|  Author | Topic: MedTech IV: R & D (Read 7,638 times) |
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|  | Re: MedTech IV: R & D
« Reply #45 on Mar 24, 2010, 9:10am » | |
Walnuts Slow Prostate Tumors in Mice, Study Finds
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New research finds that walnut consumption slows the growth of prostate cancer in mice and has beneficial effects on multiple genes related to the control of tumor growth and metabolism. (Credit: iStockphoto/Nilgun Bostanci)
ScienceDaily (Mar. 23, 2010) — Walnut consumption slows the growth of prostate cancer in mice and has beneficial effects on multiple genes related to the control of tumor growth and metabolism, researchers at UC Davis and the U.S. Department of Agriculture Western Regional Research Center in Albany, Calif. have found.
The study, by Paul Davis, nutritionist in the Department of Nutrition and a researcher with the UC Davis Cancer Center, announced the findings March 22 at the annual national meeting of the American Chemical Society in San Francisco.
Davis said the research findings provide additional evidence that walnuts, although high in fat, are healthful.
"This study shows that when mice with prostate tumors consume an amount of walnuts that could easily be eaten by a man, tumor growth is controlled," he said. "This leaves me very hopeful that it could be beneficial in patients."
Prostate cancer affects one in six American men. It is one in which environmental factors, especially diet, play an important role. Numerous clinical studies have demonstrated that eating walnuts -- rich in omega-3 polyunsaturated fats, antioxidants and other plant chemicals -- decreases the risk of cardiovascular disease. These findings prompted the U.S. Food & Drug Administration in 2004 to approve, for the first time, a qualified health claim for reducing heart disease risk for a whole food.
Davis fed a diet with whole walnuts to mice that had been genetically programmed to get prostate cancer. After 18 weeks, they found that consuming the human equivalent of 2.4 ounces of walnuts per day resulted in significantly smaller, slower-growing prostate tumors compared to mice consuming the same diet with an equal amount of fat, but not from walnuts. They also found that not only was prostate cancer growth reduced by 30 to 40 percent, but that the mice had lower blood levels of a particular protein, insulin-like growth factor (IGF-1), which has been strongly associated with prostate cancer. Additionally, Davis and his research colleagues looked at the effect of walnuts on gene activity in the prostate tumors using whole mouse gene chip technology, and found beneficial effects on multiple genes related to controlling tumor growth and metabolism.
"This is another exciting study from UC Davis nutrition researchers, where truly promising results that have a molecular footprint are having beneficial effects against cancer," said Ralph deVere White, UC Davis Cancer Center director and a prostate cancer researcher. "We have to find a way to get these kinds of studies on nutritional products funded so that we can truly evaluate their effects on cancer patients."
Davis, whose research was funded by a grant to UC Davis from the California Walnut Board, said additional research is needed to further explore how walnuts reduce tumor cell growth.
"The bottom line is that what is good for the heart -- walnuts -- may be good for the prostate as well," he said.
http://www.sciencedaily.com/releases/2010/03/100322153953.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #46 on Mar 25, 2010, 3:08am » | |
Bioengineering: What to make with DNA origami
Chemists looking to create complex self-assembling nanostructures are turning to DNA. Katharine Sanderson looks at the science beneath the fold.
Katharine Sanderson
DNA is the kind of polymer that chemists dream about. Because its complementary sequences can bind to one another, individual molecules of the right sequence will assemble all by themselves into intricate shapes and structures at the nanoscale. DNA can weave together and bind other molecules, allowing it to serve as a scaffold for complex nanomachinery.
DNA nanoengineering is dreamy, but difficult. Researchers have been putting together carefully chosen segments of DNA to form sheets, tubes, even simple machines such as tweezers since the early 1980s. But back then, designing these structures could take months to years. And because researchers were focused on designing them from scratch, they could use only the short segments, no more than 150-base-pairs long, that DNA synthesizers could manufacture. This in turn constrained the size and complexity of the designs. "The problem is that we don't just want to make small stuff, we want to make complicated small stuff, cheaply and easily," says Paul Rothemund, a computational bioengineer at the California Institute of Technology in Pasadena.
Rothemund wondered whether he could create the complicated stuff using a longer, naturally occurring piece of DNA, such as the genome of a virus, and folding it over on itself. So in 2004 and 2005 he spent months, he says, programming in his underpants, trying to work out a way to bend a 7,000-base-pair viral genome to his will. In his design he visualized how the genome could be folded into a predetermined, two-dimensional shape. Knowing the sequence of the virus at every twist and turn, he was able to write complementary DNA sequences, about 16-base-pairs long, that would essentially staple the folds in place. He ordered the 'staples' from a DNA-synthesis company, mixed them with his virus in a buffer that stabilized the DNA and then heated and cooled the mixture, allowing the single stranded viral DNA to bind with the staples (see 'Stapling a smiley'). The result, viewed using atomic-force microscopy, was the smiley face and several other shapes, created by what he called DNA origami1.
![[image]](http://img697.imageshack.us/img697/4933/tmparticlingimport20100.jpg "[image]")
P. W. K. ROTHEMUND
The ease of DNA origami was a breakthrough, dispensing with the intricacies of precise DNA engineering and other metamaterials development. "It's like being able to bake a cake and not pay attention to the ingredient ratios," says Rothemund. But with the right ingredients complex structures can be built with the kind of precision that many people have been looking for. Origami scaffolds, sheets or bricks of folded DNA, are packed with known sequences that could be used to position DNA-binding molecules just a few nanometres apart. And the new, larger structures can contain upwards of 200 sites for affixing such molecules, compared with only a handful on pre-origami structures. This type of precision engineering could be a boon to nanoengineers wanting to position components on nanoelectronic circuits or for bioengineers looking to place proteins in close, accurate proximity to one another.
Now the challenge is to go beyond the novelty of Rothemund's smileys and a dozen or so other demonstration patterns and build structures with a practical purpose. Here's what several researchers are dreaming of doing.
Make a ruler
Rothemund's technique was a door opener for Friedrich Simmel, a biophysicist at the Technical University of Munich in Germany. Suddenly, Simmel says, he was able to have even "rather sloppy" physics students making DNA structures with ease. Simmel has used DNA origami to make a ruler to measure distances between single molecules and calibrate super-high resolution microscopes.
