — to map the activity of virtually every gene in the 8) ___ simultaneously. By comparing gene activity in different areas of the brain, the team identified gene networks that correlated to specific brain regions. Then they compared the strength of these correlations between humans and chimps. Many of the human-specific gene networks identified by the scientists related to 9) ___, brain cell activity and energy metabolism. If you view the brain as the body’s engine, findings suggest that the human brain fires like a 12-cylinder engine, while the chimp brain works more like a 6-cylinder engine. It’s possible that our genes adapted to allow our brains to increase in size, operate at different speeds, metabolize energy faster and enhance 10) ___ between brain cells across different brain regions. Adapted from materials provided by University of California – Los Angeles

ANSWERS: 1) species; 2) genes; 3) brains; 4) interconnected; 5) isolation; 6) networks; 7) DNA; 8) genome; 9) learning; 10) connections

Lead researcher Dr. Peter Mazzone and his team from the Cleveland Clinic have developed a breath test that can successfully pick up lung cancer with “moderate accuracy” even in the early stages. This breath test could revolutionize the way cancer is 1) ___ and potentially save lives. The test comprises a chemical 2) ___ sensor, which detects tiny changes in the unique 3) ___ signature of the breath of people with lung cancer. Metabolic changes in lung cancer cells cause changes in the production and processing of volatile organic 4) ___. Lung cancer cells give off chemicals, called volatile 5) ___ compounds or VOCs, which are then exhaled. The researchers used the color sensor to test the breath of 122 people with different types of 6) ___ disease, and 21 healthy people. Included in the group with respiratory illness were 49 people with small cell lung cancer at various stages of development. The research team used the sensor results from 70% of the study participants to develop a predictive model, the accuracy of which was then tested on the remaining 30%. The results showed that the test was able to predict, accurately, the presence of cancer in just under three out of four of those with lung cancer. The results were not affected by age, gender, or stage of disease. Other approaches to breath testing have been used, including, gas 7) ___ and mass spectrometry, both of which require a great deal of expertise to use, plus, both are very expensive. According to the authors, as cancer is often silent in its early stages and symptoms are often not specific, it is often difficult to pick up the disease at a stage when it could be treated effectively. Diagnosis is often, therefore, only made when the disease is 8) ___. Ultimately, this line of investigation could lead to an inexpensive, non-invasive screening or diagnostic test for lung cancer.

ANSWERS: 1) detected; 2) color; 3) chemical; 4) compounds; 5) organic; 6) respiratory; 7) chromatography; 8) advanced

More information: ChemSensing has designed systems with a customized colorimetric sensor array that uses metalloporphyrins that hold metal ions tightly, but with open sites. When exposed to volatile organic compounds, the metalloporphyrins produce measurable color changes. ChemSensing’s system was first developed to identify and measure levels of potentially deadly gas exposures, as might be encountered in the case of a bioterrorist attack or a major industrial accident. It has also been used to detect bacterial food spoilage. The system used by the Cleveland Clinic’s scientists contained 36 “chemically sensate spots,” each with different sensitivities to volatile organic compounds. The authors chose a broadly sensitive system, as the identity of the key volatiles that make the breath of patients with lung cancer unique has not been clearly established.

Target Health wishes our over 2,200 readers and their family and friends a joyous New Year. Whatever holiday you may celebrate, we are all one. For our clients, most of us at Target Health will be picking up emails and addressing your needs, in spite of.the holiday respite. We will resume publication of ON TARGET on January 7, 2008.

For more information, please contact Dr. Jules T. Mitchel or Joyce Hays. For new business opportunities, contact Adrian Pencak, (Vice President, Business Development).

From Howard Hughes Medical Institute

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Wild populations of stickleback fish have evolved major changes in bony armor styles (shaded) in marine and freshwater environments. New research shows that this evolutionary shift occurs over and over again by increasing the frequency of a rare genetic variant in a single gene.

In a stunning example of evolution at work, scientists have now found that changes in a single gene can produce major changes in the skeletal armor of fish living in the wild.

The surprising results, bring new data to long-standing debates about how evolution occurs in natural habitats.

“This is one of the first cases in vertebrates where it’s been possible to track down the genetic mechanism that controls a dramatic change in skeletal pattern, a change that occurs naturally in the wild.”
David M. Kingsley

“Our motivation is to try to understand how new animal types evolve in nature,” said molecular geneticist David M. Kingsley, a Howard Hughes Medical Institute investigator at the Stanford University School of Medicine. “People have been interested in whether a few genes are involved, or whether changes in many different genes are required to produce major changes in wild populations.”

