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 Re: MedTech V: R & D
« Reply #60 on May 16, 2012, 4:51pm »

16 May 2012 Last updated at 17:05 GMT

Paralysed patients use thoughts to control robotic arm
By Fergus Walsh Medical correspondent

Two patients in the United States who are paralysed from the neck down have been able to control a robotic arm using their thoughts.

It allowed one to drink unaided for the first time in nearly 15 years.

The technique, described in the journal Nature, links a sensor implanted in the brain to a computer, which translates electrical signals into commands.

In years to come, scientists want to reconnect the brain to paralysed limbs to enable them to function again.

The project was a partnership by Brown University and the Department of Veteran Affairs, Rhode Island, and the Department of Neurology at Massachusetts General Hospital and Harvard Medical School, Boston.

In 2006 in a previous Nature paper, the team showed that the same neural interface system could be used by a paralysed patient to control a cursor on a computer screen.

The key is a tiny sensor implanted on to the surface of the motor cortex.

'True happiness'

Thinking about moving an arm or hand activates neurons in this part of the brain and the electrical activity is sent via a cable to a computer, which translates them into commands.

Both patients in this latest research project were paralysed many years ago by strokes and have no viable movement below the neck.

Video footage shows 58-year-old Cathy Hutchinson using the neural interface to control a robotic arm and bring a flask of coffee to her mouth. It was the first time in nearly 15 years that she had taken a drink unaided.

She communicates by picking out letters on a board using eye movement and wrote: "I couldn't believe my eyes when I was able to drink coffee without help. I was ecstatic. I had feelings of hope and a great sense of independence."

That was echoed by Prof John Donoghue, a neurologist at Brown University.

He said: "There was a moment of true joy, true happiness. It was beyond the fact that it was an accomplishment. I think it was an important advance in the field of brain-computer interfaces that we had helped someone do something they had wished to do for many years."

Practical use

This research shows that the part of the brain that deals with movement continues to function more than a decade after paralysis.

Furthermore, the chip continues to function long-term - Cathy Hutchinson had the sensor fitted six years earlier.

The technology is years away from practical use and the trial participants used the system under controlled conditions in their homes with a technician on hand.

Nonetheless, another of the report authors, Prof Leigh Hochberg, said the team had four goals:

* To develop effective communications systems for people with locked-in syndrome, giving them control over a cursor on a computer screen
* To create improved neural control of robotic-assistive devices for patients with paralysis
* To use the system to allow amputees to control a prosthetic limb by the neural interface
* To enable paralysed patients to reconnect their brain to their limbs using this system so that they could use their own hand to pick up a coffee cup.

Prof Hochberg freely admitted that the third and fourth goals were distant ambitions but they were the "real dream" for people with such disabilities. The researchers say it is impossible to put a timescale on when this might be achieved.

Story Landis, director of the National Institute of Neurological Disorders and Stroke, which part-funded the work, said: "This technology was made possible by decades of investment and research into how the brain controls movement.

"It's been thrilling to see the technology evolve from studies of basic neurophysiology and move into clinical trials, where it is showing significant promise for people with brain injuries and disorders."

http://www.bbc.co.uk/news/health-18092653

AND:

Paralysed patients use thoughts to control robotic arm

You know the feeling when you watch something and your jaw drops? That happened when I saw the footage of Cathy Hutchinson use a robotic arm to lift a flask of coffee to her mouth.


It was the first time since her stroke nearly 15 years previously that she had served herself a drink. She is one of two patients who took part in a trial of a neural interface system. A sensor containing a grid of 96 tiny electrodes is fixed to the brain and this picks up neural activity from the motor cortex and sends it to a computer which converts it to commands.

The footage is extraordinary because you can see the patient is controlling the robot arm by the power of thought. It would appear to open a world of possibilities - a bridge between humans and machines.

I've written a report about the research in Nature which you can read here: http://www.bbc.co.uk/news/health-18092653

'Road worth travelling'

I soon realised that I had covered this research before, in 2006: http://news.bbc.co.uk/1/hi/5167938.stm That concerned another paralysed patient, Matt Nagle. He had the same tiny sensor implanted in his brain and could use it to control a cursor on a computer screen - turning lights on and off, and switching channels on TV.

This latest research takes the project to another level.

The researchers admit this technology is very much experimental and a long way from being of practical use. But it does offer real hope to patients with locked-in syndrome, whose active brains are trapped within a paralysed body.

The system could be used to develop an effective means by which they could communicate using a computer. It could also be used to help them control a wheelchair.

As for the brain controlling prosthetic limbs for amputees or allowing paralysed patients to reconnect their brain to their limbs and enable them to function - they are both a long long way away. But that doesn't make the research any less significant. It may be a small step on a long road, but it is surely a road worth travelling.

http://www.bbc.co.uk/news/health-18087949

AND:

People With Paralysis Control Robotic Arms to Reach and Grasp Using Brain Computer Interface


[image]
One small step A 58-year-old woman, paralyzed by a stroke for almost 15 years, uses her thoughts to control a robotic arm, grasp a bottle of coffee, serve herself a drink, and return the bottle to the table. (Credit: Brown University/Braingate2.org)

ScienceDaily (May 16, 2012) — A new study in Nature reports that two people with tetraplegia were able to reach for and grasp objects in three-dimensional space using robotic arms that they controlled directly with brain activity. They used the BrainGate neural interface system, an investigational device currently being studied under an Investigational Device Exemption. One participant used the system to serve herself coffee for the first time since becoming paralyzed nearly 15 years ago.

On April 12, 2011, nearly 15 years after she became paralyzed and unable to speak, a woman controlled a robotic arm by thinking about moving her arm and hand to lift a bottle of coffee to her mouth and take a drink. That achievement is one of the advances in brain-computer interfaces, restorative neurotechnology, and assistive robot technology described in the May 17 edition of the journal Nature by the BrainGate2 collaboration of researchers at the Department of Veterans Affairs, Brown University, Massachusetts General Hospital, Harvard Medical School, and the German Aerospace Center (DLR).

A 58-year-old woman ("S3") and a 66-year-old man ("T2") participated in the study. They had each been paralyzed by a brainstem stroke years earlier which left them with no functional control of their limbs. In the research, the participants used neural activity to directly control two different robotic arms, one developed by the DLR Institute of Robotics and Mechatronics and the other by DEKA Research and Development Corp., to perform reaching and grasping tasks across a broad three-dimensional space. The BrainGate2 pilot clinical trial employs the investigational BrainGate system initially developed at Brown University, in which a baby aspirin-sized device with a grid of 96 tiny electrodes is implanted in the motor cortex -- a part of the brain that is involved in voluntary movement. The electrodes are close enough to individual neurons to record the neural activity associated with intended movement. An external computer translates the pattern of impulses across a population of neurons into commands to operate assistive devices, such as the DLR and DEKA robot arms used in the study now reported in Nature.

BrainGate participants have previously demonstrated neurally based two-dimensional point-and-click control of a cursor on a computer screen and rudimentary control of simple robotic devices.

The study represents the first demonstration and the first peer-reviewed report of people with tetraplegia using brain signals to control a robotic arm in three-dimensional space to complete a task usually performed by their arm. Specifically, S3 and T2 controlled the arms to reach for and grasp foam targets that were placed in front of them using flexible supports. In addition, S3 used the DLR robot to pick up a bottle of coffee, bring it to her mouth, issue a command to tip it, drink through a straw, and return the bottle to the table. Her BrainGate-enabled, robotic-arm control during the drinking task required a combination of two-dimensional movements across a table top plus a "grasp" command to either grasp and lift or tilt the robotic hand.

"Our goal in this research is to develop technology that will restore independence and mobility for people with paralysis or limb loss," said lead author Dr. Leigh Hochberg, a neuroengineer and critical care neurologist who holds appointments at the Department of Veterans Affairs, Brown University, Massachusetts General Hospital, and Harvard. He is the sponsor-investigator for the BrainGate2 pilot clinical trial. "We have much more work to do, but the encouraging progress of this research is demonstrated not only in the reach-and-grasp data, but even more so in S3's smile when she served herself coffee of her own volition for the first time in almost 15 years."