Simmel designed a DNA origami rectangle measuring 100 nm by 70 nm and included some staple strands labelled with fluorescent dye molecules. When the DNA folds, two labelled staples sit at opposite ends of the rectangle in precise locations. This ruler can be used to calibrate high-tech microscopes that can resolve objects smaller than the diffraction limit of light — roughly 200 nm (ref. 2). The kinds of molecules generally used for calibrating such scopes, such as loose pieces of DNA or filamentous proteins, are not ideal because they are flexible and their dimensions can change.
Simmel wants to use the ruler and related structures to help track the movement of molecular motors. Because fluorescent tags allow them to use light microscopy, as opposed to atomic-force microscopy or electron microscopy, researchers will be able to view molecular processes as they happen. That's important, Rothemund says, once scientists begin coupling proteins to DNA origami. Rulers like Simmel's will be useful to watch how those proteins behave.
Build an artificial leaf
DNA origami could allow researchers to put biomolecules together according to specification. A grail of sorts for many engineers working at the nanoscale is photosystem II, a complex of more than 20 protein subunits and accessories that helps to split water into hydrogen ions and oxygen during photosynthesis.
Attempts to recreate photosystem II, or even some of the catalysts involved in electron transport, have been disheartening. DNA origami could provide the scaffold to hold proteins in place, says Hao Yan, a biochemist at Arizona State University in Tempe. As part of a collaboration funded by the US Department of Energy at the university's Center for Bio-Inspired Solar Fuel Production, he has been looking to use DNA origami as the basis for an artificial leaf that makes hydrogen fuel from water.
Yan plans to use a cage-like DNA structure to position the proteins and to bind manganese, a crucial component of the water-oxidation process. The goal is to better direct electron flow in an artificial system that requires precise placement of components. "If we can really control all the electron-transfer sites then we can improve the efficiency," says Yan.
Put a drug in a box
Last year, Kurt Gothelf, director of the Centre for DNA Nanotechnology at Aarhus University in Denmark, and his colleagues, reported that they had made a box from DNA origami3. One strand of DNA holds the lid shut; a separate DNA 'key' springs it open. The invention prompted many to wonder what could be put into the box and subsequently released.
William Shih, a DNA nanotechnologist at Harvard Medical School in Boston, Massachusetts, is keen to exploit this kind of vessel for drug delivery, but the challenges are significant. Getting the box to pass through a cell membrane is going to be difficult, he says. He proposes covering the box with a membrane similar to those sported by some enveloped viruses.
These viruses also have special proteins to facilitate entry. Shih says that he can take viral proteins or related proteins and fix them to the outside of his DNA cages, but he faces a long list of challenges. "There's a lot of stuff," Shih says. "At this point it's just a concept."
Go for gold
Many have talked about using DNA origami as a substrate for nanoelectronic circuitry, such as in plasmonic devices.
Plasmonic devices couple light waves with charges on a metal surface and offer the speed of information transfer that light provides, but at sizes smaller than those to which technologies such as fibre optics are limited. Current lithographic techniques run into trouble when trying to arrange metallic materials such as gold into patterns with features smaller than about 100 nm in size. Rothemund says that gold spheres might be positioned using DNA origami to make structures with better optical qualities.
“Now we've got DNA origami lined up like little ducks in a row.”
He has already taken steps, in concert with IBM Almaden in San Jose, California, towards arranging metal nanoparticles. Last year they managed to arrange DNA triangles on a lithographically patterned surface4. Jennifer Cha from IBM and her colleagues subsequently showed that they could place gold nanoparticles smaller than 10 nm onto each origami structure by affixing strands of DNA to the gold that were complementary to loose ends on the DNA triangles5. The work is still quite crude, says Rothemund. They haven't got an active device yet. "Much of the next five years will be spent perfecting techniques to place DNA origami on surfaces where we want them and making this technique widely available to other scientists," he says. Importantly, they've tacked down the shapes rather than having them "bobbing around like jellyfish in solution", says Rothemund. "I didn't think anyone would solve that problem in ten years. Now we've got DNA origami lined up like little ducks in a row."
Pushing past smileys
The grand schemes go on. Researchers imagine an artificial ribosome capable of building custom enzymes, a matrix for supporting artificial organs, or a DNA origami network designed to support a neuronal network connected to electrical circuitry. Researchers are attempting all of these, but they will face some serious hurdles. Buffer solutions must be finely tuned, otherwise structures fall apart. And large, complicated structures can take up to a week to fold completely.
Change is needed to the basic, almost slapdash synthesis approach of using unpurified DNA that isn't adequately sequenced, says Shih, "just because we got away with it so far doesn't mean we want to get away with it forever".
But as long as this growing group of researchers keeps trying to make different shapes, other applications will appear. Rothemund can't predict quite how, though. "The problem is that you can do all these little cool things but they in no way form a whole system. It's not exactly clear what kinds of systems we're going to be able to build."
He's working hard to find out. "In the past six months, I've mostly been back at home, coding in my underwear again, which hopefully means good things are happening."
* References
1. Rothemund, P. W. K. Nature 440, 297-302 (2006).
2. Steinhauer, C., Jungmann, R., Sobey, T. L., Simmel, F. C. & Tinnefeld, P. Angew. Chem. Int. Edn 48, 8870-8873 (2009).
3. Andersen, E. S. et al. Nature 459, 73-76 (2009).
4. Kershner, R. J. et al. Nature Nanotech. 4, 557-561 (2009).
5. Hung, A. M. et al. Nature Nanotech. 5, 121-126 (2009).
http://www.nature.com/news/2010/100310/full/464158a.html
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #47 on Mar 26, 2010, 10:46pm » | |
Surgeons Transplant New Trachea Into Child Using His Own Stem Cells to Rebuild Airway
![[image]](http://img709.imageshack.us/img709/16/100325114400large140475.jpg "[image]")
Still image from a video showing a visualization of the transplantation operation using the new trachea. (Credit: Paolo Macchiarini)
ScienceDaily (Mar. 25, 2010) — UCL scientists and surgeons have led a revolutionary operation to transplant a new trachea into a child, using the child's own stem cells to rebuild the airway in the body.
The operation -- a world first -- involved laboratory-based scientists and hospital-based clinicians working in partnership with colleagues in Europe to treat a 10-year-old British boy.
