Synopsis: Health:


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#Chip lets scientists see how cancer spreads Johns hopkins university rightoriginal Studyposted by Phil Sneiderman-JHU on November 12 2014a new lab chip is giving researchers an unprecedented look at the complex process that spreads cancer from its birthplace

By showing scientists precisely how tumor cells travel the tool may help them plot new strategies for preventing metastasis

which leads to more than 90 percent of cancer deaths. The work is published in the journal Cancer Research.

There s still so much we don t know about exactly how tumor cells migrate through the body partly

because even using our best imaging technology we haven t been able to see precisely how these individual cells move into blood vessels says lead researcher Andrew D. Wong a graduate student in materials science and engineering at Johns hopkins university.

The material resembles the human tissue that surrounds tumors when cancer cells break away and try to relocate elsewhere.

and begin to form deadly new tumors. Wong then replicated the processes in a small transparent chip that incorporates the artificial blood vessel and the surrounding simulated tissue material.

Cancer researchers should now have a much clearer look at the complex physical and biochemical interplay involved in leaving a tumor moving through surrounding tissue and approaching a blood vessel.

Cancer cells would have a tough time leaving the original tumor site if it weren t for their ability to enter our bloodstream

So it s actually the entry of cancer cells into the bloodstream that allows the cancer to spread very quickly.

or even stop the spread of cancer. Next the researchers plan to use the device to try out various cancer-fighting drugs within this device to get a better look at how the medications perform

and how they might be improved. The device is protected by a provisional patent. A grant from Johns Hopkins Institute for Nanobiotechnology and a National Cancer Institute grant supported the work.

Source: Johns Hopkins Universit t


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#Paper circuit might diagnose Ebola in the field The first case of the Ebola outbreak currently ravaging West Africa appeared in Guinea in December 2013.

Partly because confirming the diagnosis required that epidemiologists fly from Europe to Africa collect blood samples fly back to Europe

##This could really be a game-changer for a lot of applications including diagnostics##say James Collins who is a professor of biomedical engineering and medicine at Boston University and a core faculty member at Harvard s Wyss Institute.##

##The best diagnostic tools currently use antibodies to sense things like hormones or viruses in a patient s bloodstream.

A standard pregnancy test for example tests for a hormone produced when a fertilized egg implants into a women s uterus.

##The antibody-based tests are exquisitely sensitive and we can t compete with that sensitivity yet##says Keith Pardee a postdoctoral fellow in Collins lab coauthor of the Cell paper and a Wyss Institute research scientist.##

##But to make a custom antibody it costs between $4000 and $30000 and it will take between four and six months.##

and scan for infection for exampleâ##synthetic gene circuits are especially useful for detecting things like contaminants pesticides heavy metals and counterfeit drugs.##

##The technology can be embedded in any porous material such as cloth potentially opening the door for wider applications says Collins. He envisions smart scrubs for health care workers that can sense exposure to a virus;

bandages that signal when a wound is infected with antibiotic-resistant bacteria; or smart clothing that tells a runner she s getting dehydrated.##


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Copsin belongs to the group of defensins a class of small proteins produced by many organisms to combat microorganisms that cause disease.

The human body also produces defensins to protect itself against infections. They have been found for example on the skin and in the mucous membranes.

Whether copsin will one day be used as an antibiotic in medicine remains to be seen. This is by no means certain

while humans have been using antibiotics in medicine for just 70 years with many of them already becoming useless due to resistance?

In addition to being used as an antibiotic in medicine it may also be possible to use copsin in the food industry as well.

This is because copsin kills many pathogens including Listeria a type of bacteria that can cause severe food poisoning


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and other medical professionals measure and improve the diets of children and adults alike.####There is great interest in the development of objective biomarkers of dietary intake especially biomarkers that can be measured noninvasively##says coauthor Susan T. Mayne professor of epidemiology at Yale university and a developer of the device.##

##Our earlier studies demonstrated a correlation between skin carotenoids and fruit and vegetable intakeâ##this new paper demonstrates that the biomarker was sensitive to changes in fruit and vegetable intake in the intervention setting.##

Diets rich in fruit and vegetables have been linked to important health outcomes including reductions in cardiovascular disease type 2 diabetes and some forms of cancer.

Brenda Cartmel a senior research scientist and lecturer at the Yale School of Public health is a co-author of the paper along with researchers from the USDA/Agricultural research service Grand Forks Human nutrition Research center and the University of Utah.


