#Wireless tattoo patch tracks health 24/7 A thin, soft stick-on patch that can stretch and move with the skin uses off-the shelf chip-based electronics to continuously track health
and wirelessly send updates to your cellphone or computer. The patches stick to the skin like a temporary tattoo
and incorporate a unique microfluidic construction with wires folded like origami to allow the patch to bend
and flex without being constrained by the rigid electronics components. Researchers say the patches could revolutionize clinical monitoring such as EKG and EEG testingo bulky wires, pads,
or tape required. They report their findings in Science. e designed this device to monitor human health 24/7
but without interfering with a person daily activity, says Yonggang Huang, professor of civil and environmental engineering and mechanical engineering at Northwestern University. t is as soft as human skin
and can move with your body, but at the same time it has many different monitoring functions. What is very important about this device is it is powered wirelessly
and can send high-quality data about the human body to a computer, in real time. Researchers did a side-by-side comparison with traditional EKG
and EEG monitors and found the wireless patch performed equally to conventional sensors, while being significantly more comfortable for patients.
STRESS TESTS AND SLEEP STUDIES Such a distinction is crucial for long-term monitoring situations, such as stress tests or sleep studies
when the outcome depends on the patient ability to move and behave naturally, or for patients with fragile skin such as premature newborns.
John A. Rogers, professor of materials science and engineering at the University of Illinois and a coauthor of the current study, previously demonstrated skin electronics made of very tiny, ultrathin, specially designed and printed components.
While those also offer high-performance monitoring, the ability to incorporate readily available chip-based components provides many important
complementary capabilities in engineering design, at very low cost. ur original epidermal devices exploited specialized device geometriesuper thin, structured in certain ways,
Rogers says. ut chip-scale devices, batteries, capacitors, and other components must be reformulated for these platforms.
RIGAMIWIRES here a lot of value in complementing this specialized strategy with our new concepts in microfluidics
Researchers turned to soft microfluidic designs to address the challenge of integrating relatively big, bulky chips with the soft
The chip components are suspended on tiny raised support points, bonding them to the underlying patch
squiggly wires connecting the electronics componentsadios, power inductors, sensors, and more. The serpentine-shaped wires are folded like origami,
the chips don have to. Skin-mounted devices could give those interested in fitness tracking a more complete and accurate picture of their activity level,
STRETCHABLE ELECTRONICS elative motion causes a lot of background noise. If you have mounted these skin devices and an ability to locate them on multiple parts of the body,
For example, data analysis could detect motions associated with Parkinson disease at its onset. he application of stretchable electronics to medicine has a lot of potential,
it could be possible to catch health conditions before experiencing pain, discomfort, and illness. The National security Science and Engineering Faculty Fellowship of Energy
the Korean Foundation for International Cooperation of Science and Technology, and the Department of energy supported the work.
Source: Northwestern Universit o
#Microchip could detect infection in artificial joints A tiny microchip could improve postoperative care for patients with knee replacements
and other surgical implants by detecting early signs of infection. Alexander Star, an associate professor of chemistry at the University of Pittsburgh, says the new chip,
which is engineered to detect ph levels in the body, will be able to alert doctors to encroaching bacterial infection,
which causes acidosis, a drop in ph levels in nearby tissue. The chip, festooned with tiny carbon nanotubes (engineered segments of carbon that are efficient electrical conductors) and treated with a proprietary polymer
reads ph levels and transmits the information to a radio frequency identification reader held by a doctor.
The wirelessly powered chip can be attached to implants and can stay in the body long term.
One in 100 Americans has an artificial joint, Star says, nd bacterial infections are a common complication of the implant.
Infection can damage the body surrounding the implant, and bacterial films, resistant to antibiotics, can colonize the implant itself.
To catch infection early without having to resort to invasive measures could lead to faster treatment. his is a very attractive detection mechanism for monitoring the condition of the implant
Star says. t may alleviate the need for further surgical intervention. A paper on the chip appears online in Scientific Reports.
Star and his team have developed similar chip/nanotube sensors that can be affixed to a toothbrush to detect bad breath (the presence of hydrogen sulfide)
and another that can identify the beginning of an asthma attack by measuring nitric oxide. Another Star-developed chip measures acetone in breath, an indicator of diabetes.