The boy, who has not been named, is recovering from surgery but his condition is stable and he is breathing unaided.
He was born with a rare condition called Long Segment Tracheal Stenosis -- a tiny windpipe that does not grow and restricts breathing.
Shortly after birth, he underwent a conventional trachea transplant at Great Ormond Street Hospital for Children (GOSH), but his condition deteriorated last November when a metal stent implanted in that operation began to erode into the aorta, a key artery, causing severe bleeding.
Scientists and surgeons at UCL, GOSH, the Royal Free Hampstead NHS Trust, and the Careggi University Hospital in Florence, Italy, developed a new technique to treat the life-threatening condition.
They stripped cells from a donated trachea, used it to replace the entire length of the damaged airway, and then used the child's own bone marrow stem cells to seal the airway in the body.
Dr Mark Lowdell, Director of Cellular Therapy at Royal Free Hospital and a senior lecturer at UCL Medical School, received the donor trachea from Italy and some bone marrow from the patient at the beginning of surgery.
He and his colleagues prepared two different types of stem cells from the bone marrow together with some growth signalling chemicals and returned them to GOSH with the donor trachea.
Professor Paolo Macchiarini, from Careggi University Hospital, who is an Honorary Consultant at GOSH and Honorary Professor at UCL, applied the cells and the growth factors to the trachea in the operating theatre.
Martin Elliot, Professor of Cardiothoracic Surgery at UCL and Director of the Tracheal Service at GOSH, led the operation to repair the damaged aorta and implant the new trachea.
The application of this technology -- which has never been used on a child before -- should reduce greatly the risk of rejection of the new trachea, as the child's stem cells will not generate any immune response.
Professor Martin Birchall, UCL lead for translational regenerative medicine, who is also a head and neck surgeon specialising in airways and voice, led on ethics and regulatory approvals.
Professor Birchall and Professor Macchiarini achieved the world's first stem cell-based organ transplant on an adult patient in 2008.
Since moving to a Chair at the UCL Ear Institute in 2009, Professor Birchall has developed a research programme with Professor Elliott which includes, for example, the absorbable stent (supporting tube) used in this 10-year-old patient.
When the patient presented to Professor Elliott, Professor Birchall pulled together the various team members into a functional unit capable of delivering a stem cell implant as quickly as possible.
He said: "Professor Macchiarini's seminal work, together with the UCL team, has now saved the life of two adults and one child. We have shown that stem cell-based treatments can save lives and can be used in the creation of living structures which draw upon the body's own natural healing mechanisms for their support.
"The step-wise progression in technique from first patient to the present has delivered a highly streamlined, rapid process. This means that such treatments potentially can be moved out of the hands of a tiny number of specialist centres into many hospitals around the world, including those in developing countries."
http://www.sciencedaily.com/releases/2010/03/100325114400.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #48 on Mar 26, 2010, 10:54pm » | |
Playing 'Pong' With the Blink of an Eye
![[image]](http://img682.imageshack.us/img682/1623/100326101113large188401.jpg "[image]")
Imperial student demonstrates how neurotechnology works. (Credit: Image courtesy of Imperial College London)
ScienceDaily (Mar. 26, 2010) — University students have developed a computer game that is operated by eye movements, which could allow people with severe physical disabilities to become 'gamers' for the first time.
The students, from Imperial College London, have adapted an open source game called 'Pong', where a player moves a bat to hit a ball as it bounces around the screen. The adaptation enables the player to move the bat using their eye.
To play the game, the user wears special glasses containing an infrared light and a webcam that records the movement of one eye.
The webcam is linked to a laptop where a computer program syncs the player's eye movements to the game.
The prototype game is very simple but the students believe that the technology behind it could be adapted to create more sophisticated games and applications such as wheelchairs and computer cursors controlled by eye movements.
One of the major benefits of the new technology is that it is inexpensive, using off-the-shelf hardware and costing approximately £25 to make.
Eye movement systems that scientists currently use to study the brain and eye motion cost around £27,000, say the researchers.
Dr Aldo Faisal, the team's supervisor from the Department of Computing and the Department of Bioengineering at Imperial College London, says:
"Remarkably, our undergraduates have created this piece of neurotechnology using bits of kit that you can buy in a shop, such as webcams. The game that they've developed is quite simple, but we think it has enormous potential, particularly because it doesn't need lots of expensive equipment. We hope to eventually make the technology available online so anyone can have a go at creating new applications and games with it and we're optimistic about where this might lead. We hope it could ultimately provide entertainment options for people who have very little movement. In the future, people might be able to blink to turn pages in an electronic book, or switch on their favourite song, with the roll of an eye."
Mr Ian Beer, who is a third year undergraduate from the Department of Computing, adds: "This game is just an early prototype, but we're really excited that from our student project we've managed to come up with something that could ultimately help people who have really limited movement. It would be fantastic to see lots of people across the world creating new games and applications using our software."
Researchers in Dr Faisal's lab are now refining the technology so that it can monitor movements in both eyes. This would enable a user to carry out more complicated tasks such as plotting a journey on screen. This might ultimately allow them to use eye movements to steer a motorised wheelchair.
Student team includes: William Abbot, Department of Biomedical Engineering; Oliver Rogers, Department of Maths and Department of Computing; Tim Treglown, Department of Maths and Department of Computing; Aaron Berk, Department of Computing; Ian Beer, Department of Computing.
A video demonstrating how the computer game works can be downloaded and embedded from YouTube: http://www.youtube.com/watch?v=9gU8RqttXeo
http://www.sciencedaily.com/releases/2010/03/100326101113.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #49 on Mar 26, 2010, 10:57pm » | |
Your Fat May Help You Heal: Researcher Extracts Natural Scaffold for Tissue Growth
![[image]](http://img138.imageshack.us/img138/5378/1003251430592076340.jpg "[image]")
Adipogel forms a viscous droplet when isolated on a petri dish. After further processing, it can be used as a natural extracellular matrix to support new tissue growth. (Credit: N. Sharma)
ScienceDaily (Mar. 26, 2010) — It frequently happens in science that what you throw away turns out to be most valuable. It happened to Deepak Nagrath, but not for long.