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and has been shown to cause cancer. Because biochar can be produced from various waste biomass including agricultural residues this new technology provides an alternative


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#Lab mice bred to test Ebola vaccines University of North carolina at Chapel hill University of Washington rightoriginal Studyposted by Mark Derewicz-UNC on November 3 2014researchers have developed the first genetic strain

It s a critical step toward developingâ#treatments and vaccines.####You can t look for a cure for Ebola

unless you have an animal model that mimics the Ebola virus disease spectra##says study coauthor Ralph Baric professor of epidemiology at the University of North carolina at Chapel hill.

Typical laboratory mice usually do not develop humanlike Ebola disease including the severe symptoms that can prove fatal in humans.

So the researchers asked whether all mice are immune to Ebola or whether some strains of mice are susceptible;

and if some are susceptible could they harness the power of mouse genetics to figure out what genes make someone susceptible to the disease.

and successfully test a strain of mice to permit active research on potential Ebola vaccines and treatments.

when infected with the virus. The team was able to show that a combination of genes were involved in producing a range of disease symptoms such that the genetic variation of the mice directly led to the variety of symptoms that the disease produced.

##A basic understanding of how our genetics influence susceptibility to viral infections and affect disease development is absolutely critical to creating much needed therapeutic interventions.##

##says William Fischer an assistant professor of medicine who has treated Ebola patients in Africa.####We can decrease Ebola fatality rates with intensive critical care

but this is difficult to do in places with limited human and material resources. Rationally designed treatments and vaccines are needed desperately##adds Fischer who was not part of this research project.

Martin Ferris coauthor of the paper published in Science and a research assistant professor of genetics in the UNC School of medicine says:##

##Public perception of Ebola infection typically focuses on the high mortality rate following hemorrhagic fever but Ebola actually produces a range of disease symptoms.##

##During an outbreak it is often difficult to assess the role that genetic variation plays in determining disease severity in people.

And if we re going to develop treatments then we need to know about this genetic variation.##


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#How to coax doctors out of their comfort zones Hearing about a new therapy from an influential colleague increases a doctor s odds of trying it out.

It s difficult to get doctors to adopt new therapies because you are invading people s comfort zones

and the way they usually do things says lead author Curtis Weiss assistant professor of medicine at Northwestern University Feinberg School of medicine and a physician at Northwestern Memorial Hospital.

By analyzing physician social networks the researchers examined how doctors are connected professionally and pass information to each other and how that leads to increasing adoption.

The current belief is physicians catch a new therapy in what is known as a contagion model.

One doctor sees another doctor prescribing a drug or ordering a test and she will catch

whose utility is difficult if not impossible to gauge says senior author Luis Amaral professor of chemical and biological engineering at the Mccormick School of engineering and Applied science and a professor of medicine at Feinberg.

It s a surprisingly long road from Food and Drug Administration approval of a new drug or technique to doctors actually using the new drug in their practices notes Weiss whose research focuses on how to get doctors to adopt best practices.

and discussed at medical conferences and then doctors in that field were supposed to integrate that into their clinical practice Weiss says.

The problem with that is doctors are busy and don t always read the journals or go to those conferences.

But the bigger issue is even if you read the article and go to the conference if you don t see a patient with that condition for six months you may have forgotten the therapy.

And there s no follow up or reinforcement after the conference about how to use it. The authors analyzed the social networks of critical care physicians in the medical intensive care unit (ICU) at Northwestern Memorial Hospital.

The test case was a new high-impact serum assay or blood test that measures an enzyme shown to be a marker of life-threatening bacterial infections and sepsis in critically ill patients.

The assay has been reported in medical literature as an effective marker but is not yet a part of the guidelines for care.

The current way to diagnose infection is a culture but those results take 48 to 72 hours.

A quicker diagnosis may improve patient treatment. Prior to the study Northwestern didn t have the assay available in its lab. Weiss learned the assay was going to become available and convinced the lab director not to tell anyone before the experiment.

Weiss and Amaral then seeded information about the new serum to two other ICU physicians chosen at random.

which time 20 out of 36 doctors adopted the assay. We discovered the persuasion model was more accurate in explaining the number

Optimized interventions could help increase adoption of best practices in hospitals around the country and increase quality of care Weiss says.

and emphasize using the new therapy (or best practice) closer to the point at which they would actually use it.