A National Energy technology Laboratory grant supported the research
#Silly Putty component helps build carpet for stem cells The sponginess of the environment where human embryonic stem cells are growing affects the type of specialized cells they eventually become, a new study shows.
The researchers coaxed human embryonic stem cells to turn into working spinal cord cells more efficiently by growing the cells on a soft,
ultrafine carpet made of a key ingredient in Silly Putty. Their study is appears online in Nature Materials.
This research is the first to directly link physical, as opposed to chemical, signals to human embryonic stem cell differentiation.
Differentiation is the process of the source cells morphing into the body more than 200 cell types that become muscle
bone, nerves, and organs, for example. Jianping Fu, assistant professor of mechanical engineering at University of Michigan, says the findings raise the possibility of a more efficient way to guide stem cells to differentiate
and potentially provide therapies for diseases such as amyotrophic lateral sclerosis (Lou Gehrig disease), Huntington, or Alzheimer. In the specially engineered growth systemhe arpetsfu
and his colleagues designedicroscopic posts of the Silly Putty component polydimethylsiloxane serve as the threads.
By varying the post height, the researchers can adjust the stiffness of the surface they grow cells on.
Fu is collaborating with doctors at the University of Michigan Medical school. Eva Feldman, professor of neurology, studies amyotrophic lateral sclerosis, or ALS.
It paralyzes patients as it kills motor neurons in the brain and spinal cord. Researchers like Feldman believe stem cell therapiesoth from embryonic and adult varietiesight help patients grow new nerve cells.
and whether the process could work, and they hope to try it in humans in the future. rofessor Fu
discoveries like this provide tools for modeling disease in the laboratory and for developing cell-replacement therapies.
and preventing tumor growth. Fu says his findings could also provide insights into how embryonic stem cells differentiate in the body. ur work suggests that physical signals in the cell environment are important in neural patterning,
a process where nerve cells become specialized for their specific functions based on their physical location in the body,
of the H1n1 flu virus. Flu epidemics cause up to half a million deaths each year, and emerging strains continually threaten to spread to humans and cause even deadlier pandemics.
The findings, published in Immunity, pave the way for an urgently needed therapy that is highly effective against the flu virus
and potentially other viral infections. rugs that specifically target PGE2 pathways have already been developed and tested in animals,
so our results have excellent potential for clinical translation, not only for the treatment of influenza,
but other viral respiratory infections that interact with similar host immune pathways, says senior author Maziar Divangahi, an assistant professor in the Faculty of medicine at Mcgill University.
Despite the worldwide use of vaccination and other antiviral interventions, the flu virus remains a persistent threat to human health.
To investigate molecular pathways that could be targeted by new interventions, Divangahi and his team focused on drugs such as aspirin and ibuprofen,
commonly used to manage flu-like symptoms. By inhibiting a molecule called cyclooxygenase (COX ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDS) lower the production of five major prostanoidsmmune molecules that contribute to pain
and fever. ut since these drugs inhibit all prostanoids, each may contribute differently towards the immunity against influenza virus,
says Francois Coulombe, a Mcgill Phd student and the study first author. nderstanding their individual role is crucial in developing a new therapy.
Divangahi research team found that mice genetically engineered to lack a member of the prostanoid family,
PGE2, showed remarkably enhanced immunity to flu infection. Most importantly, the vast majority of these mice infected with a lethal dose of the H1n1 flu virus survived.
Similarly mice treated with a compound that inhibits PGE2 showed enhanced antiviral immunity and produced better survival rates following infection with a lethal dose of the flu virus compared with untreated mice. revious studies produced conflicting results due to the inhibition of all prostanoids
, not just PGE2, Divangahi says. ur findings suggest that different prostaglandins have different roles in antiviral immunity
and that specific inhibition of PGE2 will be an effective therapy against influenza viral infection by boosting immune responses. i
#Stop copying protein to knock out flu virus The Influenza a virus makes a protein that helps it outwit one of the body natural defense mechanisms.