The Rice assistant professor in chemical and biomolecular engineering was looking for ways to grow cells in a scaffold, and he discarded the sticky substance secreted by the cells.
"I thought it was contamination, so I threw the plates away," said Nagrath, then a research associate at Harvard Medical School.
That substance, derived from adipose cells -- aka body fat -- turned out to be a natural extracellular matrix, the very thing he was looking for.
Nagrath, who joined Rice in 2009, and his co-authors have since built a biological scaffold that allows cells to grow and mature. He hopes the new material, when suffused with stem cells, will someday be injected into the human body, where it can repair tissues of many types without fear of rejection.
The research by Nagrath and his co-authors appeared last week in the Federation of American Societies for Experimental Biology (FASEB) Journal.
The basic idea is simple: Prompt fat cells to secrete what bioengineers call "basement membrane." This membrane mimics the architecture tissues naturally use in cell growth, literally a framework to which cells attach while they form a network. When the cells have matured into the desired tissue, they secrete another substance that breaks down and destroys the scaffold.
Structures that support the growth of living cells into tissues are highly valuable to pharmaceutical companies for testing drugs in vitro. Companies commonly use Matrigel, a protein mixture secreted by mouse cancer cells, but for that reason it can't be injected into patients.
"Fat is one thing that is in excess in the body. We can always lose it," Nagrath said. The substance derived from the secretions, called Adipogel, has proven effective for growing hepatocytes, the primary liver cells often used for pharmaceutical testing.
"My approach is to force the cells to secrete a natural matrix," he said. That matrix is a honey-like gel that retains the natural growth factors, cytokines (substances that carry signals between cells) and hormones in the original tissue.
Nagrath's strategy for growing cells isn't the only approach being pursued, even at Rice: Another method reported last week in Nature Nanotechnology uses magnetic levitation to grow three-dimensional cell cultures.
But Nagrath is convinced his strategy is ultimately the most practical for rebuilding tissue in vivo, and not only because it may cost significantly less than Matrigel. "The short-term goal is to use this as a feeder layer for human embryonic stem cells. It's very hard to maintain them in the pluripotent state, where they keep dividing and are self-renewing," he said.
Once that goal is achieved, Adipogel may be just the ticket for transplanting cells to repair organs. "You can use this matrix as an adipogenic scaffold for stem cells and transplant it into the body where an organ is damaged. Then, we hope, these cells and the Adipogel can take over and improve their functionality."
Nagrath's co-authors are Nripen S. Sharma, a research associate at Rutgers University, and Martin Yarmush, the Helen Andrus Benedict Professor of Surgery and Bioengineering at Harvard Medical School.
The National Institutes of Health and the Shriners Hospitals for Children supported their research.
Journal Reference:
1. Sharma et al. Adipocyte-derived basement membrane extract with biological activity: applications in hepatocyte functional augmentation in vitro. The FASEB Journal, 2010; DOI: 10.1096/fj.09-135095
http://www.sciencedaily.com/releases/2010/03/100325143059.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #50 on Apr 1, 2010, 12:31am » | |
Scientists Reverse Alzheimer's-Like Memory Loss in Fruit Flies
![[image]](http://img88.imageshack.us/img88/3669/100329152521large970828.jpg "[image]")
In a new study, neuroscientists succeeded in preventing memory loss in fruit flies caused by brain plaques similar to those thought to cause Alzheimer's disease in humans (Credit: iStockphoto)
ScienceDaily (Mar. 30, 2010) — By blocking the cellular signaling activity of a protein, a team of neuroscientists at Cold Spring Harbor Laboratory (CSHL) has prevented memory loss in fruit flies caused by brain plaques similar to those thought to cause Alzheimer's disease in humans. The study also resolves a long-standing controversy about the role of this protein, PI3 kinase, which was previously thought to have a protective function against the disease.
"Our work suggests that the peptides, or fragments, of β-amyloid associated with Alzheimer's disease directly increase the activity of PI3 kinase, which in turn causes memory loss and increases the accumulation of plaque in the brain," explains CSHL Professor Yi Zhong, who led the research team. The study appears online, ahead of print, March 29 in the Proceedings of the National Academy of Sciences.
β-amyloid peptides are known to alter a slew of cellular signaling proteins such as PI3 kinase, causing a wide range of cellular dysfunctions within the brain's neurons, thus impairing brain activity. But exactly how these dangerous peptides cause signaling havoc and trigger memory loss has been a mystery, largely because such studies have been performed in cultured cells, not in living organisms.
Zhong and his colleagues addressed the question in a biological system that closely recapitulates the disease pathology seen in humans: fruit flies engineered to produce human β-amyloid in their brains. The team previously showed that these flies develop many key features of Alzheimer's, including age-dependent memory loss, massive neurodegeneration, β-amyloid deposits and plaque accumulation.
Searching for the molecular basis of memory loss, the team discovered the importance of PI3-kinase by studying a type of neurotransmission called long-term depression (LTD), in which nerve signal transmissions at particular synapses, or junctions between nerve cells, is depressed for an extended period, usually lasting hours. LTD is known to be pathologically enhanced when β-amyloid is present in fly brain.
The team has now found that LTD enhancement in the β-amyloid-producing flies is due to increased activity of PI3-kinase. A reduction of this activity via injections of PI3 kinase-blocking drugs or by switching off the gene that encodes PI3 kinase both restored normal LTD signals. With these measures, the team not only improved memory in aging fruit flies, but also decreased the buildup of β-amyloid deposits.
These findings on β-amyloid's effect on PI3 kinase activity might explain another mystery about the disease. Among patients, the disease is sometimes known as "brain diabetes" because brain tissue gradually becomes resistant to insulin, further impairing brain function. Insulin is one of the molecules that normally induce PI3-kinase activity, which in turn mediates the cell's response to insulin.
"Our results now suggest that the Alzheimer's brains might become insulin-resistant because PI3 kinase activity is already at the maximum due to its activation by β-amyloid and therefore is no longer able to respond to insulin," explains Zhong. "It might be possible to tackle these various disease symptoms by targeting PI3 kinase."
This work was supported in part by grants from the National Institutes of Health and the U.S. Army Neurofibromatosis Research Program.