Interventions also can regularly audit doctors adoption. It could say hey you only used this 30 percent of the time


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The ability to better understand the difference between normal and pathological activity within the brain may lead to the ability to predict


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Biomedical engineers exploring ways to toughen up engineered cartilage and keep natural tissues strong outside the body report new developments in the Proceedings of the National Academy of Sciences.##

or approved for use in humans a current method for treating serious joint problems is with transplants of native cartilage.

##The ramifications of the work presented in the PNAS paper are tremendous with respect to tissue grafts used in surgery as well as new tissues fabricated using the principles of tissue engineering##says Kyriacos A. Athanasiou a professor of biomedical engineering and orthopedic surgery and chair


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The researchers demonstrate that these converted cells survived at least six months after injection into the brains of mice

They are affected the primary cells in Huntington s disease an inherited genetic disorder that causes involuntary muscle movements and cognitive decline usually beginning in middle-adulthood.

In regard to potential future therapies the ability to convert adult human cells presents the possibility of using a patient s own skin cells

To study the cellular properties associated with the disease the investigators now are taking skin cells from patients with Huntington s disease


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A new study shows the girls with a family history of depression respond to stress by releasing much higher levels of the hormone cortisol.

Telomeres also shorten as a result of exposure to stress. Previous studies have uncovered links in adults between shorter telomeres and premature death more frequent infections and chronic diseases.

I did not think that these girls would have shorter telomeres than their low-risk counterparts they'e too young says Ian Gotlib professor of psychology at Stanford university.

For the study published in Molecular Psychiatry researchers recruited 10-to 14-year-old healthy girls with a family history of depression

so girls at high-risk girls should learn stress reduction techniques Gotlib says. Other studies show that neurofeedback


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or two fist-size servings of these nonstarchy vegetables reduced their risk for liver problems Type 2 diabetes and other complications of obesity.


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and Sierra Leona could be infected with Ebola by late January according to the US Centers for Disease Control and Prevention.

and difficulty of diagnosing the disease when a patient is seen first. Conventional fluorescent label-based virus detection methods require expensive lab equipment significant sample preparation transport and processing times and extensive training to use.

The device could be used to diagnose Ebola and other hemorrhagic fever diseases in resource-limited countries.

and hemorrhagic fever diseases our collaborative research effort has produced a highly sensitive device with the potential to perform rapid diagnostics in clinical settings.##

and handling our system can reduce potential exposure to health care workers##says Connor a researcher at Boston University s National Emerging Infectious diseases Laboratories (NEIDL).#

##The shoebox-sized prototype diagnostic device known as the single particle interferometric reflectance imaging sensor (SP-IRIS) detects pathogens by shining light from multicolor LED sources on viral nanoparticles bound to the sensor

surface by a coating of virus-specific antibodies. Interference of light reflected from the surface is modified by the presence of the particles producing a distinct signal that reveals the size and shape of each particle.

and fastâ##ideally delivering answers within 30 minutesâ##through further technology development and preclinical trials.

Based on the team s current rate of progress a field-ready instrument could be ready to enter the medical marketplace in five years.


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If cancer markers are found in a cell the circuit could for example activate a cellular suicide program.

Healthy cells without cancer markers would remain unaffected by this process. Biocomputers differ significantly from their counterparts made of silicon


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and Marburg s comparative evolution could##affect design of vaccines and programs that identify emerging pathogens##researchers write in the journal Peerj.

The research does not address the age of the modern-day Ebola virus. Instead it shows that Ebola

Taylor and coauthor Jeremy Bruenn professor of biological sciences research viral##fossil genes##â##chunks of genetic material that animals and other organisms acquire from viruses during infection.

Understanding the virus ancient past could aid in disease prevention Taylor says. If a researcher were trying to create a single vaccine effective against both Ebola

and Marburg it could be helpful to know that their evolutionary lineages diverged so long ago.

Knowing more about filoviruses in general could provide insight into which host species might serve as##reservoirs##that harbor undiscovered pathogens related to Ebola


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#Diabetes may raise risk for heart valve disease Rice university right Original Studyposted by Mike Williams-Rice on October 21 2014 There appears to be a link between high blood sugar and heart valve hardening.

and their activities says Peter Kamel a medical student at Baylor College of Medicine who completed the research as an undergraduate at Rice university.