The answer, based on new research, is that evolution can occur quickly, with just a few genes changing slightly, allowing newcomers to adapt and populate new and different environments.

In collaboration with zoologist Dolph Schluter, at the University of British Columbia, Vancouver, Canada, and Rick Myers and colleagues at Stanford, Kingsley and graduate student Pamela F. Colosimo focused on a well-studied little fish called the stickleback. The fish—with three bony spines poking up from their backs—live both in the seas and in coastal fresh water habitats all around the northern hemisphere.

Sticklebacks are enormously varied, so much so that in the 19th century naturalists had counted about 50 different species. But since then, biologists have realized most populations are recent descendants of marine sticklebacks. Marine fish colonized new freshwater lakes and streams when the last ice age ended 10,000 to 15,000 years ago. Then they evolved along separate paths, each adapting to the unique environments created by large scale climate change.

“There are really dramatic morphological and physiological adaptations” to the new environments, Kingsley said.

For example, “sticklebacks vary in size and color, reproductive behavior, in skeletal morphology, in jaws and teeth, in the ability to tolerate salt and different temperatures at different latitudes,” he said.

Kingsley, Schluter and their co-workers picked one trait—the fish’s armor plating—on which to focus intense research, using the armor as a marker to see how evolution occurred. Sticklebacks that still live in the oceans are virtually covered, from head to tail, with bony plates that offer protection. In contrast, some freshwater sticklebacks have evolved to have almost no body armor.

“It’s rather like a military decision, to be either heavily armored and slow, or to be lightly armored and fast,” Kingsley said. “Now, in countless lakes and streams around the world these low-armored types have evolved over and over again. It’s one of the oldest and most characteristic differences between stickleback forms. It’s a dramatic change: a row of 35 armor plates turning into a small handful of plates – or even no plates at all.”

Using genetic crosses between armored and unarmored fish from wild populations, the research team found that one gene is what makes the difference.

“Now, for the first time, we’ve been able to identify the actual gene that is controlling this trait,” the armor-plating on the stickleback, Kingsley said

The gene they identified is called Eda , originally named after a human genetic disorder associated with the ectodysplasin pathway, an important part of the embryonic development process. The human disorder, one of the earliest ones studied, is called ectodermal dysplasia.

“It’s a famous old syndrome,” Kingsley said. “Charles Darwin talked about it. It’s a simple Mendelian trait that controls formation of hair, teeth and sweat glands. Darwin talked about `the toothless men of Sind,’ a pedigree (in India) that was striking because many of the men were missing their hair, had very few teeth, and couldn’t sweat in hot weather. It’s a very unusual constellation of symptoms, and is passed as a unit through families.”

Research had already shown that the Eda gene makes a protein, a signaling molecule called ectodermal dysplasin. This molecule is expressed in ectodermal tissue during development and instructs certain cells to form teeth, hair and sweat glands. It also seems to control the shape of – bones in the forehead and nose.

Now, Kingsley said, “it turns out that armor plate patterns in the fish are controlled by the same gene that creates this clinical disease in humans. And this finding is related to the old argument whether Nature can use the same genes and create other traits in other animals.”

Ordinarily, “you wouldn’t look at that gene and say it’s an obvious candidate for dramatically changing skeletal structures in wild animals that end up completely viable and healthy,’ he said. ” Eda gene mutations cause a disease in humans, but not in the fish. So this is the first time mutations have been found in this gene that are not associated with a clinical syndrome. Instead, they cause evolution of a new phenotype in natural populations.”

The research with the wild fish also shows that the same gene is used whenever the low armor trait evolves. “We used sequencing studies to compare the molecular basis of this trait across the northern hemisphere,” said Kingsley. “It doesn’t matter where we look, on the Pacific coast, the East coast, in Iceland, everywhere. When these fish evolve this low-armored state they are using the same genetic mechanism. It’s happening over and over again. It makes them more fit in all these different locations.”

Because this trait evolves so rapidly after ocean fish colonize new environments, he added, “we wondered whether the genetic variant (the mutant gene) that controls this trait might still exist in the ocean fish. So we collected large numbers of ocean fish with complete armor, and we found a very low level of this genetic variant in the marine population.”