Hochberg adds that even after nearly 15 years, a part of the brain essentially "disconnected" from its original target by a brainstem stroke was still able to direct the complex, multidimensional movement of an external arm -- in this case, a robotic limb. The researchers also noted that S3 was able to perform the tasks more than five years after the investigational BrainGate electrode array was implanted. This sets a new benchmark for how long implanted brain-computer interface electrodes have remained viable and provided useful command signals.

John Donoghue, the VA and Brown neuroscientist who pioneered BrainGate more than a decade ago and who is co-senior author of the study, said the paper shows how far the field of brain-computer interfaces has come since the first demonstrations of computer control with BrainGate.

"This paper reports an important advance by rigorously demonstrating in more than one participant that precise three-dimensional neural control of robot arms is not only possible, but also repeatable," said Donoghue, who directs the Brown Institute for Brain Science. "We've moved significantly closer to returning everyday functions, like serving yourself a sip of coffee, usually performed effortlessly by the arm and hand, for people who are unable to move their own limbs. We are also encouraged to see useful control more than five years after implant of the BrainGate array in one of our participants. This work is a critical step toward realizing the long-term goal of creating a neurotechnology that will restore movement, control, and independence to people with paralysis or limb loss."

In the research, the robots acted as a substitute for each participant's paralyzed arm. The robotic arms responded to the participants' intent to move as they imagined reaching for each foam target. The robot hand grasped the target when the participants imagined a hand squeeze. Because the diameter of the targets was more than half the width of the robot hand openings, the task required the participants to exert precise control. (Videos of these actions are available on the Nature website.)

In 158 trials over four days, S3 was able to touch the target within an allotted time in 48.8 percent of the cases using the DLR robotic arm and hand and 69.2 percent of the cases with the DEKA arm and hand, which has the wider grasp. In 45 trials using the DEKA arm, T2 touched the target 95.6 percent of the time. Of the successful touches, S3 grasped the target 43.6 percent of the time with the DLR arm and 66.7 percent of the time with the DEKA arm. T2's grasp succeeded 62.2 percent of the time.

T2 performed the session in this study on his fourth day of interacting with the arm; the prior three sessions were focused on system development. Using his eyes to indicate each letter, he later described his control of the arm: "I just imagined moving my own arm and the [DEKA] arm moved where I wanted it to go."

The study used two advanced robotic arms: the DLR Light-Weight Robot III with DLR five-fingered hand and the DEKA Arm System. The DLR LWR-III, which is designed to assist in recreating actions like the human arm and hand and to interact with human users, could be valuable as an assistive robotic device for people with various disabilities. Patrick van der Smagt, head of bionics and assistive robotics at DLR, director of biomimetic robotics and machine learning labs at DLR and the Technische Universität München, and a co-senior author on the paper said: "This is what we were hoping for with this arm. We wanted to create an arm that could be used intuitively by varying forms of control. The arm is already in use by numerous research labs around the world who use its unique interaction and safety capabilities. This is a compelling demonstration of the potential utility of the arm by a person with paralysis."

DEKA Research and Development developed the DEKA Arm System for amputees, through funding from the United States Defense Advanced Research Projects Agency (DARPA). Dean Kamen, founder of DEKA said, "One of our dreams for the Luke Arm [as the DEKA Arm System is known informally] since its inception has been to provide a limb that could be operated not only by external sensors, but also by more directly thought-driven control. We're pleased about these results and for the continued research being done by the group at the VA, Brown and MGH." The research is aimed at learning how the DEKA arm might be controlled directly from the brain, potentially allowing amputees to more naturally control this prosthetic limb.

Over the last two years, VA has been conducting an optimization study of the DEKA prosthetic arm at several sites, with the cooperation of veterans and active duty service members who have lost an arm. Feedback from the study is helping DEKA engineers to refine the artificial arm's design and function. "Brain-computer interfaces, such as BrainGate, have the potential to provide an unprecedented level of functional control over prosthetic arms of the future," said Joel Kupersmith, M.D., VA chief research and development officer. "This innovation is an example of federal collaboration at its finest."

Story Landis, director of the National Institute of Neurological Disorders and Stroke, which funded the work in part, noted: "This technology was made possible by decades of investment and research into how the brain controls movement. It's been thrilling to see the technology evolve from studies of basic neurophysiology and move into clinical trials, where it is showing significant promise for people with brain injuries and disorders."

In addition to Hochberg, Donoghue, and van der Smagt, other authors on the paper are Daniel Bacher, Beata Jarosiewicz, Nicolas Masse, John Simeral, Joern Vogel, Sami Haddadin, Jie Liu, and Sydney Cash.

Story Source:

The above story is reprinted from materials provided by Brown University.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Leigh R. Hochberg, Daniel Bacher, Beata Jarosiewicz, Nicolas Y. Masse, John D. Simeral, Joern Vogel, Sami Haddadin, Jie Liu, Sydney S. Cash, Patrick van der Smagt, John P. Donoghue. Reach and grasp by people with tetraplegia using a neurally controlled robotic arm. Nature, 2012; 485 (7398): 372 DOI: 10.1038/nature11076

http://www.sciencedaily.com/releases/2012/05/120516140000.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."

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 Re: MedTech V: R & D
« Reply #61 on May 17, 2012, 11:33am »

Successful Stem Cell Differentiation Requires DNA Compaction, Study Finds

[image]
These are phase contrast images showing that H1 triple-knockout (bottom) embryonic stem cells were unable to adequately form neurites and neural networks compared to wild-type embryonic stem cells (top). (Credit: Yuhong Fan)

ScienceDaily (May 11, 2012) — New research findings show that embryonic stem cells unable to fully compact the DNA inside them cannot complete their primary task: differentiation into specific cell types that give rise to the various types of tissues and structures in the body.

Researchers from the Georgia Institute of Technology and Emory University found that chromatin compaction is required for proper embryonic stem cell differentiation to occur. Chromatin, which is composed of histone proteins and DNA, packages DNA into a smaller volume so that it fits inside a cell.

A study published on May 10, 2012 in the journal PLoS Genetics found that embryonic stem cells lacking several histone H1 subtypes and exhibiting reduced chromatin compaction suffered from impaired differentiation under multiple scenarios and demonstrated inefficiency in silencing genes that must be suppressed to induce differentiation.

"While researchers have observed that embryonic stem cells exhibit a relaxed, open chromatin structure and differentiated cells exhibit a compact chromatin structure, our study is the first to show that this compaction is not a mere consequence of the differentiation process but is instead a necessity for differentiation to proceed normally," said Yuhong Fan, an assistant professor in the Georgia Tech School of Biology.

Fan and Todd McDevitt, an associate professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University, led the study with assistance from Georgia Tech graduate students Yunzhe Zhang and Kaixiang Cao, research technician Marissa Cooke, and postdoctoral fellow Shiraj Panjwani.

The work was supported by the National Institutes of Health's National Institute of General Medical Sciences (NIGMS), the National Science Foundation, a Georgia Cancer Coalition Distinguished Scholar Award, and a Johnson & Johnson/Georgia Tech Healthcare Innovation Award.

To investigate the impact of linker histones and chromatin folding on stem cell differentiation, the researchers used embryonic stem cells that lacked three subtypes of linker histone H1 -- H1c, H1d and H1e -- which is the structural protein that facilitates the folding of chromatin into a higher-order structure. They found that the expression levels of these H1 subtypes increased during embryonic stem cell differentiation, and embryonic stem cells lacking these H1s resisted spontaneous differentiation for a prolonged time, showed impairment during embryoid body differentiation and were unsuccessful in forming a high-quality network of neural cells.

"This study has uncovered a new, regulatory function for histone H1, a protein known mostly for its role as a structural component of chromosomes," said Anthony Carter, who oversees epigenetics grants at NIGMS. "By showing that H1 plays a part in controlling genes that direct embryonic stem cell differentiation, the study expands our understanding of H1's function and offers valuable new insights into the cellular processes that induce stem cells to change into specific cell types."