That protein could be a good target for antiviral drugs, researchers suggest. Better antiviral drugs could help the millions of people annually infected by flu,
When an influenza virus infects a human cell, it uses some of the host cellular machinery to make copies of itself,
says Robert Krug, professor of molecular biosciences at University of Texas at Austin. In addition to countering the body defense mechanisms,
FAST-SPREADING EPIDEMICS The need for new antiviral drugs against the influenza virus is great.
Because flu vaccines are not 100 percent effective, antiviral drugs play an important role in fast-spreading epidemics.
Yet Influenza a viruses are developing resistance to antiviral drugs currently in use. Krug and his team discovered that the viral NS1 protein is associated often,
#New clues to why RSV sends babies to the hospital Researchers have pinpointed a viral protein that plays a major role in making respiratory syncytial virus (RSV) the most common cause of hospitalization in children under one
and potential treatments for an infection that strikes nearly all children before they reach the age of three
and causes severe disease in 3 percent of infected children. RSV infection leads to the hospitalization of between 75,000 and 125,000 babies under one year of age in the United states every year.
Globally RSV is the second-leading cause of infant mortality due to infectious disease behind only malaria. ee known for a long time that RSV has increased an propensity,
compared to other respiratory viruses, for causing obstruction and inflammation in the narrowest airways of the infant lung,
leading to severe bronchiolitis, says Raymond Pickles, associate professor of microbiology and immunology. ut what wee now shown is that RSV has increased an ability to cause airway obstruction because, during an RSV infection,
the virus expresses a specific RSV-encoded nonstructural protein, or NS2, in epithelial cells, causing the cells to shed from the airway lining and into the airway lumen.
This leads to obstruction of airflow in the small airways and overwhelming inflammation. Published in the Journal of Clinical Investigation, the study shows it this NS2 protein
and its effect on epithelial-cell shedding that makes RSV by far the most common cause of bronchiolitis in otherwise healthy young children.
and other common respiratory viruses that might account for the increased disease caused by RSV, Pickles says. e compared the ability of RSV
which compose the lining of the lung airway. ut comparing these consequences of infection did not provide hints as to why RSV and PIV3 produced such differences in disease severity.
though, that the epithelial cells infected by RSV looked very different during infection compared to those infected by PIV3.
CELLS BALL UP AND PUFF OUT In experiments led by graduate student Rachael Liesman, the researchers decided to engineer PIV3 to express the RSV NS2 gene.
They found that infection of the narrowest airways of the lung by PIV3 alone caused moderate levels of inflammation,
but after infection by PIV3 expressing RSV NS2, the epithelial cells lining the narrow airways were shed rapidly into the airway lumen.
what has been found in human infants who had died because of RSV infection. Pickles says convinced that the RSV NS2 gene is a major driver for the well-recognized increased ability of RSV to cause lung disease, especially in the extremely narrow small airways of human infants.
Pickles is now on the trail of a human biomarker that would tell doctors if an RSV-infected infant is at greater risk of developing severe lung disease.
A biomarker would be key in the development of a needed diagnostic tool and would aid clinical trials that aim to develop anti-RSV therapeutics.
TOO SICK TO SEND HOME? hen young children arrive at the hospital with an RSV infection,
it challenging and frustrating to guess which children you can safely send home, versus those you should admit to the hospital
because they might require supportive care in an intensive care unit, says Michelle Hernandez, a pediatric immunologist. ny information that will help us make these decisions not only helps us ensure that we provide the best care for these kids,
but also helps us use health care resources more wisely. Using animal models, Pickles has already found candidate molecular biomarkers that indicate
if the epithelial cells in the tiniest airways are expressing the RSV NS2 protein. He is now initiating studies to look for the same biomarkers in human infants infected with RSV f we can find biomarkers informing us that the most vulnerable parts of the lung have already been infected by RSV,
then it could be possible to identify much more quickly the children at more risk for developing severe lung disease
and to get those babies in a treatment protocol at an earlier time, he says.
Regarding whether these findings could lead to better RSV treatments, it may be possible to suppress the ability of NS2 to shed the airway epithelial cells.
Thwarting this shedding effect wouldn stop infection or stifle the typical symptoms of RSV infection
but it might limit the virus ability to spread into the tiniest airways, which are the most likely to be obstructed by cells shed during infection.