Journal Reference:
1. Hsueh-Cheng Chiang, Lei Wang, Zuolei Xie, Alice Yau, and Yi Zhong. PI3 kinase signaling is involved in A%u03B2-induced memory loss in Drosophila. Proceedings of the National Academy of Sciences, 2010; DOI: 10.1073/pnas.0909314107
http://www.sciencedaily.com/releases/2010/03/100329152521.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #51 on Apr 3, 2010, 7:11pm » | |
Beta-blockers 'cut cancer spread'
Blood pressure drugs may be able to reduce the ability of breast cancer to spread around the body, researchers have told a European conference.
A joint UK and German study found that cancer patients taking beta-blockers had a lower risk of dying.
The drugs may block hormones that trigger the spread of cancer cells.
However, experts stressed that more evidence from bigger studies would be needed before the drug could be given as part of routine treatment.
Breast cancer, which affects more than 30,000 people in the UK each year, is most easily tackled when tumours are confined to the breast only.
When cancer cells migrate to other parts of the body, and start growing, a process known as metastasis, the likelihood of successful treatment begins to fall.
The biological processes which trigger metastasis are still not fully understood.
The latest research, presented at the European Breast Cancer Conference in Barcelona, builds on earlier laboratory studies which suggest that the ability of cancer cells to increase in number and spread is boosted by the presence of stress hormones.
Beta-blockers attach themselves to the same receptors on cancer cells used by these hormones, potentially reducing their ability to stimulate the cell and trigger spread.
They are already taken by approximately two million people in the UK.
To test this theoretical cancer-fighting ability, Dr Des Powe, from Queen's Medical Centre, Nottingham, in collaboration with Professor Frank Entschladen from Witten University in Germany, looked at three groups of breast cancer patients, a total of 466 people.
The first group had high blood pressure, also called hypertension, and were taking beta-blockers, the second had high blood pressure, but were taking something different for it, while the third had no blood pressure problems.
In the 43 who were taking beta-blockers, there was a significant reduction in both cancer metastasis, and new tumours within the breast. Overall they had a 71% lower chance of dying from breast cancer compared with the other groups.
Small-scale research
Dr Powe said: "It is reasonable to speculate, therefore, that some non-hypertensive women with breast cancer will respond favourably to beta-blocker treatment, though doses and side-effects would need to be investigated in clinical trials."
However, he said that the study was "relatively small" and its results would need to be reproduced in a larger group of patients.
"We are very encouraged by these first results which have already shown that by using a well-established, safe and cost effective drug, we can take another step on the road towards targeted therapy in breast cancer."
Meg McArthur, from Breakthrough Breast Cancer, welcomed the findings: "Although this is early stage research, these results show that beta blockers could play a role in reducing the risk of metastatic breast cancer. This is a positive step forward as it could potentially lead to survival improvements for people affected with this condition.
"However, as the study is quite small, we would like to see further research in this area."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8589066.stm
Published: 2010/03/26 12:47:03 GMT
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #52 on Apr 3, 2010, 7:12pm » | |
Prostate cancer prevention clue
A drug already used in men with enlarged prostates seems to cut the risk of prostate cancer developing, a large international study has shown.
A four-year trial in more than 6,500 men found those who took dutasteride had a 23% lower risk of prostate cancer than those who took a dummy pill.
The men in the study, published in the New England Journal of Medicine, were all at high risk of the disease.
UK experts welcomed the results but said longer-term research was needed.
It is not the first time that this class of drugs has been found to have potential effects on the prevention of prostate cancer.
In 2003, researchers showed a similar drug, finasteride, cut the risk of prostate cancer by a quarter in healthy men but also found that the tumours that were detected were more aggressive.
Both drugs are prescribed in men who have an enlarged but benign prostate gland - an extremely common condition that happens with age and can cause symptoms such as frequent and painful urination.
High-risk patients
The latest trial, which was funded by GlaxoSmithKline which makes dutasteride, looked at men aged between 50 and 75 years who were high risk for prostate cancer because they had high PSA scores - a blood test which may indicate disease - but had been found not to have prostate cancer.
They were treated with a daily dose of dutasteride or a dummy pill.
Over the study, prostate cancer was found in 659 of the men taking the drug and 858 of the men taking a placebo.
Among men with a family history of prostate cancer, the drug reduced the relative risk of a prostate cancer diagnosis by 31.4%.
The researchers believe that most of the tumours detected during the trial - which tended to be moderately aggressive - would have been present from the beginning but were too small to be detected.
They say this supports the idea that the drug shrinks early prostate tumours or prevents them from growing to a size at which they would be detected and need treatment.
Study leader Dr Gerald Andriole, chief of urologic surgery at Washington University School of Medicine, said the drug might potentially offer thousands of men a chance to reduce their risk of the disease.
"This means more men could avoid unnecessary treatment for prostate cancer along with the costs and harmful side effects that can occur with treatment."
The National Institute for Health and Clinical Excellence (NICE) are already looking into whether dutasteride should be used for prostate cancer prevention and are due to report later this year.
Martin Ledwick, Cancer Research UK's head information nurse, said the results in the high risk population were interesting.
But he added: "Further research to see if the effects are maintained in the longer term is an important next step."
Dr Helen Rippon, head of research management at The Prostate Cancer Charity, agreed: "Of course, we don't yet know what will happen to these men in the coming years and whether they will still go on to develop the disease and it will be many years before we know if the drug can provide any long-term benefit to men."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8597157.stm
Published: 2010/03/31 23:01:49 GMT
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #53 on Apr 3, 2010, 7:13pm » | |
Sleeping sickness 'breakthrough'
Scientists say they have identified a potential treatment for sleeping sickness, a killer disease that infects about 60,000 people in Africa a year.
British and Canadian experts say drugs could attack an enzyme the parasite causing the illness needs to survive.
They say the orally-administered drug could be ready for human clinical trials in about 18 months.
The disease, spread by the bite of a tsetse fly, is caused by a parasite attacking the central nervous system.
It has similar symptoms to malaria, making it difficult to diagnose. Left untreated, it moves to the spinal column and brain, resulting in mental confusion and eventual death.
Fatal side effects
The "breakthrough" came at the University of Dundee in Scotland, where scientists were funded to research diseases neglected by major drugs companies.
Professor Paul Wyatt, director of the programme, said: "This is one of the most significant findings made in recent years in terms of drug discovery and development for neglected diseases."