During spontaneous differentiation, the majority of the H1 triple-knockout embryonic stem cells studied by the researchers retained a tightly packed colony structure typical of undifferentiated cells and expressed high levels of Oct4 for a prolonged time. Oct4 is a pluripotency gene that maintains an embryonic stem cell's ability to self-renew and must be suppressed to induce differentiation.

"H1 depletion impaired the suppression of the Oct4 and Nanog pluripotency genes, suggesting a novel mechanistic link by which H1 and chromatin compaction may mediate pluripotent stem cell differentiation by contributing to the epigenetic silencing of pluripotency genes," explained Fan. "While a significant reduction in H1 levels does not interfere with embryonic stem cell self-renewal, it appears to impair differentiation."

The researchers also used a rotary suspension culture method developed by McDevitt to produce with high efficiency homogonous 3D clumps of embryonic stem cells called embryoid bodies. Embryoid bodies typically contain cell types from all three germ layers -- the ectoderm, mesoderm and endoderm -- that give rise to the various types of tissues and structures in the body. However, the majority of the H1 triple-knockout embryoid bodies formed in rotary suspension culture lacked differentiated structures and displayed gene expression signatures characteristic of undifferentiated stem cells.

"H1 triple-knockout embryoid bodies displayed a reduced level of activation of many developmental genes and markers in rotary culture, suggesting that differentiation to all three germ layers was affected." noted McDevitt.

The embryoid bodies also lacked the epigentic changes at the pluripotency genes necessary for differentiation, according to Fan.

"When we added one of the deleted H1 subtypes to the embryoid bodies, Oct4 was suppressed normally and embryoid body differentiation continued," explained Fan. "The epigenetic regulation of Oct4 expression by H1 was also evident in mouse embryos."

In another experiment, the researchers provided an environment that would encourage embryonic stem cells to differentiate into neural cells. However, the H1 triple-knockout cells were defective in forming neuronal and glial cells and a neural network, which is essential for nervous system development. Only 10 percent of the H1 triple-knockout embryoid bodies formed neurites and they produced on average eight neurites each. In contrast, half of the normal embryoid bodies produced, on average, 18 neurites.

In future work, the researchers plan to investigate whether controlling H1 histone levels can be used to influence the reprogramming of adult cells to obtain induced pluripotent stem cells, which are capable of differentiating into tissues in a way similar to embryonic stem cells.

Story Source:

The above story is reprinted from materials provided by Georgia Institute of Technology Research News.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Yunzhe Zhang, Marissa Cooke, Shiraj Panjwani, Kaixiang Cao, Beth Krauth, Po-Yi Ho, Magdalena Medrzycki, Dawit T. Berhe, Chenyi Pan, Todd C. McDevitt, Yuhong Fan. Histone H1 Depletion Impairs Embryonic Stem Cell Differentiation. PLoS Genetics, 2012; 8 (5): e1002691 DOI: 10.1371/journal.pgen.1002691

http://www.sciencedaily.com/releases/2012/05/120511104205.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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 Re: MedTech V: R & D
« Reply #62 on May 25, 2012, 1:04am »

23 May 2012 Last updated at 13:32 GMT

Clot drug 'helps stroke recovery', Edinburgh University study suggests

Stroke victims given a clot-busting drug after an attack recover better than those without the treatment, an Edinburgh study has suggested.


More than 3,000 patients worldwide took part in the trial of rt-PA.

The drug was given intravenously to patients who have had acute ischaemic stroke, when an artery that carries blood to the brain is blocked.

Stroke damage can be permanent or fatal, with problems including paralysis and problems with speech.

The international trial, led by the University of Edinburgh, found that following treatment with the drug, more stroke survivors were able to look after themselves.

A patient's chances of completely recovering within six months of a stroke were also increased.

For every 1,000 patients given rt-PA within three hours of stroke, 80 more will survive and live without help from others than if they had not been given the drug, according to the research.

But patients are also at risk of death within seven days of treatment because the drug can cause a secondary bleed in the brain.

Without treatment with rt-PA, one-third of people who have a stroke die and another third are left permanently dependent and disabled.

For those who do not experience bleeding, the drug improves patients' longer-term recovery.

Researchers said the trial showed the benefits of treating patients with the drug as soon as possible.

The findings of the study are published in The Lancet medical journal, alongside an analysis of all other trials of the drug from the past 20 years.

Clot data

The study involved stroke patients in 12 countries between 2000 and 2011, half of whom were treated with intravenous rt-PA and half were not. About half of participants were aged over 80.

In 2002 rt-PA was given an EU licence on condition it was used on patients under 80 within three hours of them having an ischaemic stroke.

Professor Joanna Wardlaw, from Edinburgh University, said: "We have looked at data from more than 7,000 stroke patients worldwide.

"What we see is that the drug increases patients' longer-term recovery. But we need to find out why some people bleed and how to reduce this to increase the effectiveness of clot-busting treatment."

The trial was supported by the University of Edinburgh, the Stroke Association UK, the Medical Research Council, EME, the Health Foundation UK and NHS Lothian Health Board.

http://www.bbc.co.uk/news/uk-scotland-edinburgh-east-fife-18175505
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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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 Re: MedTech V: R & D
« Reply #63 on May 25, 2012, 1:09am »

22 May 2012 Last updated at 00:32 GMT

The end of drug discovery?
By Smitha Mundasad BBC Radio 4

[image]
Will we find new cures for the 21st Century?

Half a century ago, in the drug industry's golden era, we were bestowed with countless pills to lower blood pressure, control blood sugar and get rid of infections. But today it costs about $1bn to bring a new medicine to market, a process that can take 15 years.

The industry faces multiple crises as budgets are squeezed and tough scientific challenges loom.

Academics and patients' groups are concerned we will not have the drugs necessary to treat future ills.

Last year, the World Health Organization's director general, Margaret Chan, warned that the world was heading for a "post-antibiotic era".

She raised fears that many common infections might no longer have a cure and could once again "kill unabated".

Major problems, Dr Chan suggested, included growing resistance to antibiotics.

And as the population ages, many of us will battle with neurological conditions such as Alzheimer's and Parkinson's, where new drugs are also lacking.

'Inefficient model'

But the old model of drug discovery is no longer working well.

This so-called blockbuster method - which commits large sums of money to finding a drug that promises to treat a huge proportion of the population, and generate swathes of cash to cover other experimental losses - can no longer sustain the industry.

The model is inefficient. Nine times out of 10, molecules which show promise at the early stage are destined for failure at later trials.

Pharmaceutical companies are also under pressure as patents for some of their most lucrative drugs expire.

Manufacturers face an uphill struggle with science too. Some argue that in its most successful years, the big pharmaceutical firms picked off the "low-hanging fruit" - the compounds that were easiest to discover and turn into drugs.

Chas Bountra, professor of translational medicine at Oxford University, says: "We don't understand enough about human disease or enough about the mode of action of existing drugs. Take paracetamol for example. We all take it but we don't know how it works, we don't know what the site of action of paracetamol is.

"So if we don't know that, how can we design better, more superior molecules?"

But finding new targets - proteins in the body that could be modified by a drug to help relieve disease - is like a lottery, he says.

"There are more than 20,000 proteins in the human body, and any of those proteins could be a target for drug discovery. Our ability, even in 2012, to be able to say one protein is going to work in this patient group or subset of patients is appalling."

'Better visibility'

Alongside many other people working on drug development, he points to another difficulty that threatens the process - duplication.

"We don't publish our failures, or if we do publish them, we publish too late. As a consequence other academics, other companies, carry on working on the same target, carry on wasting resources and careers and exposing patients to molecules that have a chance of failure," Prof Bountra says.

But Prof Patrick Vallance, president of pharmaceuticals research and development at GlaxoSmithKline, thinks the industry is becoming more open: "One of the things we have done is to be very public about when things go into the clinic.