This would lead to a less severe infection and fewer hospitalizations. Suppressing the effects of the RSV NS2 protein may also allow our immune system more time to deal with the RSV infection before the small airways become clogged with cells shedding from the lining of the airway,
Pickles says. hese are questions we are aiming to answer in studies already underway
#Gastric banding treats diabetes in overweight people Gastric banding can play a vital role in the treatment of type 2 diabetes in people who are overweightot just those who are obese.
Monash University researchers found that weight loss surgery (gastric banding) for overweight people with diabetes had a profound impact on the illness. his is randomized the first controlled trial demonstrating that treatment of type 2 diabetes
in overweight people by substantial weight loss is safe and hugely beneficial, says Professor Paul Orien from Monash University Centre for Obesity Research and Education (CORE).
s there are no alternative options that can achieve such a result, this study indicates a potentially attractive path for the overweight person with diabetes and for those providing the care.
The study, published in the Lancet Diabetes and Endocrinology, looked at people who suffered diabetes
and were overweight, but not obese. The connection between excessive body weight and diabetes is well known,
but while the benefits of weight loss for obese people suffering type 2 diabetes have been well document,
it has not been clear if those who were overweight would enjoy the same benefits.
The study enrolled 50 people with diabetes who were overweight but not obese, with a body mass index between 25 and 30. e provided a comprehensive program of multidisciplinary care to all of the participants,
but randomly allocated half of them to receive an additional treatment of adjustable gastric banding,
Orien explains. he surgery was conducted as an outpatient procedure with no significant adverse effects. We were pleased to see was that after two years into the trial,
more than half of the banded group were in remission of their diabetes while only eight percent of the non banded group were in remission.
The results showed a strong relationship between the amount of weight loss and remission of diabetes
clearly showing that successful ways of reducing weight such as gastric banding should have a high priority in the treatment of diabetes e
#Dog genes may offer clues to cleft palate in humans Researchers have identified the genetic mutation responsible for a form of cleft palate in a breed of dog,
the Nova scotia Duck Tolling Retriever. They hope the discovery, which provides the first dog model for the craniofacial defect,
Although cleft palate is one of the most common birth defects in children, affecting approximately one in 1, 500 live human births in the United states,
The findings appear online this week in the journal PLOS Genetics. his discovery provides novel insight into the genetic cause of a form of cleft palate through the use of a less conventional animal model says study leader Professor Danika Bannasch,
a veterinary geneticist at the UC Davis School of veterinary medicine. t also demonstrates that dogs have multiple genetic causes of cleft palate that we anticipate will aid in the identification of additional candidate genes relevant to human cleft palate.
Bannasch explains that common breeding practices have made the dog a unique animal model to help understand the genetic basis of naturally occurring birth defects.
By conducting a genome-wide study of these particular retrievers with a naturally occurring cleft palate,
researchers identified a mutation responsible for the development of cleft palate in the breed. Dogs with this mutation also have shortened a lower jaw
similar to humans who have Pierre Robin Sequence. The disorder, a subset of cleft palate, affects one in 8,
Children born with cleft palate may develop hearing loss and difficulties with speech and eating. They also may be increased at risk for neurological deficits.
The Center for Companion Animal health at the School of veterinary medicine and the National institutes of health supported the research
#Scientists find off switch for scleroderma Researchers have identified a signaling pathway that switches on scleroderma,
a rare and sometimes fatal disease that causes skin and other tissue to thicken. There is currently no cure for the condition.
The team also says they have found the chemical compounds that can turn the switch off. ur findings provide a new approach to developing better treatment options where few have existed,
says Richard Neubig, chairperson of the department of pharmacology and toxicology in the College of Osteopathic Medicine at Michigan State. here are two kinds of scleroderma, localized and systemic,
with the latter often proving to be life threatening, Neubig says. his research shows that by inhibiting this main signaling pathway,
we can block fibrosishe thickening of tissue that occurs with the disease. Localized scleroderma affects the skin and causes a loss of flexibility.
Systemic sclerosis can spread throughout the body, hardening organs such as the lungs, heart, gut, and kidneys.
Scleroderma is an autoimmune disorder. It estimated 300,000 Americans suffer from the disease with about one-third of those having the systemic form.
Localized scleroderma patients usually live normal lifespans. Yet about half of systemic patients especially with widespread skin involvement and internal organ fibrosis, will see their lives cut short.