So, he said, “the marine fish actually carry the genes for this alternative state, but at such a low level it is never seen;” all the ocean fish remain well-armored. “But they do have this silent gene that allows this alternative form to emerge if the fish colonize a new freshwater location.”

Also, comparing what happens to the ectodysplasin signaling molecule when its gene is mutated in humans, and in fish, shows a major difference. The human protein suffers “a huge amount of molecular lesions, including deletions, mutations, many types of lesions that would inactivate the protein,” Kingsley said.

But in contrast, “in the fish we don’t see any mutations that would clearly destroy the protein.” There are some very minor changes in many populations, but these changes do not affect key parts of the molecule. In addition, one population in Japan used the same gene to evolve low armor, but has no changes at all in the protein coding region. Instead, Kingsley said, “the mutations that we have found are, we think, in the (gene’s) control regions, which turns the gene on and off on cue.” So it seems that evolution of the fish is based on how the Eda gene is used; how, when and where it is activated during embryonic growth.

Also, to be sure they’re working with the correct gene, the research team used genetic engineering techniques to insert the armor-controlling gene into fish “that are normally missing their armor plates. And that puts the plates back on the sides of the fish,” Kingsley said.

“So, this is one of the first cases in vertebrates where it’s been possible to track down the genetic mechanism that controls a dramatic change in skeletal pattern, a change that occurs naturally in the wild,” he noted.

“And it turns out that the mechanisms are surprisingly simple. Instead of killing the protein (with mutations), you merely adjust the way it is normally regulated. That allows you to make a major change in a particular body region – and produces a new type of body armor without otherwise harming the fish.”

Image: David Kingsley, HHMI at Stanford University, modified from Cuvier (1829).

From Howard Hughes Medical Institute

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Ocean sticklebacks are dark colored fish that often migrate into new environments. Multiple stickleback populations have evolved lighter gill and skin colors following colonization of new lakes and streams at the end of the last ice age. Ocean (upper) compared to freshwater creek (lower) sticklebacks, both collected near Vancouver, British Columbia. Scientists have identified a genetic change controlling rapid evolution of skin color in fish, and shown that the same mechanism also contributes to recent evolution of skin color in humans.

When humans began to migrate out of Africa about 100,000 years ago, their skin color gradually changed to adapt to their new environments. And when the last Ice Age ended about 10,000 years ago, marine ancestors of ocean-dwelling stickleback fish experienced dramatic changes in skin coloring as they colonized newly formed lakes and streams. New research shows that despite the vast evolutionary gulf between humans and the three-spined stickleback fish, the two species have adopted a common genetic strategy to acquire the skin pigmentation that would help each species thrive in their new environments.

The researchers, led by Howard Hughes Medical Institute investigator David Kingsley, published their findings in the December 14, 2007, issue of the journal Cell. Kingsley and first author Craig Miller are at the Stanford University School of Medicine, and other co-authors are from the University of Porto in Portugal, the University of British Columbia, the University of Chicago, and the Pennsylvania State University Further studies of stickleback, they say, may reveal other malleable pieces of genetic machinery both fish and humans have used for adaptation.

“The genetic mechanisms that can produce these changes may be so constrained that evolution will tend to use the same sorts of genes in different organisms.”
David M. Kingsley

The stickleback has become a premier model organism for studying evolution because of its extraordinary evolutionary history, said Kingsley. “Sticklebacks have undergone one of the most recent and dramatic evolutionary radiations on earth,” he said. When the last Ice Age ended, giant glaciers melted and created thousands of lakes and streams in North America, Europe, and Asia. These waters were colonized by the stickleback’s marine ancestors, which subsequently adapted to life in freshwater. “This created a multitude of little evolutionary experiments, in which these isolated populations of fish adapted to the new food sources, predators, water color, and water temperature that they found in these new environments,” Kingsley explained.

Among those adaptations were new colorations that helped the fish camouflage themselves, distinguish species, and attract mates in their new environments. Until now, however, scientists had not understood what genetic factors drove the changes in skin pigmentation.

Human populations have also undergone pigmentation changes as they have adapted to life in new environments. The ecological reasons for those changes may be quite different from the forces driving the evolution of pigmentation in sticklebacks, said Kingsley. As human populations migrated out of Africa into northern climates, the need for darker pigmentation necessary to protect against the intense tropical sun diminished. With skin that was more transparent to sunlight, humans were better able to produce sufficient vitamin D in their new climate.