"And we publish our results - we make our protocols available to reviewers when papers are submitted. Those sorts of things help to start better visibility of what is in the pipeline."

GlaxoSmithKline has put 13,500 structures which have the potential to kill malaria into the public domain.

Prof Vallance says the firm has done this because it is a "tough problem to crack".

He adds: "Why not let everyone have a look at those compounds and see if they can think of something smarter than we are doing, and see if they can group them in a certain way or spot a pattern we have missed?"

But, he argues, we have to be realistic about this. "There will always be a degree of duplication, because that comes with the competition."

Prof Bountra's group at Oxford has also made a decision to publish all their successes and failures.

Moving forward

Prof Paul Workman at the Institute of Cancer Research points to another pressing issue: "With the problems of the financial crisis there has developed something of a vacuum that many of us describe as 'the valley of death'.

"This is the valley between basic research and innovation on the one hand, and patient benefit and commercial success on the other, with this chasm in between into which there is a lack of funding and a lot of failure."

One possible solution is for charitable foundations such as the Wellcome Trust to offer funding to fill this gap.

Prof Workman, on the other hand, works on a model where many processes of drug discovery and development come under one roof.

"We go all the way from discerning a new biological concept to developing the chemicals that block a certain pathway or gene function, and then all the way into clinical trials," he says.

He points out that they don't do the whole thing alone, often partnering with smaller and larger companies in later stages.

Prof Workman is optimistic that the science is moving forward, and bringing new chances of success with it: "The science is taking us in the opposite direction to blockbuster drugs, to personalised medicine. You would identify the patient who would benefit from what drug according to a gene test.

"A relatively small number of patients will benefit but they will benefit extremely well."

What all these newer models of drug development have in common, it seems, is collaboration - perhaps presenting a cultural change for an industry that many people believe has had competition at the centre of its working.

But, says Prof Vallance, while there is need for more collaboration in the early stages of drug development for some of the more complex diseases, that will turn into competition at a later point.

"There will be fierce competition to get the best drug first, to make sure you do the right trial and show you've got the best medicine."

http://www.bbc.co.uk/news/health-18095669
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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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 Re: MedTech V: R & D
« Reply #64 on Jun 25, 2012, 2:54am »

24 June 2012 Last updated at 23:52 GMT

Voice algorithms spot Parkinson's disease
By Jane Wakefield Technology reporter, TEDGlobal, Edinburgh

Parkinson's is a devastating disease for those living with the condition and currently there is no cure.

Diagnosis can also be slow as there are no blood tests to detect it.

But now mathematician Max Little has come up with a non-invasive, cheap test which he hopes will offer a quick new way to identify the disease.

He will be kicking off the TEDGlobal conference in Edinburgh calling for volunteers to contribute to a huge voice database.

Mr Little has discovered that Parkinson's symptoms can be detected by computer algorithms that analyse voice recordings.

In a blind test of voices, the system was able to spot those with Parkinson's with an accuracy of 86%.

Mr Little was recently made a TED Fellow.

The non-profit organisation behind the TED (Technology, Entertainment and Design) conference creates 40 such fellowships each year. The programme aims to target innovators under the age of 40 and offers them free entry to conferences and other events.

Intel founder

Mr Little became interested in understanding voice from a mathematical perspective while he was studying for a PhD at Oxford University in 2003.

"I was looking for a practical application and I found it in analysing voice disorders, for example when someone's voice has broken down from over-use or after surgery on vocal chords," he told the BBC.

"I didn't occur to me at the time that people with Parkinson's and other movement disorders could also be detected by the system."

But a chance meeting with someone from Intel changed that.

Andy Grove, one of Intel's founders and ex-chief executive, was diagnosed with Parkinson's in 2000 and has since pledged millions of his personal fortune to fund research into the disease.

This includes funds for the chipmaker to develop its own projects to monitor the symptoms.

"They were using devices that detect breakdown in dexterity and accelerometers but they had also recorded the voices of around 50 patients with Parkinson's," explained Mr Little.

The recordings were detailed as the team had recorded the patients once a week over a six-month period.

"They had an enormous amount of data but they didn't know what to do with it. So we wondered whether my technique would work," said Mr Little.

"They set me a blind test to see if I can tell them which ones had Parkinson's. I had 86% accuracy using the techniques I'd developed."

Voice tremors

[image]
The technology works partly by tracking the motion of vocal chords

The system "learns" to detect differences in voice patterns.

"This is machine learning. We are collecting a large amount of data when we know if someone has the disease or not and we train the database to learn how to separate out the true symptoms of the disease from other factors."

Voice patterns can change for a number of reasons, including throat surgery, heavy smoking and even just having a common cold.

But Mr Little believes the system will be smart enough to tell the difference.

"It is not as simple as listening for a tremor in the voice. That tremor has to be in context of other measures and the system has to take in other factors such as if someone has a cold."

Now he is looking for volunteers to contribute to a vast voice bank to help the database to learn even more.

He is aiming to record up to 10,000 voices and has set up local numbers in 10 countries around the world. In the UK the number is 01865 521168.

Anyone can call and they need to state whether or not they have been diagnosed with the disease.

There is also a website where people can find out more about the project: http://www.parkinsonsvoice.org/

"The more people that call in, the better," he said.

"If we get 10,000 recordings we'd be very happy but even a tenth of that would be great,"

Clinical trials

He hopes that the technology will be available to doctors within the next two years.

"We're not intending this to be a replacement for clinical experts, rather, it can very cheaply help identify people who might be at high risk of having the disease and for those with the disease, it can augment treatment decisions by providing data about how symptoms are changing in-between check-ups with the neurologist," he said.

There could also be a role for the technology in clinical trials.

"The technology makes it easy for people to report their progress whilst on a new drug, for example," he added.

"If you can catch the disease early it will make a huge difference to care costs. It could become a key technology in reducing the burden of care on the NHS."

http://www.bbc.com/news/technology-18427851
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« Reply #65 on Jun 25, 2012, 1:35pm »

Boosting Blood System Protein Complex Protects Against Radiation Toxicity

ScienceDaily (June 24, 2012) — New research in Nature Medicine shows that boosting a protein pathway in the body's blood making system protects mice from otherwise fatal radiation poisoning.

Scientists in the multi-institutional study -- posted online by the journal on June 24 -- say their findings open the potential for new treatments against radiation toxicity during cancer treatment or environmental exposures -- such as in a nuclear explosion or accident.

By identifying a target-specific intervention to protect the hematopoietic system against radiation toxicity, the study addresses a largely unmet challenge, according to the researchers.

"These findings suggest that pharmacologic augmentation of the activity of the Thbd-aPC pathway by recombinant Thbd (thrombomodulin) or aPC (activated protein C) might offer a rational approach to the mitigation of tissue injury and lethality caused by ionizing radiation," the scientists write in their manuscript. "Recombinant human aPC has undergone extensive clinical testing in patients, and recombinant soluble human Thbd is currently being investigated for efficacy in antithrombotic therapy in humans. Our data encourage the further evaluation of these proteins for their radio-mitigating activities."

The study reveals a previously unknown function of the Thbd-aPC pathway in radiation mitigation. The pathway is normally known for its ability to prevent the formation of blood clots and help the body fight infections. The researchers found the pathway helps blood cells in the bone marrow recover from injury caused by radiation exposure. They demonstrated that pharmacologic boosting of this pathway with two drugs tested for the treatment of thrombosis or infection (recombinant Thbd and aPC respectively) can be used in mice to prevent death caused by exposure to lethal doses of radiation.

In all instances of treatment with recombinant soluble Thbd or aPC, the result was accelerated recovery of hematopoietic progenitor cell activity in bone marrow and a reduction in the harmful effects of lethal total body irradiation. When treatment was with aPC, these benefits occurred even when treatment was delayed for 24 hours.

The scientists caution their study involves early laboratory research in mice, so it remains to be tested how the findings may translate to human treatment. Researchers also need to determine exactly why the protective function of the targeted Thbd-aPC protein pathway seems to work so well in mice.