He said the research, published in the journal Nature, represented "significant strides" in the development of a full blown drug against the disease.
The World Health Organization estimates there are between 50,000 and 70,000 cases of the disease a year, with a further 60 million people at risk of infection.
The research in Dundee was backed by partners at the University of York in England and the Structural Genomics Consortium in Toronto, Canada.
The two drugs currently available to treat sleeping sickness both have associated problems.
One is arsenic-based with side effects that kill one in 20 patients and the other - eflornithine - is costly, only partially effective and requires prolonged hospital treatment, the scientists said.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/africa/8597774.stm
Published: 2010/03/31 23:40:45 GMT
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #54 on Apr 5, 2010, 12:21am » | |
Pig cells give hope for diabetes cure
By Brigid Glanville in Auckland
Posted 3 hours 19 minutes ago
There is renewed hope of a cure for type 1 diabetes after successful human trials involving pig cells.
In New Zealand and Europe more than a dozen humans have had pigs cells transplanted into their bodies to control diabetes.
So far two patients have been able to stop using insulin.
The trial is now being considered in Australia.
Michael Helyer, 54, has had type 1 diabetes since he was a child, but 14 years ago became the first man in the world to have pig cells transplanted into his pancreas.
The cells were designed to mimic the body's natural production of insulin.
"At peak performance my cells were producing 30 per cent of my requirement," he said.
"What that means is that you can reduce your insulin dose by 30 per cent. Your chances of having a terrible low blood sugar episode are much diminished."
The cells continued to work inside Mr Helyer's body for nine years.
As the first human to be trialed, the number of cells transplanted was very small. But some of the recent transplant patients have been able to stop using insulin altogether.
Professor Bob Elliot, a researcher with Living Cell Technologies, says patients were transplanted up to three times without problems.
"To our delight we got more success in terms of efficacy than we expected," he said.
"Out of the eight [people] that we did, a couple came off insulin for varying periods of time up to many, many months."
Type 1 diabetes effects 30 million people worldwide. Professor Elliot and his team of researchers hope this could be a cure.
"What we're more interested in as a shorter-term objective is to improve diabetes control," he said.
There has been concern though that this treatment could result in the transmission of viruses from pigs to humans.
It caused Australian authorities to place a ban on pig cell transplants, but that ban has now been lifted.
"The pigs used must be free of any disease that's capable of being transmitted to man," Professor Elliot said.
"By good fortune we lit upon a herd of pigs that had been abandoned in a sub-Antarctic island some 200 years ago, and in that 200 years they have lost any form of infection capable of being transmitted to man.
"The pigs we used are derived from those. They're not currently housed on that island, they're housed in a very special containment facility which keeps that nice pristine, infection-free, bug-free status."
With no moratorium in place, Living Cell Technologies hopes to conduct more human trials in Australia by the end of the year.
http://www.abc.net.au/news/stories/2010/04/05/2864294.htm?section=world
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #55 on Apr 6, 2010, 7:24pm » | |
Blocking gene boosts radiotherapy
A gene which hinders the ability of radiotherapy to kill cancer cells has been detected by UK researchers.
The team found that if they blocked the POLQ gene - which has a role in repairing damaged DNA - radiotherapy was more effective.
It is hoped that the discovery, which came about after a trawl through 200 candidate genes, could lead to new drugs to boost radiotherapy.
The findings are published in the journal Cancer Research.
Many thousands of cancer patients will have some form of radiotherapy as part of their treatment, and it is estimated to contribute to 40% of cases where cancer is eliminated.
The researchers from the University of Oxford said tumours can differ widely in the way they respond to radiotherapy - but the reasons for these differences are largely unknown.
In order to find a potential target for increasing the chances that radiotherapy would work, they looked specifically at genes involved in repairing DNA damage.
After pinpointing the POLQ gene, they found that blocking it in several different types of cancer cell in the laboratory, including laryngeal and pancreatic tumours, rendered the cells more vulnerable to the effects of radiation.
Selective
Previous research had shown that the POLQ gene is not particularly active in normal healthy tissue.
Doing the same experiment in healthy cells, the team found that blocking the gene did not have any effect on the sensitivity of normal tissue to radiation.
The researchers said the fact that the POLQ seemed to more abundant in cancer cells than normal cells made it a good target for boosting the effects of radiotherapy.
Study leader Dr Geoff Higgins, a Cancer Research UK scientist at the Gray Institute for Radiation Oncology and Biology, said: "We've sieved through a vast pool of promising genetic information and identified a gene that could potentially be targeted by drugs to improve the effectiveness of radiotherapy.
"Blocking the activity of this gene resulted in a greater number of tumour cells dying after radiotherapy and provides new avenues for research."
Professor Gillies McKenna, director of the institute, added: "The next stage is to translate this discovery into a treatment that will benefit patients."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8596797.stm
Published: 2010/04/02 23:00:34 GMT
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #56 on Apr 10, 2010, 1:58am » | |
Significant Findings About Protein Architecture May Aid in Drug Design, Generation of Nanomaterials
ScienceDaily (Apr. 9, 2010) — Researchers in Singapore are reporting this week that they have gleaned key insights into the architecture of a protein that controls iron levels in almost all organisms. Their study culminated in one of the first successful attempts to take apart a complex biological nanostructure and isolate the rules that govern its natural formation.
The Nanyang Technological University team's work on the protein ferritin, the results of which appear in this week's issue of the Journal of Biological Chemistry, is expected to have significant ramifications on the fields of drug design and nanomaterials.
"Engineering the structure of a protein is one of the ultimate dreams of structural biologists," wrote one of the journal's peer reviewers, "and approaching that dream is greatly enabled through studies aimed at finding out what governs the nanoarchitecture of the protein."
Brendan P. Orner, the assistant professor who oversaw the team's work, described the protein ferritin as a potential model for explaining complicated protein structure in general.
Across the biological kingdoms, ferritin regulates the distribution of iron, which is necessary for a number of cellular functions but also forms reactive ions that can be lethal to cells. Shaped like a spherical nanocage, ferritin is made up of 24 proteins, and it sequesters the reactive iron ions in its hollow interior. In humans, ferritin prevents iron deficiency and overload.