To begin to understand the genetic basis of skin pigmentation changes in fish, Kingsley and his colleagues crossed stickleback species that had different pigmentation patterns and used genetic markers and the recently completed sequence map of the fish’s genome to search for the mechanism regulating stickleback pigmentation. They searched for chromosome segments in the offspring that were always associated with inheritance of dark or light gills and skin. Through detailed mapping of one such segment, Kingsley and his colleagues found that a gene called Kitlg (short for “Kit ligand”) was associated with pigmentation inheritance. Kitlg was an excellent candidate for regulating pigmentation because mutant forms of the corresponding gene in mice produce changes in fur color, said Kingsley.

The Kitlg gene is involved in a variety of biological processes, including germ cell development, pigment cell development, and hematopoiesis. Light-colored fish have regulatory mutations that reduce expression of the Kitlg gene in gills and skin, but that do not reduce the gene’s function in other tissues. “By altering expression of this gene in one particular place in the body, the fish can fine tune the level of expression of that factor in some tissues but not others,” said Kingsley. “That lets evolution produce a big local effect on a trait like color while preserving the other functions of the gene.”

Humans also have a Kitlg gene, and Kingsley and his colleagues wondered if it played a role in regulating the pigmentation of human skin. One clue they had came from previous research by other groups that had revealed that the human Kitlg gene has undergone different changes among different human populations, suggesting that it is evolutionarily significant.

Kingsley and his colleagues tested whether the different human versions of the Kitlg gene are associated with changes in skin color. Humans with two copies of the African form of the Kitlg gene had darker skin color than people with one or two copies of the new Kitlg variant that is common in Europe and Asia.

“Although multiple chromosomal regions contribute to the complex trait of pigmentation in both fish and humans, we have identified one gene that plays a central role in color changes in both species,” said Kingsley.

“Since fish and humans look so different, people are often surprised that common mechanisms may extend across both organisms,” he said. “But there are real parallels between the evolutionary history of sticklebacks and humans. Sticklebacks migrated out of the ocean into new environments about ten thousand years ago. And they breed about once every one or two years, giving them five thousand to ten thousand generations to adapt to new environments.”

Although modern humans arose in Africa, they are thought to have migrated out of Africa in the last 100,000 years. “Humans breed about once every 20 years, giving them about 5,000 generations or so to emerge from an ancestral environment and colonize and adapt to new environments around the world,” Kingsley added. “So despite the difference in total years, the underlying process is actually quite similar. Whether it be fish or humans, there were small migrating populations encountering new environments and evolving significant changes in some traits in a relatively short time. And the genetic mechanisms that can produce these changes may be so constrained that evolution will tend to use the same sorts of genes in different organisms.”

Kingsley and his colleagues are now exploring the genetic basis of other evolved traits in the stickleback that could find a parallel in humans. “And given the degree to which evolutionary mechanisms appear to be shared between populations and organisms, we’re optimistic about finding the particular genes that underlie other recent adaptations to changing environments in both fish and humans,” he said.

Photo: Frank Chan, Craig Miller, and David Kingsley; Stanford University

Van Jones, calls himself, the black Al Gore. In addition, we call him a beautiful green hero. His talk is inspiring and easy to listen to. Let him motivate you, as he has done for so many.

Activist, Van Jones is tackling two of our biggest problems – urban poverty and environmental peril – with a fresh, dynamic plan. His vision for providing America’s poor with “green jobs instead of jails” touts a Green Revolution that includes everyone.

Target Health Inc. was at Jones’ presentation at PopTech Conference this past October 2007. Of all the cutting edge presenters, Van Jones was the most memorable of all. Below, we share with you, a video of his talk.

Enjoy!

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The Howard Hughes Medical Institute (HHMI) has selected 12 colleges and universities to participate in a nationwide genomics course that will involve first-year college students in authentic research. The new course is the first major initiative from HHMI’s Science Education Alliance, which seeks to enhance the teaching of science and inspire new generations of scientists.

In Fall 2008, first-year students at the six undergraduate institutions and six research-intensive institutions will take part in a year-long research course — the Phage Genomics Research Initiative – which is being developed by the Science Education Alliance (SEA).