Researchers noted that the protective benefits of Thbd-aPC occurred only in vivo in irradiated mouse models. The researchers reported that overexpressed Thbd in irradiated laboratory cell cultures did not offer the same protective benefits, as the cells did not survive. This indicates the protective benefits of Thbd on blood making cells in irradiated mouse models depends on the help of additional cells or molecules in the body, which the researchers are trying to identify in a follow-up study.

The study involves extensive multi-scientist collaborations that combined previously independent lines of research by groups at Cincinnati Children's Hospital Medical Center and the University of Ulm, Germany (led by Hartmut Geiger, PhD, Division of Experimental Hematology/Cancer Biology and the Department of Dermatology/Allergic Diseases); the University of Arkansas, Little Rock (led by Martin Hauer-Jensen, MD, PhD, Division of Radiation Health, the College of Pharmacy and the Central Arkansas Veterans Healthcare System); the Blood Research Institute in Milwaukee, Wis. (led by Hartmut Weiler, PhD); and The Scripps Research Institute in La Jolla, Calif. (led by John H. Griffin, PhD, Department of Molecular and Experimental Medicine).

The research team said the current study exemplifies a global shift to multi-investigator projects that allow a combination of varied expertise by scientists tackling complex problems from the perspective of their respective fields. This approach requires the willingness of investigators to share unpublished data and engage in an open collaboration. The researchers also said the study underscores the importance of continued federal funding for leading edge basic research that can benefit human health.

Story Source:

The above story is reprinted from materials provided by Cincinnati Children's Hospital Medical Center, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Hartmut Geiger, Snehalata A Pawar, Edward J Kerschen, Kalpana J Nattamai, Irene Hernandez, Hai Po H Liang, Jose Á Fernández, Jose A Cancelas, Marnie A Ryan, Olga Kustikova, Axel Schambach, Qiang Fu, Junru Wang, Louis M Fink, Karl-Uwe Petersen, Daohong Zhou, John H Griffin, Christopher Baum, Hartmut Weiler & Martin Hauer-Jensen. Pharmacological targeting of the thrombomodulin–activated protein C pathway mitigates radiation toxicity. Nature Medicine, 24 June 2012 DOI: 10.1038/nm.2813

http://www.sciencedaily.com/releases/2012/06/120624134951.htm
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« Reply #66 on Jun 25, 2012, 1:41pm »

Arsenic for Better Drugs and Cleaner Crops

ScienceDaily (June 25, 2012) — Research carried out at the University of Gothenburg may lead to more effective arsenic-containing drugs. The results may also lead to more resistant plants, and crops with a limited absorption and storage of arsenic.

Even though arsenic is toxic for many organs in the human body, it is used in the treatment of some forms of cancer, and it is an active component of drugs against parasitic diseases.

Healing arsenic

Arsenic is used in therapeutic medicine, but we know relatively little about the mechanisms by which cells develop resistance to arsenic, which may lead to a lower therapeutic effect.

Proteins control cellular processes

Scientist Doryaneh Ahmadpour at the Department of Chemistry and Molecular Biology, University of Gothenburg, has carried out experiments with common baker's yeast, in order to find out how inflow and outflow take place in cells.

"The knowledge we obtain from determining these mechanisms in yeast can be subsequently used in the long term to produce more effective drugs containing arsenic. A membrane protein known as Fps1 is particularly interesting. This protein transports the trivalent form of arsenic (arsenite) into and out from the cell," says Doryaneh Ahmadpour.

She has worked with scientist Michael Thorsen to show how the Fps1 protein is regulated and how the inflow into the cell of arsenic is influenced by another protein, Hog1.

The results suggest that a reduction in the activity of Hog1 is an effective way of increasing the ability of the cell to absorb arsenic. This may make the cell more sensitive to arsenic and thus give more effective treatment.

Resistance to arsenic can be increased in a similar manner, by increasing the activity of Hog1, which reduces the inflow of arsenic into the cells.

"We have shown also that a protein known as Slt2 regulates the outflow of arsenic from the cell, and increases the resistance of the cell to arsenic. It is possible, in the same way, to regulate the cellular resistance against arsenic by controlling the activity of Slt2."

Arsenic as a problem

Arsenic is a toxic metalloid that is naturally found in earth crust. It can be leached out by water or spread by industrial activity.

Arsenic is a global problem due to the increasing contamination of water, soil and crops, not only in the industrialized world but also in developing countries.

"High levels of arsenic in groundwater can lead to humans being exposed to toxic levels in food and water. This affects mainly people in regions in which the crops are watered with arsenic-contaminated water, leading to arsenic being stored in the plants."

Resistant crops

Increased knowledge about arsenic can be used to produce plants with a high absorption, and these can be used to clean contaminated land. The knowledge can also be used to produce food crops, known as "safe crops," with a limited absorption and storage of arsenic.

The thesis has been successfully defended.

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The above story is reprinted from materials provided by University of Gothenburg, via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

http://www.sciencedaily.com/releases/2012/06/120625085312.htm
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« Reply #67 on Jul 17, 2012, 11:01am »

Galaxy-Exploring Camera to Be Used in the Operating Room

ScienceDaily (July 12, 2012) — Neurosurgeons and researchers at Cedars-Sinai Medical Center and the Maxine Dunitz Neurosurgical Institute are adapting an ultraviolet camera to possibly bring planet-exploring technology into the operating room.

If the system works when focused on brain tissue, it could give surgeons a real-time view of changes invisible to the naked eye and unapparent even with magnification of current medical imaging technologies. The pilot study seeks to determine if the camera provides visual detail that might help surgeons distinguish areas of healthy brain from deadly tumors called gliomas, which have irregular borders as they spread into normal tissue.

"Our goal is to revolutionize the way neurological disorders are treated. Ultraviolet imaging is one of several intraoperative technologies we are pursuing," commented Keith L. Black, MD, chair of the Department of Neurosurgery.

The tumors' far-reaching tentacles pose big challenges for neurosurgeons: Taking out too much normal brain tissue can have catastrophic consequences, but stopping short of total removal gives remaining cancer cells a head start on growing back. Delineating the margin where tumor cells end and healthy cells begin never has been easy, even with recent advances in medical imaging systems, said Black, director of the Maxine Dunitz Neurosurgical Institute and the Johnnie L. Cochran, Jr. Brain Tumor Center and the Ruth and Lawrence Harvey Chair in Neuroscience

But the ultraviolet camera might be able to see below the surface, he said. Because tumor cells are more active and require more energy than normal cells, a specific chemical (nicotinamide adenine dinucleotide hydrogenase or NADH) accumulates in tumor cells but not in healthy cells. NADH emits ultraviolet light that may be captured by the camera and displayed in a high-resolution image. The camera, on loan from NASA's Jet Propulsion Laboratory, employs the ultraviolet technology used in space to study planets and distant galaxies.

"The ultraviolet imaging technique may provide a 'metabolic map' of tumors that could help us differentiate them from normal surrounding brain tissue, providing useful, real-time, intraoperative information," said Ray Chu, MD, a neurosurgeon leading the study with co-principal investigator Babak Kateb, MD, research scientist at Cedars-Sinai's Maxine Dunitz Neurosurgical Institute and chairman of the board of the Society for Brain Mapping and Therapeutics.

Kateb observed: "This study and equipment-sharing arrangement represents the leading edge of an effort by Cedars-Sinai to develop the next generation of solutions for brain tumors, injuries and other neurological disorders right here at Cedars-Sinai's Maxine Dunitz Neurosurgical Institute by introducing paradigm-shifting technologies into the field."

In the clinical trial, the highly sensitive camera is placed near the surgical field, recording images as the neurosurgeon exposes and removes the tumor. Images are not used in decision-making or surgical technique but later are correlated with tumor appearance, laboratory findings, and MRI and CT scans to assess the ultraviolet technology's value in the operating room.

John S. Yu, MD, vice chair of the Department of Neurosurgery, and Adam N. Mamelak, MD, neurosurgeon and co-director of Cedars-Sinai's Pituitary Center, also are participating in the study.