That results in patients with diabetes having problems with vision and with their nerves and kidneys as well.

The results that high glucose concentration can also cause pathologic remodeling by the aortic-valve cells could suggest that diabetes is also directly a cause of aortic-valve disease he adds.

We know that calcific aortic-valve disease is associated heavily with metabolic syndrome which can lead to type 2 diabetes.

It s not as common as the link between atherosclerosis and diabetes but it s definitely an appreciable strong subset.

To understand any heart valve-related disease we need to understand the mechanism of how the cells interact with excess lipids

and sugars and we re just starting to scratch the surface she says. So work like this is pretty fundamental.


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#Therapy cures hearing loss from loud noises University of Michigan rightoriginal Studyposted by Kara Gavin-U. Michigan on October 21 2014scientists restoredâ#hearing to mice that were deafened partly by noise.

The work reported in the journal elife suggests the protein might be a target for treating people who have suffered hearing loss due to noise or aging.

##It has become apparent that hearing loss due to damaged ribbon synapses is a very common and challenging problem

He also notes that the research may have implications for neurodegenerative diseases. Researcher from Harvard university collaborated on the project

which was funded by the National Institute on Deafness and Other Communication Disorders the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Hearing Health Foundation.


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One way that Staphylococcus aureus and other pathogens can become resistant to antibiotics is to change the way they generate energy

and become small and weak colony variantssays Eric Skaar professor of pathology microbiology and immunology at Vanderbilt University.

and grow poorly in the laboratory cause such persistent infections in humans? Current studies support the notion that antibiotic-resistant staph bacteria including methicillin-resistant (MRSA) strains can exchange nutrients with each other

and even with other bacterial species including the normal microbes of the microbiome to increase their virulence during an infection.

& Microbe challenge infectious disease dogma Skaar says. The thinking has been that if an infection becomes resistant to antibiotics then the resistant organisms appeared clonally meaning they're all genetically the same.

Skaar and colleagues wondered if perhaps instead there are a bunch of organisms that became resistant in different ways

Next they tested the idea in a mouse model of the bone infection osteomyelitis. Antibiotic-resistant small colony variant S. aureus is the cause of chronic and difficult to treat osteomyelitis and also of lung infections in patients with cystic fibrosis (CF.

-or menaquinone-deficient) caused only minimal bone infection but mixed together they caused a fully virulent and bone-destroying infection.

In bone these bacteria are trading molecules Skaar says. Researchers then isolated samples of staph small colony variants and normal bacteria from the lungs of CF patients.

The microbiome of a cystic fibrosis patient s lungs can provide nutrients to these small colony variants

Our findings show that these antibiotic-resistant infections are not what we thought they were they're not a single strain of bacteria with a single lesion leading to the small colony variant phenotype.

Instead they re a mixed population of organisms that are sharing nutrients. They act like a big group of bullies until you hit them with drugs then they stop sharing resources

We're now a little bit smarter about how these organisms are behaving in an infection which

Preventing the nutrient exchange for example may offer a new therapeutic strategy against these antibiotic-resistant organisms The National institutes of health supported the research.


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#Drug flips cells to limit damage after heart attack University of North carolina at Chapel hill rightoriginal Studyposted by Mark Derewicz-UNC on October 16 2014a new way to generate more blood vessels after a heart attack can reduce damage

This switch is driven by p53 the well-documented tumor-suppressing protein. Researchers showed that increasing the level of p53 in scar-forming cells significantly reduced scarring

and improved heart function after heart attack. The finding published in the journal Nature shows that it is possible to limit the damage wrought by heart attacks which strike nearly one million people in the United states each year.

Heart disease accounts for one in four deaths every year.####Scientists have thought that fibroblasts are differentiated terminally meaning they can t adopt the fate of other kinds of cells;

##It appears that injury itself can induce fibroblasts to change into endothelial cells so the heart heals better.

##After a heart attack fibroblasts replace damaged heart muscle with scar tissue. This scarring can harden the walls of the heart

To explore this idea they induced heart attacks in mice and then studied the fibroblasts to see if the cells expressed markers characteristic of endothelial cells.

To their surprise almost a third of the fibroblasts in the area of the cardiac injury expressed these endothelial markers.