“The phage genomics course is the beginning of the transformation that the Science Education Alliance hopes to bring to science education.”
Tuajuanda C. Jordan

The SEA, headquartered at HHMI’s Janelia Farm Research Campus in Northern Virginia, will foster the development of a national network of scientists and educators who work collaboratively to develop and distribute new materials and methods to the education community. HHMI has built the SEA using the knowledge and experience it has gained from supporting science education advances in the United States over the last 20 years.

“The phage genomics course is the beginning of the transformation that the Science Education Alliance hopes to bring to science education,” said Tuajuanda C. Jordan, a biochemist and director of the SEA. “The institutions that we have chosen really see the long-term impact that the program can have on their students and their institutions. The participating faculty have support at all levels for implementing and expanding on the program.”

The SEA is a new direction for HHMI, which for two decades has funded science education programs run by faculty and teachers at institutions across the United States. By creating the SEA, HHMI is taking a more active role in catalyzing change in science education. The Institute is staffing the SEA program with its own employees, who are building the alliance with the help of HHMI’s extensive network of grantees and educators. HHMI is committing a total of $4 million over the first four years of the program.

“The initial institutions we have selected represent a broad sampling of high quality higher education,” said Peter J. Bruns, vice president for grants and special programs at HHMI. “Although diverse in size and location, all participating schools share a desire to bring authentic discovery to freshman instruction. I am impressed by their commitment to the project and eagerly wait to see what a working alliance of such a diverse, yet commonly committed community, will yield.”

Approximately 20 students at each institution will participate in the two-semester phage genomics research course, in which they will be taught to use sophisticated research techniques. Students will isolate bacterial viruses (phages) from their local soil, prepare the viral DNA for sequencing, and annotate and compare the sequenced genome. The goal is to immerse students in the process of doing science, and equip them with the critical thinking and communication skills necessary for successful research careers. “We also hope their work will make a significant contribution to the field of genomics,” said Jordan.

For faculty who will teach the phage genomics course, joining the SEA will help move the science curriculum at their institutions beyond “cookbook” style laboratory experiments and bring hands-on research to a larger group of students. “I’ve become increasingly dissatisfied with the way we teach the science of biology. It is mostly fact learning rather than inquiry learning, and that’s just a tragedy. It’s not the way we should teach science,” said Kit J. Pogliano, a professor of biology at the University of California, San Diego, who will teach the phage genomics course with her husband and fellow faculty member, Joseph A. Pogliano.

“We’ve been seeking ways to engage more of our students in research and inquiry-directed learning experiences,” said Pogliano. “This sort of an experiment – having a big group of students doing research over the course of a year in a formalized lab course, rather than in individual faculty labs — is something we’ve thought about doing. But like many state schools, we just didn’t have the finances to put together a big project like that ourselves. This was a great way to jump-start the process.”

At the University of Louisiana at Monroe (ULM), biology professor Ann M. Findley said her institution serves students of diverse backgrounds with varying levels of preparedness and “extremely limited prior exposure to experimental science.”

“ULM’s participation in the HHMI-SEA initiative will not only furnish our students with an exciting introduction to the process of doing science, it will also provide us with the opportunity to demonstrate that, when presented with a challenging laboratory environment and a committed support system, all engaged students can effectively transcend their high school preparation to become contributing members of this exciting national experiment,” said Findley.

Earlier this Fall, HHMI invited all four-year institutions to apply to participate in the Phage Genomics Research Initiative. HHMI received 44 applications and selected 12 institutions.

Each institution will receive up to three years of support from HHMI to assist with faculty training, reagents, computing support, and DNA sequencing services for the course. Faculty from participating institutions will attend three training workshops at Janelia Farm before teaching the phage genomics course.

Twelve more institutions will join the program in the fall of 2009, and another 12 in the fall of 2010. When the Phage Genomics Research Initiative is running at capacity, 36 institutions and approximately 720 students will be participating. After three years of initial support by SEA, institutions wishing to continue offering the course must provide their own financial resources to cover reagents, sequencing, and computing costs.

Participants in the 2008-2009 course will benefit from a pilot phage genomics course currently running at the University of Pittsburgh. SEA staff will use student and faculty experiences in the pilot course to refine the curriculum and develop additional resources for professors and students.