The ultraviolet imaging study, which will include 20 patients, is open to adults undergoing open-skull surgery for any brain tumor that is within range of the camera lens. Enrollment information is available by contacting Suzane Brian, study research assistant, in the Department of Neurosurgery.

Story Source:

The above story is reprinted from materials provided by Cedars-Sinai Medical Center.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

http://www.sciencedaily.com­/releases/2012/07/120712092234.htm
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« Reply #68 on Jul 27, 2012, 6:45am »

World's first dengue vaccine beats virus strains

Updated July 26, 2012 13:27:48

The world's first vaccine against dengue fever has protected against three of the virus's four strains in a keenly awaited clinical trial in Thailand.

French drugmaker Sanofi says the proof of efficacy is a key milestone in the 70-year quest to develop a viable dengue shot.

The company says the results also confirm the safety profile of its vaccine candidate.

The mosquito-borne disease is a threat to nearly 3 billion people and is caused by four different types of virus.

Sanofi's vaccine generated an antibody response for all four dengue virus types, but evidence of protection was only demonstrated against three of the four strains circulating in Thailand.

The Phase IIb study involved 4,002 Thai children aged four to 11 years and was conducted during a dengue epidemic.

Large-scale late-stage Phase III clinical studies with 31,000 participants are under way with Sanofi's vaccine in 10 countries in Asia and Latin America.

The company's vaccine unit Sanofi Pasteur has already invested $US423 million in a new French factory to make the three-dose vaccine.

Analysts expect a commercial launch will be viable in 2015.

Other drug companies are also working on dengue vaccines but Sanofi's product is several years ahead.

Most patients survive dengue fever but it is estimated to kill about 20,000 every year, many of them children less able to fight it off.

http://www.abc.net.au/news/2012-07-26/an-dengue-vaccine/4156196?section=world
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« Reply #69 on Aug 2, 2012, 5:54am »

31 July 2012 Last updated at 00:55 GMT

'Spray-patch' could mend hearts
By James Gallagher Health and science reporter, BBC News

A 10,000 volt 3D electric sprayer, which fires out a stream of heart cells, could be the latest tool in mending broken hearts.

[image]

It can create thin sheets of beating cells that researchers hope they can use to patch-up pieces of damaged heart.

The need is huge. Heart attacks may no longer be a death sentence, but as more people survive them it means more are living with a damaged heart.

When a bit of heart muscle dies it is replaced by tough scars, just as it does after you cut your leg. But scar tissue does not beat, so it can leave the heart struggling to pump blood. In some cases it can make even the simplest of tasks as exhausting as running a marathon.

It is for this reason that British Heart Foundation researchers are trying to develop the patches. The thin sheets of heart cells could be layered onto the heart to help it beat or maybe even sprayed directly onto scar tissue inside the heart.

Spray on

In a windowless laboratory in the heart of London a mechanical engineer, Dr Suwan Jayasinghe, has assembled the pieces of the bio-electric sprayer.

First a syringe is filled with heart cells. In the future it is thought these cells could be taken from a patient's heart and grown or a patient's stem cells could be converted into heart cells.

These are then passed through a needle. However, unlike a graffiti artist's spray can, this is not enough to get the thin accurate spray of cells needed to build the heart tissue.

[image]
Scar tissue forms after a heart attack

Instead 10,000 volts going through the needle create an electric field to control the cells.

"You get the formation of a fine jet which then breaks up into a myriad of droplets and those droplets are what form the sheet," said Dr Jayasinghe.

"The beautiful thing is that we can add various other cell types into this cell suspension and create three dimensional cardiac tissues that are fully functional."

Under a microscope it is then possible to see the cells beating in the patch. The next test is to see if the patches can actually help a damaged heart to beat, by testing them in animals.

Precision

Researcher Dr Anastasis Stephanou said: "Hopefully we can show that these engineered cardiac sheets improve the function of a damaged heart.

"What we're hoping in the long term is to use this technology to actually repair the damaged heart so the patients wont have to wait long-term for a donor heart.

"A heart is made up of different cell types, so we would be able to design the technology where we would be able to place the right number of cell types to develop the actual cardiac tissue.

"So we feel the technology we have is quite superior in terms of the other cardiac tissue engineering technologies that are available."

Professor Peter Weissberg, medical director at the British Heart Foundation which funds the research, said: "Creating heart muscle is a huge challenge and involves a mix of different cells and blood vessels that need to line-up perfectly with one another.

"This groundbreaking research is trying to find a way to build 'pieces of the heart' outside the body. We hope that one day these pieces can be grafted onto damaged hearts to help them pump more strongly again.

"This research could offer hope to the 750,000 people living with heart failure in the UK."

http://www.bbc.co.uk/news/health-18899486
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« Reply #70 on Aug 5, 2012, 12:02am »

3 August 2012 Last updated at 00:39 GMT

'Spray-on skin' helps heal leg ulcers
By James Gallagher Health and science reporter, BBC News

A "spray-on skin" which coats a wound with a layer of skin cells could help healing, according to US and Canadian researchers.

The spray was tested on 228 people with leg ulcers, which are painful open wounds that can last for months.

The findings, published in the Lancet, showed that ulcers treated with the spray were more likely to heal and did so more quickly: http://www.thelancet.com/journals/lancet....0644-8/abstract

Experts said faster healing could save money despite the cost of the spray.

Leg ulcers are hard to treat. The best treatment, compression bandages, will heal only about 70% of ulcers after six months. Other options include taking skin from somewhere else on the body and grafting it over the wound.

Instead the spray puts a coating of donated skin cells and blood-clotting proteins over the ulcer.

In the study, patients who were given the spray-on-skin every 14 days showed the most improvement.

The researchers said the size of the wound "began to decrease rapidly" as soon as the treatment started. In the patients who had the spray, 70% were healed after three months compared with 46% who received other treatment.

The spray was developed by Healthpoint Biotherapeutics in the US, which also funded the research.

Vast improvement

One of the scientists involved, Dr Herbert Slade, said: "The treatment we tested in this study has the potential to vastly improve recovery times and overall recovery from leg ulcers, without the need for a skin graft.

"This means not only that the patient doesn't acquire a new wound where the graft is taken from, but also that the spray-on solution can be available as soon as required - skin grafts take a certain amount of time to prepare, which exposes the patient to further discomfort and risk of infection."

The study largely tested the safety of the spray and the best dose to use, further studies will decide if it is a practical treatment for leg ulcers.

Leg ulcers are most commonly caused by high blood pressure in the veins of the legs which damage the skin, causing it to break down and develop into an open wound.

Irene Anderson, a lecturer in leg ulcer theory at the University of Hertfordshire, said: "A dressing or other application may have a positive effect on the wound for a period of time but ultimately if the underlying condition is not managed the leg will break down again.

"We do know that leg ulcers are becoming increasingly complex and when using the range of treatments available there needs to be clear evidence that there will be a beneficial effect to ensure cost effectiveness and to make sure that patients are not given false expectations of a cure."

Commenting on the study, Prof Matthias Augustin from the University Medical Centre in Hamburg, Germany, said compression would be the main treatment for some time.

"The temporary higher costs for additional cell and tissue-engineered therapy can be justified as an investment in improved healing," he added.

http://www.bbc.co.uk/news/health-19093302
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« Reply #71 on Aug 7, 2012, 1:42am »

Microswimmers: Micron-Scale Swimming Robots Could Deliver Drugs and Carry Cargo Using Simple Motion

[image]
Illustration shows the rigid propulsive flaps on each side of the micro-swimmer, while the steering flap on the front is being deformed by a light source. The green cones represent velocity vectors through the middle of the micro-swimmer. (Credit: Courtesy of Alexander Alexeev)

ScienceDaily (Aug. 6, 2012) — When you're just a few microns long, swimming can be difficult. At that size scale, the viscosity of water is more like that of honey, and momentum can't be relied upon to maintain forward motion.