"The rules that govern self-assembling nanosystems, like the ferritin model, are poorly understood," Orner explained. "We systematically analyzed the interactions between the 24 ferritin units that make up the nanocage and identified the hot spots that are crucial to the cage's formation."
Their goal was to discover which amino acids are responsible for assembling the cage, and they found that it is possible to both disassemble ferritin by removing single side chains of amino acids and, surprisingly, to stabilize the structure by removing other side chains.
Understanding the assembly of the nanocage could open the door to drug design that will disrupt the structure and function of defective proteins that cause or contribute to disease. It also may aid in the creation of biological nanostructures in which scientists can grow special particles and materials with a variety of properties and applications.
"Cell biology provides many structures that are on the nanoscale and have amazing complexity and symmetry," Orner said. "The problem is that many of these structures are, like ferritin, self-assembled proteins, and, if we are going to use them for nanomaterials applications, we need to understand the fundamentals that make them form this way naturally."
Orner and his team members are particularly interested in growing nanoparticles of precise dimensions inside ferritin shells. Already, they have developed a new method to grow gold nanoparticles in them.
"Slight deviations in size or shape can radically change nanoparticles' properties, particularly in the case of metals and semiconductors," Orner said. "Our ferritin proteins are hollow, so, when we grow mineral or metal clusters inside them, the growth stops when the nanoparticles reach the limits of the protein shell."
By studying the rules that control the folding and assembly of such a protein in nature, Orner said, the investigators hope to be able to manipulate them one day to create new proteins with novel sizes and shapes and, therefore, generate nanoparticles of novel sizes and shapes inside them.
"Those nanoparticles could be used for in-vitro assays to do high-throughput drug screening of some protein-protein interactions involved in virus infection and cancer, for example," he said.
Orner's team included doctoral students Yu Zhang and Rongli Fan, undergraduate students Siti Raudah, Huihian Teo and Gwenda Teo, and scholar Xioming Sun. Their research was funded by the Singapore Ministry of Education and Nanyang Technological University.
Their resulting article has been named a "Paper of the Week" by the Journal of Biological Chemistry, putting it in the top 1 percent of papers reviewed by the editorial board in terms of significance and overall importance.
Journal Reference:
1. Zhang et al. Alanine-shaving Mutagenesis to Determine Key Interfacial Residues Governing the Assembly of a Nano-cage Maxi-ferritin. Journal of Biological Chemistry, 2010; 285 (16): 12078 DOI: 10.1074/jbc.M109.092445
http://www.sciencedaily.com/releases/2010/04/100409105403.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #57 on Apr 10, 2010, 2:03am » | |
Tiny Worms Employed to Unlock Keys to Herbal Medicines
ScienceDaily (Apr. 9, 2010) — A team of researchers at the University of Maryland, Baltimore (UMB), writing in the science journal PLos ONE, have developed a biologic method to tease out which compounds from herbal medicines and medicinal herbal mixtures produce their reputed medicinal benefits.
"This provides the first step to find, from all of the hundreds of compounds in herbs, which ones have potential for medicinal purposes. And you can do this very quickly and efficiently," said co-author Laura Dosanjh, graduate student with the School of Pharmacy at UMB.
Science has not been very helpful in determining the efficacy of herbal medicines in the United States. The U.S. Food and Drug Administration, for example, has so far sided with science only once to approve an herb-based treatment with multiple active ingredients -- an ointment for genital warts made from green tea leaves.
Now, using tiny worms that live only 20 days, the team sorted out which compounds found in two common Chinese herbal formulations showed most potential for their stated purpose: extending life expectancy.
Cinnamon and ginseng won, showing the most promise.
A team led by Yuan Luo PhD, MS, associate professor at the School, conducted a first-of-its- kind, "systematic evaluation" of a mixture of 10 herbs called Shi-Quan-Da-Bu-Tang (SQDB), reportedly effective for fatigue and energy; and an 11-herb formula called Huo Luo Xiao Ling Dan (HLXL) used as a the treatment of arthritic joint pain. Both mixtures are reputed to have benefits for healthy living and longevity in humans.
The researchers tested the mixtures, as well as each separate herb in them, on the laboratory worm model C. elegans. This particular worm─which biochemists often use as their 'lab rat'─ shares genes for aging and other traits with humans and other organisms.
Cinnamon bark (Cinnamomum cassia) from HLXL extended life span of the worms by 14.5 percent and cinnamon bark from SQDB extended the life 10.8 percent.
Ginseng root (Panax ginseng) from SQDB extended life span by 7.7 percent. Ginseng is not an ingredient in HLXL.
Significantly, cinnamon, ginseng, and SQDB also thinned out levels of hydrogen peroxide, which can destroy cells. They each also enhanced expression of small heat shock proteins, an indicator for cellular response to stress that plays an important role in maintenance of cell functions.
Furthermore, the life span-extending herbs appreciatively reduced in the expression in C. elegans of a toxicity factor, amyloid, which is a hallmark in the human brain of pathological development of Alzheimer's disease.
In a 1998 national survey published in the Journal of American Medical Association, 49 percent of American adults said they had used herbal medicines within the previous year. However, proof of efficacy of herbal medicines, even their modes of action in the body, are extremely difficult challenges, said, Luo.
Herbal medicines are usually mixtures of herbs. That presents a severe challenge for the Food and Drug Administration to understand which compounds or combinations of compounds in the herbs are effective or not effective.
Said Dosanjh, "Because it's very difficult to sort out so many herbs with so many constituents together, we needed to find a model. And there is a high level of [common genetic origins] with the nematode and humans."
Luo added, "To isolate a single compound from an herb and test it for a medical condition, it often doesn't work; not like the whole herb works."
In recent years, scientists have learned to use C. elegans worm as a model system in for studying gene-environment interactions. In their experiments, the School of Pharmacy researchers first used "wild" C. elegans to screen the herbal mixtures and single herbs. They determined which herbs aided lifespan of the worms, then tested those herbs on well-characterized mutant worms. Each mutant was missing a single gene known for lifespan and/or stress resistance. C. elegans is valuable to science because its very short life cycle is suitable for conducting rapid experiments and between 60 to 80 percent of the 20,000 genes in C. elegans genome have similar origins to human genes. The genes are found consistently along the evolutionary paths including the worms and humans.