Because a heart attack is such a stressful event Ubil created a list of genes that were known to be involved in cellular responses to stress.

or apoptosis which reduces the likelihood that they will go on to form tumors.####As luck would have it that was the first gene

##or overexpressed in the fibroblasts after heart injury and this seemed to regulate fibroblasts becoming endothelial cells.

and used it to treat mice for a few days after cardiac injury. The drug had dramatic results doubling the number of fibroblasts that turned into endothelial cells.

They had more blood vessels at the site of injury and their heart function was better.##

##By increasing the number of blood vessels in the injury region we were able to greatly reduce the effects of the heart attack.##

##Ubil says his study shows that this could be a novel strategy for treating heart attacks.

and this could potentially benefit people who have heart attacks.####Deb adds:####We are also currently investigating

whether such an approach could be applied for treating scarring in other organs after injury.####The American Heart Association and the National institutes of health funded the work.


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Researchers would like to place very small implants deep inside our bodies to monitor health or treat pain.

But providing electric power to implants without wires or batteries has been a big obstacle. Now engineers are developing a way to send power safely

and wirelessly to smart chips programmed to perform medical tasks and report back the results.

and execute medical commands and report the completed activity via a tiny built-in radio antenna.""We think this will enable researchers to develop a new generation of tiny implants designed for a wide array of medical applications"says Amin Arbabian assistant professor of electrical engineering at Stanford university.

Arbabian's team recently presented a working prototype of this wireless medical implant system at the IEEE Custom Integrated circuits Conference in San jose California.

The researchers chose ultrasound to deliver wireless power to their medical implants because it has been used safely in many applications such as fetal imaging

and can provide sufficient power to implants a millimeter or less in size. Now Arbabian and his colleagues are collaborating with other researchers to develop sound-powered implants for a variety of medical applications including studying the nervous system

and treating the symptoms of Parkinson's disease.""Tiny wireless nodes such as these have the potential to become a key tool for addressing neurological disorders"says Florian Solzbacher professor of electrical and computer engineering at University of Utah and director of its Center for Engineering Innovation.

The implant chip is powered by piezoelectricity which is caused electricity by pressure. In a piezoelectric material pressure compresses its molecular structure much like a child jumping on a bed compresses the mattress.

When the pressure abates the piezoelectric material's molecular structure like the mattress springs back into shape.

Every time a piezoelectric structure is compressed and decompressed a small electrical charge is created. Researchers created pressure by aiming ultrasound waves at a tiny piece of piezoelectric material mounted on the device."

"The implant is like an electrical spring that compresses and decompresses a million times a second providing electrical charge to the chip"says Marcus Weber who worked on the team with fellow graduate students Jayant Charthad and Ting Chia Chang.

In the future the team plans to extend the capabilities of the implant chip to perform medical tasks such as running sensors

or delivering therapeutic jolts of electricity right where a patient feels pain. Finally the"smart chip"contains a radio antenna to beam back sensor readings or signal the completion of its therapeutic task.

The current prototype is the size of the head of a ballpoint pen. Researchers hope to design a next-generation implant one-tenth that size.

"This requires being able to interface with cells using arrays of micro implants across the entire 3d structure of the brain."

"Arbabian's team wants to test many other applications using this basic technology to wirelessly power small implants deep inside the body."

"Many biosensing and stimulation applications require small deep medical implants"he says.""We believe our platform provides the recipe for building small devices that can be powered wirelessly


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#Brain surgery robot would go through the cheek Vanderbilt University Posted by David Salisbury-VU on October 16 2014for people with severe epilepsy treatment can mean drilling through the skull deep into the brain

if it was possible to address epileptic seizures in a less invasive way? They decided it would be possible.

In addition the needle is inserted in tiny millimeter steps so the surgeon can track its position by taking successive MRI scans.

According to project leader Eric Barth associate professor of mechanical engineering the next stage in the surgical robot s development is testing it with cadavers.

'##At the same time Robert Webster associate professor of mechanical engineering had developed a system of steerable surgical needles.####The idea for this came about when Eric and

The engineers identified epilepsy surgery as an ideal high-impact application through discussions with Joseph Neimat associate professor of neurological surgery.

and identify the location where the epileptic fits originate. But the straight needles they use can t reach the source region

Comber and Barth shadowed Neimat through brain surgeries to understand how their device would work in practice.##

and unlimited access would make surgeries minimally invasive. We could do a dramatic surgery with nothing more than a needle stick to the cheek.##

##The engineers have designed the system so that much of it can be made using 3d printing in order to keep the price low.


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