Microorganisms, of course, have evolved ways to swim in spite of these challenges, but tiny robots haven't quite caught up. Now a team of researchers at the Georgia Institute of Technology has used complex computational models to design swimming micro-robots that could overcome these challenges to carry cargo and navigate in response to stimuli such as light.

When they're actually built some day, these simple micro-swimmers could rely on volume changes in unique materials known as hydrogels to move tiny flaps that will propel the robots. The micro-devices could be used in drug delivery, lab-on-a-chip microfluidic systems -- and even as micro-construction robots working in swarms.

The simple micro-swimmers were described July 23 in the online advance edition of the journal Soft Matter, published by the Royal Society of Chemistry in the United Kingdom.

"We believe that our simulations will give experimentalists a reason to pursue development of these micro-swimmers to go beyond what is available now," said Alexander Alexeev, an assistant professor in the George W. Woodruff School of Mechanical Engineering at Georgia Tech. "We wanted to demonstrate the principle of how robots this small could move by determining what is important and what would need to be used to build a real system."

The simple swimmer designed by Alexeev and collaborators Hassan Masoud and Benjamin Bingham consists of a responsive gel body about ten microns long with two propulsive flaps attached to opposite sides. A steering flap sensitive to specific stimuli would be located at the front of the swimmer.

The responsive gel body would undergo periodic expansions and contractions triggered by oscillatory chemical reactions, oscillating magnetic or electric fields, or by cycles of temperature change. These expansions and contractions -- the chemical swelling and de-swelling of the material -- would create a beating motion in the rigid propulsive flaps attached to each side of the micro-swimmer. Combined with the movement of the gel body, the beating motion would move the micro-swimmer forward.

The trajectory of the micro-swimmer would be controlled by a flexible steering flap on its front. The flap would be made of a material that deforms based on changes in light intensity, temperature or magnetic field.

"The combination of these flaps and the oscillating body creates a very nice motion that we believe can be used to propel the swimmer," said Alexeev. "To build a device that is autonomous and self-propelling at the micron-scale, we cannot build a tiny submarine. We have to keep it simple."

Key to the operation of the micro-swimmer would be the latest generation of hydrogels, materials whose volume changes in a cyclical way. The hydrogels would serve as "chemical engines" to provide the motion needed to move the device's propulsive flaps. Such materials currently exist and are being improved upon for other applications.

"We are using the state-of-the art in materials science, changing the properties of the material," explained Masoud, a Ph.D. candidate in the School of Mechanical Engineering. "We have combined the materials with the principles of hydrodynamics at the small scale to develop this new swimmer."

As part of their modeling, the researchers examined the effects of flaps of different sizes and properties. They also studied how flexible the micro-swimmer's body needed to be to produce the kind of movement needed for swimming.

"You can't swim at the small scale in the same way you swim at the large scale," Alexeev said. "There is no inertia, which is how you keep moving at the large scale. What happens at the small scale is counter-intuitive to what you expect at the large scale."

The computational fluid modeling the researchers used allowed them to study a wide range of parameters in materials, oscillation rates and flexibility. What they learned, Alexeev said, will give experimentalists a starting point for actually building prototypes of the flexible gel robots.

"We have captured the solid mechanics of the periodically-oscillating body, the fluid dynamics of moving through the viscous liquid, and the coupling between the two," he said. "From a computational fluid dynamics standpoint, it's not an easy problem to model at this scale."

Ultimately, the researchers hope to work with an experimental team to actually build the micro-swimmers. Combining their theoretical work with actual experiments could be a powerful approach to building robots on this size scale.

"This is a simulation that we hope to see in real life one day," Alexeev said. "We have learned how experimentalists can pursue fabrication of these devices without extensive trial-and-error. We can use the simulations to look inside what will happen by using the laws of physics to explain it."

The researchers envision groups of micro-swimmers carrying cargo through microfluidic chips or other devices. Swarms of them could one day work together as tiny construction robots moving materials to desired locations for assembly.

But the micro-swimmers won't win any Olympic competitions. Alexeev estimates that their top speed could be on the order of a few micrometers per second -- which should be enough to accomplish their mission.

"If your body is micrometers in size, that kind of speed is really not too bad," he said. "The swimming speed will be rather slow, but at that size scale, you don't really need to go very fast since you only need to go short distances."

Story Source:

The above story is reprinted from materials provided by Georgia Institute of Technology, Research Communications.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Hassan Masoud, Benjamin I. Bingham, Alexander Alexeev. Designing maneuverable micro-swimmers actuated by responsive gel. Soft Matter, 2012; DOI: 10.1039/C2SM25898F

http://www.sciencedaily.com/releases/2012/08/120806093924.htm
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« Reply #72 on Aug 23, 2012, 1:50am »

Targeting Inflammation to Prevent, Treat Cancers

ScienceDaily (Aug. 22, 2012) — Laboratory mice bred without the gene lacked a pro-inflammatory protein called TREM-1 and protected them from developing liver cancer after exposure to carcinogens.

The study, published in Cancer Research, a journal for the American Association for Cancer Research, could lead to drug therapies to target TREM-1, said Dr. Anatolij Horuzsko, an immunologist at the GHSU Cancer Center and principal investigator on the study.

"We have long suspected that chronic inflammation is a very powerful tool in the initiation of cancer, and also in the progression or metastasis of cancer," said Horuzsko. "We [looked] at the molecules that control inflammatory responses to gain a better understanding of how this process works. One important triggering receptor for inflammation is TREM-1."

TREM-1's role in promoting inflammation is useful in cases such as battling viral or bacterial infections and in maintaining normal tissue function. But as Horuzsko's team discovered, in abnormal conditions -- such as liver damage due to alcohol abuse or other irritants -- production of TREM-1 goes haywire. A chronic, low-level state of inflammation is produced as TREM-1 leads to the development of other inflammatory agents, which causes more damage, increases cell production and creates mutated cells. These mutated cells then reproduce -- planting the seeds that can lead to cancer.

During the 14-month study, Horuzsko and his team used mouse studies to gather data on the effect of TREM-1 in the liver cells and identify potential sources for therapies. Because a mouse's life span is about three years, the length of the study mimicked a similar 20- to 30-year cancer progression of liver cancer in humans.

Two sets of mice -- one with the TREM-1 gene removed -- were exposed to the cancer-causing agent diethylnitrosamine, or DEN, which is present in tobacco smoke, chemicals and other products. Within just 48 hours of DEN injection, the control mice were already showing signs of liver cell injury and death and high levels of TREM-1 expression in the liver's Kupffer cells. These specialized liver cells normally destroy bacteria and worn-out red blood cells. Eight months later, these mice also showed massive liver tumors.

But the mice with the gene removed remained healthy, showing very few changes -- and very small, if any, tumors after eight months. The only difference between the two groups was the appearance of TREM-1 in the Kupffer cells.

Horuzko's team hopes the findings -- and their potential in TREM-1-related cancer treatment -- will be applicable to other cancers as well. "TREM-1 could be a target for any inflammation-associated cancer," said Horuzsko. "In the future, we could use a drug to target TREM-1 in the body. We are already working in this direction."

Horuzsko's team also identified another potential target for drug therapy during the study -- a product of liver cell injury and death called HMGB1. HMGB1 is a previously unknown activating ligand, or agent, that stimulates Kupffer cells to produce the TREM-1 protein and start the inflammatory process.

"Advanced drug therapies for cancer are a growing field of research, and immune therapies are an important part of our mission," said Dr. Samir N. Khleif, Director of the GHSU Cancer Center. "Studies like Dr. Horuzsko's are leading the way to identify targeted therapies that will become our future standards of care. As we open the door to new scientific discoveries, this enables us to provide better care to patients and families with cancer. "

The GHSU Cancer Center is the region's only dedicated clinical cancer and cancer research center, offering Phase 1 clinical trials. The center is also working to become Georgia's second National Cancer Institute-designated cancer center.

The Cancer and Inflammation Program at the National Cancer Institute also provided work on this study, which was funded by National Institutes of Health grants.