The institutions that will participate in the SEA phage genomics research initiative in academic year 2008-2009 are:

* Carnegie Mellon University
Pittsburgh, Pennsylvania
* The College of William and Mary
Williamsburg, Virginia
* Hope College
Holland, Michigan
* James Madison University
Harrisonburg, Virginia
* Oregon State University
Corvallis, Oregon
* Spelman College
Atlanta, Georgia
* University of California, San Diego
San Diego, California
* University of California, Santa Cruz
Santa Cruz, California
* University of Louisiana at Monroe
Monroe, Louisiana
* University of Mary Washington
Fredericksburg, Virginia
* University of Maryland-Baltimore County
Baltimore, Maryland
* Washington University in St. Louis
St. Louis, Missouri

The Biology of Algae – A tiny world we may not think about very often, but which is extremely important to the planet, especially algae in the oceans. Take a look at this NASA article, that shows how algae and climate change are connected.

News release issued by Rice University — Rice University biomedical engineers have developed a new technique for growing cartilage from human embryonic stem cells, a method that could be used to grow replacement cartilage for the surgical repair of knee, jaw, hip, and other joints.

“Because native cartilage is unable to heal itself, researchers have long looked for ways to grow replacement cartilage in the lab that could be used to surgically repair injuries,” said lead researcher Kyriacos A. Athanasiou, the Karl F. Hasselmann Professor of Bioengineering. “This research offers a novel approach for producing cartilage-like cells from embryonic stem cells, and it also presents the first method to use such cells to engineer cartilage tissue with significant functional properties.”

Using a series of stimuli, the researchers developed a method of converting the stem cells into cartilage cells. Building upon this work, the researchers then developed a process for using the cartilage cells to make cartilage tissue. The results show that cartilages can be generated that mimic the different types of cartilage found in the human body, such as hyaline articular cartilage — the type of cartilage found in all joints — and fibrocartilage — a type found in the knee meniscus and the jaw joint. Athanasiou said the results are exciting, as they suggest that similar methods may be used to convert the stem cell-derived cartilage cells into robust cartilage sections that can be of clinical usefulness.

Tissue engineers, like those in Athanasiou’s research group, are attempting to unlock the secrets of the human body’s regenerative system to find new ways of growing replacement tissues like muscle, skin, bone and cartilage. Athanasiou’s Musculoskeletal Bioengineering Laboratory at Rice University specializes in growing cartilage tissues.

The idea behind using stem cells for tissue engineering is that these primordial cells have the ability to become more than one type of cell. In all people, there are many types of “adult” stem cells at work. Adult stem cells can replace the blood, bone, skin and other tissues in the body. Stem cells become specific cells based upon a complex series of chemical and biomechanical cues, signals that scientists are just now starting to understand.

Unlike adult stem cells, which can become only a limited number of cell types, embryonic stem cells can theoretically become any type of cell in the human body.

Athanasiou’s group has been one of the most successful in the world at studying cartilage cells and, especially, engineering cartilage tissues. He said that for his research the primary advantage that embryonic stem cells have over adult stem cells is their ability to remain malleable.

“Identifying a readily available cell source has been a major obstacle in cartilage engineering,” Athanasiou said. “We know how to convert adult stem cells into cartilage-like cells. The more problematic issue comes in trying to maintain a ready stock of adult stem cells to work with. These cells have a strong tendency to convert from stem cells into a more specific type of cell, so the clock is always ticking when we work with them.”

By contrast, Athanasiou said his research group has found it easier to grow and maintain a stock of embryonic stem cells. Nonetheless, he is quick to point out that there is no clear choice about which type of stem cell works best for cartilage engineering.

“We don’t know the answer to that,” Athanasiou said. “It’s extremely important that we study all potential cell candidates, and then compare and contrast those studies to find out which works best and under what conditions. Keep in mind that these processes are very complicated, so it may well be that different types of cells work best in different situations.”

Athanasiou began studying embryonic stem cells in 2005. Since funding for the program was limited, he asked two new graduate students in his group if they were interested in pursuing the work as a secondary project to their primary research. Those students, Eugene Koay and Gwen Hoben, are co-authors of the newly published study. Both are enrolled in the Baylor College of Medicine Medical Scientist Training Program, a joint program that allows students to concurrently earn their medical degree from Baylor while undertaking Ph.D. studies at Rice.

The results are available online and slated to appear in the September issue of the journal Stem Cells. The study involved cells from an NIH-sanctioned stem cell line.

The research was funded by Rice University.

news release issued by Rice University.

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