"The good news is that this is a way of testing to show the medicinal effect. It is now testable. We have statistical evidence for the first time in C. elegans for a multi-compound drug," said Luo. "Most [scientists] are not using whole organisms for screening herbs. This is simple and clean, it is a system to look at specific genes. Now we have to further validate the human relevancy.
The School of Pharmacy study was published in the Feb. 2010 issue of PLoS ONE, Vo. 5.
Journal Reference:
1. Young-Beob Yu, Laura Dosanjh, Lixing Lao, Ming Tan, Bum Sang Shim, Yuan Luo Dosanjh Laura. Cinnamomum cassia Bark in Two Herbal Formulas Increases Life Span in Caenorhabditis elegans via Insulin Signaling and Stress Response Pathways. PLoS ONE, 22 Feb 2010 DOI: 10.1371/journal.pone.0009339
http://www.sciencedaily.com/releases/2010/03/100329082009.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #58 on Apr 10, 2010, 2:05am » | |
DNA Nanotechnology: 'Magic Bullets' Breakthrough Offers Promising Applications in Medicine
![[image]](http://img697.imageshack.us/img697/5548/1003171619503010903.jpg "[image]")
Researchers have created the first examples of DNA nanotubes that encapsulate and load cargo, and then release it rapidly and completely when a specific external DNA strand is added. (Credit: Image courtesy of McGill University)
ScienceDaily (Apr. 9, 2010) — A team of McGill Chemistry Department researchers led by Dr. Hanadi Sleiman has achieved a major breakthrough in the development of nanotubes -- tiny "magic bullets" that could one day deliver drugs to specific diseased cells. Sleiman explains that the research involves taking DNA out of its biological context. So rather than being used as the genetic code for life, it becomes a kind of building block for tiny nanometre-scale objects.
Using this method, the team created the first examples of DNA nanotubes that encapsulate and load cargo, and then release it rapidly and completely when a specific external DNA strand is added. One of these DNA structures is only a few nanometres wide but can be extremely long, about 20,000 nanometres. (A nanometre is one-10,000th the diameter of a human hair.)
Until now, DNA nanotubes could only be constructed by rolling a two-dimensional sheet of DNA into a cylinder. Sleiman's method allows nanotubes of any shape to be formed and they can either be closed to hold materials or porous to release them. Materials such as drugs could then be released when a particular molecule is present.
One of the possible future applications for this discovery is cancer treatment. However, Sleiman cautions, "we are still far from being able to treat diseases using this technology; this is only a step in that direction. Researchers need to learn how to take these DNA nanostructures, such as the nanotubes here, and bring them back to biology to solve problems in nanomedicine, from drug delivery, to tissue engineering to sensors," she said.
The team's discovery was published on March 14, 2010 in Nature Chemistry. The research was made possible with funding from the National Science and Engineering Research Council and the Canadian Institute for Advanced Research.
Journal Reference:
1. Pik Kwan Lo, Pierre Karam, Faisal A. Aldaye, Christopher K. McLaughlin, Graham D. Hamblin, Gonzalo Cosa & Hanadi F. Sleiman. Loading and selective release of cargo in DNA nanotubes with longitudinal variation. Nature Chemistry, 14 March 2010 DOI: 10.1038/nchem.575
http://www.sciencedaily.com/releases/2010/03/100317161950.htm
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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Big Bunny
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| | Re: MedTech IV: R & D
« Reply #59 on Apr 10, 2010, 5:19pm » | |
Inkjet-like device "prints" cells right over burns
By Maggie Fox, Health and Science Editor
Posted 2010/04/09 at 9:51 am EDT
WINSTON-SALEM, North Carolina, Apr. 9, 2010 (Reuters) — Inspired by a standard office inkjet printer, U.S. researchers have rigged up a device that can spray skin cells directly onto burn victims, quickly protecting and healing their wounds as an alternative to skin grafts.
![[image]](http://img411.imageshack.us/img411/3431/20100409t135118z01btre6.jpg "[image]")
An undated software screen grab of a device used to bioprint skin cells onto burns. Inspired by a standard office inkjet printer, U.S. researchers have rigged up a device that can spray skin cells directly onto burn victims, quickly protecting and healing their wounds as an alternative to skin grafts. REUTERS/Wake Forest Institute of Regenerative Medicine/Handout
They have mounted the device, which has so far only been tested on mice, in a frame that can be wheeled over a patient in a hospital bed, they reported Wednesday.
A laser can take a reading of the wound's size and shape so that a layer of healing skin cells can be precisely applied, said the team at Wake Forest University in Winston-Salem, North Carolina.
"We literally print the cells directly onto the wound," said student Kyle Binder, who helped design the device. "We can put specific cells where they need to go."
Tests on mice showed the spray system, called bioprinting, could heal wounds quickly and safely, the researchers reported at the Translational Regenerative Medicine Forumb.
"We were able to close the entire wound in two weeks," Binder said. Mice with plugs of skin removed that were not treated took five weeks to heal, he said.
The team will eventually seek U.S. Food and Drug Administration approval to test the device on humans, said George Christ, a professor of regenerative medicine at the school.
They are working with the U.S. Armed Forces Institute of Regenerative Medicine to come up with ways to help soldiers wounded in Iraq and Afghanistan. It could be used to close various types of wounds as well as burns.
Binder and colleagues dissolved human skin cells from pieces of skin, separating and purifying the various cell types such as fibroblasts and keratinocytes.
They put them in a nutritious solution to make them multiply and then used a system similar to a multicolor office inkjet printer to apply first a layer of fibroblasts and then a layer of keratinocytes, which form the protective outer layer of skin.
The wound on the mouse was completely closed by three weeks, they reported. Experts say victims of massive burns usually die of infection within two weeks unless they receive skin grafts, and normal grafting often leaves severe scars.
The sprayed cells also incorporated themselves into surrounding skin, hair follicles and sebaceous glands, probably because immature cells called stem cells were mixed in with the sprayed cells, the researchers said.
"You have to give a lot of credit to the cells. When you put them into the wound, they know what to do," Binder said.
The next step is to try the system on pigs, whose skin more closely resembles the skin of humans. Binder said it may also be useful for treating diabetic foot ulcers, a common problem.
http://www.newsdaily.com/stories/tre6382qm-us-wounds-printer/
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"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
John F. Kennedy |
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