Story Source:

The above story is reprinted from materials provided by Georgia Health Sciences University. The original article was written by Christen Carter.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

J. Wu, J. Li, R. Salcedo, N. F. Mivechi, G. Trinchieri, A. Horuzsko. The Proinflammatory Myeloid Cell Receptor TREM-1 Controls Kupffer Cell Activation and Development of Hepatocellular Carcinoma. Cancer Research, 2012; 72 (16): 3977 DOI: 10.1158/0008-5472.CAN-12-0938

http://www.sciencedaily.com/releases/2012/08/120822154658.htm
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 Re: MedTech V: R & D
« Reply #73 on Aug 23, 2012, 1:29pm »

Artificial Intelligence Allows Automated Worm Sorting

[image]
Georgia Tech associate professor Hang Lu holds a microfluidic chip that is part of a system that uses artificial intelligence and cutting-edge image processing to automatically examine large number of nematodes used for genetic research. (Credit: Georgia Tech Photo: Gary Meek)

ScienceDaily (Aug. 19, 2012) — Research into the genetic factors behind certain disease mechanisms, illness progression and response to new drugs is frequently carried out using tiny multi-cellular animals such as nematodes, fruit flies or zebra fish. Often, progress relies on the microscopic visual examination of many individual animals to detect mutants worthy of further study.

Now, scientists have demonstrated an automated system that uses artificial intelligence and cutting-edge image processing to rapidly examine large numbers of individual Caenorhabditis elegans, a species of nematode widely used in biological research. Beyond replacing existing manual examination steps using microfluidics and automated hardware, the system's ability to detect subtle differences from worm-to-worm -- without human intervention -- can identify genetic mutations that might not have been detected otherwise.

By allowing thousands of worms to be examined autonomously in a fraction of the time required for conventional manual screening, the technique could change the way that high throughput genetic screening is carried out using C. elegans.

Details of the research were scheduled to be reported August 19th in the advance online publication of the journal Nature Methods. The research has been supported by the National Institutes of Health (NIH), the National Science Foundation (NSF) and the Alfred P. Sloan Foundation.

"While humans are very good at pattern recognition, computers are much better than humans at detecting subtle differences, such as small changes in the location of dots or slight variations in the brightness of an image," said Hang Lu, the project's lead researcher and an associate professor in the School of Chemical & Biomolecular Engineering at the Georgia Institute of Technology. "This technique found differences that would have been almost impossible to pick out by hand."

Lu's research team is studying genes that affect the formation and development of synapses in the worms, work that could have implications for understanding human brain development. The researchers use a model in which synapses of specific neurons are labeled by a fluorescent protein. Their research involves creating mutations in the genomes of thousands of worms and examining the resulting changes in the synapses. Mutant worms identified in this way are studied further to help understand what genes may have caused the changes in the synapses.

One aspect the researchers are studying is why synapses form in the wrong locations, or are of the wrong sizes or types. The differences between the mutants and the normal or "wild type" worms indicate inappropriate developmental patterns caused by the genetic mutations.

Because of the large number of possible genes involved in these developmental processes, the researchers must examine thousands of worms -- perhaps as many as 100,000 -- to exhaust the search. Lu and her research group had earlier developed a microfluidic "worm sorter" that speeds up the process of examining worms under a microscope, but until now, there were two options for detecting the mutants: a human had to look at each animal, or a simple heuristic algorithm was used to make the sorting decision. Neither option is objective or adaptable to new problems.

Lu's system, an optimized version of earlier work by her group, uses a camera to record three-dimensional images of each worm as it passes through the sorter. The system compares each image set against what it has been taught the "wild type" worms should look like. Worms that are even subtly different from normal can be sorted out for further study.

"We feed the program wild-type images, and it teaches itself to recognize what differentiates the wild type. It uses this information to determine what a mutant type may look like -- which is information we didn't provide to the system -- and sorts the worms based on that," explained Matthew Crane, a graduate student who performed the work. "We don't have to show the computer every possible mutant, and that is very powerful. And the computer never gets bored."

While the system was designed to sort C. elegans for a specific research project, Lu believes the machine learning technology -- which is borrowed from computer science -- could be applied to other areas of biology that use model genetic organisms. The system's hardware and software are currently being used in several other laboratories beyond Georgia Tech.

"Our automated technique can be generalized to anything that relies on detecting a morphometric -- or shape, size or brightness difference," Lu said. "We can apply this to anything that can be detected visually, and we think this could be expanded to studying many other problems related to learning, memory, neuro-degeneration and neural developmental diseases that this worm can be used to model."

Individual C. elegans are less than a millimeter long and thinner than a strand of hair, but have 302 neurons with well-defined synapses. While research using single cells can be simpler to do, studies using the worms are good in vivo models for many important processes relevant to human health.

Other researchers who contributed to this paper include student Jeffrey Stirman from Georgia Tech's interdisciplinary program in bioengineering, Professor James Rehg from Georgia Tech's School of Interactive Computing, and three researchers from the Department of Biology at Stanford University's Howard Hughes Medical Institute: Chan-Yen Ou, Peri Kurshan, and Professor Kang Shen.

The autonomous processing facilitated by the new system could allow researchers to examine more animals more rapidly, potentially opening up areas of study that are not feasible today.

"We are hoping that the technology will really change the approach people can take to this kind of research," said Lu. "We expect that this approach will enable people to do much larger scale experiments that can push the science forward beyond looking what individual mutations are doing in a specific situation."

Story Source:

The above story is reprinted from materials provided by Georgia Institute of Technology, Research Communications, via Newswise. The original article was written by John Toon.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Matthew M Crane, Jeffrey N Stirman, Chan-Yen Ou, Peri T Kurshan, James M Rehg, Kang Shen, Hang Lu. Autonomous screening of C. elegans identifies genes implicated in synaptogenesis. Nature Methods, 2012; DOI: 10.1038/NMETH.2141

http://www.sciencedaily.com/releases/2012/08/120819153447.htm
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"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."

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 Re: MedTech V: R & D
« Reply #74 on Aug 26, 2012, 11:00am »

Virus Detector Harnesses Ring of Light in 'Whispering Gallery Mode'

ScienceDaily (Aug. 24, 2012) — By affixing nanoscale gold spheres onto a microscopic bead of glass, researchers have created a super-sensor that can detect even single samples of the smallest known viruses. The sensor uses a peculiar behavior of light known as "whispering gallery mode," named after the famous circular gallery in St. Paul's Cathedral in London, where a whisper near the wall can be heard around the gallery.

In a similar way, waves of light are sent whirling around the inside of a small glass bead, resonating at a specific frequency. Just as a small object on a vibrating violin string can change its frequency -- ever so slightly -- so too can a virus landing on the sensor change the resonant frequency of the light. With the initial glass sphere, researchers were able to detect changes in frequency from viruses about the size of influenza, a relatively large virus.

The system, however, was not sensitive enough to detect anything smaller, such as the Polio virus. The researchers were able to increase the sensitivity of the device nearly seventyfold by adding gold nanospheres to the surface of the glass, which created what the researchers referred to as "plasmonic hot spots" -- areas where the light waves coupled with waves of electrons.

This hybrid sensor not only detected the presence of the MS2 virus -- the current light-weight in the world of RNA viruses -- it also was able to determine the weight of the virus by measuring the precise frequency change of the light.

With a few minor adjustments, the sensor should also be able to detect single proteins, such as cancer markers that appear in the blood long before outward signs of cancer can be detected. The results were published in the American Institute of Physics (AIP) journal Applied Physics Letters.

Story Source:

The above story is reprinted from materials provided by American Institute of Physics (AIP), via Newswise.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

V. R. Dantham, S. Holler, V. Kolchenko, Z. Wan, S. Arnold. Taking whispering gallery-mode single virus detection and sizing to the limit. Applied Physics Letters, 2012; 101 (4): 043704 DOI: 10.1063/1.4739473

http://www.sciencedaily.com/releases/2012/08/120824081919.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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