Scleroderma many pathways he majority of drug treatments that exist today for fibrosis basically look at reducing just the inflammation,
says Dinesh Khanna, associate professor of internal medicine at the University of Michigan. here are other drugs that block one or two of the signaling pathways that cause the disease,
but scleroderma has many of these pathways. Published in the Journal of Pharmacology and Experimental Therapeutics, the new research could significantly change the quality of life for scleroderma patients
and greatly increase the lifespan of systemic patients, Neubig says. ur research shows promise for the development of a new drug that can reverse the fibrosis process by flipping the main switch on all of the signaling pathways.
By validating this core switch as a viable drug target, we can now continue our work to improve the chemical compounds
so they will work with doses that are appropriate for people. It definitely promising. A donation from Jon and Lisa Rye, a Michigan family who has experienced the effects of scleroderma,
and the family crowdfunding site, the Scleroderma Cure Fund, helped support the research h
#Anticancer drug reverses schizophrenia symptoms in teen mice An experimental anticancer drug appears to reverse schizophrenia-related behavior
and restore some lost brain cell function in young mice with a rodent version of the illness,
researchers say. The compound, called FRAX486, appears to halt an out-of-control biological runingprocess in the schizophrenic brain that unnecessarily destroys important connections among brain cells,
according to a new study published online in the Proceedings of the National Academy of Sciences. y using this compound to block excess pruning in adolescent mice,
we also normalized the behavior deficit, says study leader Akira Sawa, professor of psychiatry and behavioral sciences at Johns hopkins university School of medicine. hat we could intervene in adolescence
and still make a difference in restoring brain function in these mice is intriguing. FRAX486 is a PAK inhibitor,
one of a class of drugs shown in animal experiments to confer some protection from brain damage due to Fragile X syndrome,
an inherited disease in humans marked by mental retardation. There also is some evidence, experts say, that PAK inhibitors can be used to treat Alzheimer disease.
And because the PAK protein itself can initiate cancer and cell growth PAK inhibitors have also been tested for cancer.
Working with mice that mimic schizophrenia and related disorders, the researchers were able to partially restore disabled neurons
so they could connect to other nerve cells. The findings in adolescent mice are an especially promising step in efforts to develop better therapies for schizophrenia in humans,
researchers say, because schizophrenia symptoms typically appear in late adolescence and early adulthood. Schizophrenia is a chronic,
severe mental disorder that affects about one in 100 people, the National institute of mental health says. Patients may experience hallucinationsften hearing nonexistent voicesnd delusions
and they may not make sense when they speak. Among other problems, they may also appear agitated
or have cognitive problems such as difficulty focusing or issues with working memory. MISSING SPINES The researchers began their study by chemically turning down expression in their mice of a gene known as Disrupted-in-Schizophrenia 1. DISC1,
as it is called, makes a protein that appears to regulate neurons in the cerebral cortex responsible for igher-orderfunctions, like information processing.
In studies of rodent brain cells, the researchers found that a DISC1 deficit caused deterioration of vital parts of the neuron called spines
which help neurons communicate with one another. Reduced amounts of DISC1 protein also impact the development of a protein called Kalirin-7 (KAL7),
which is needed to regulate another protein called Rac1. Without enough DISC1, KAL7 can adequately control Rac1 production and the development of neuronal spines.
Excess Rac1 apparently erases spines and leads to excess PAK in the mice. By using FRAX486 to reduce the activity of PAK,
the researchers were able to protect against the deterioration of the spines caused by too little DISC1,
halting the process. This normalized the excess pruning and resulted in the restoration of missing spines.
The scientists were able to see this by peering into the brains of the mice with DISC1 mutations on the 35th and 60th day of their lives, the equivalent of adolescence and young adulthood.
Sawa cautions that it has not yet been shown that PAK is elevated in the brains of people with schizophrenia.
to follow up on the mouse study to determine if a haywire PAK cascade also occurs in humans.
There is a neuropsychiatric phenomenon in which any organism will react less to a strong, startling sound when they have first been primed by hearing a weaker one.
In schizophrenia the first noise makes no impact on the reaction to the second one.
and appeared to be safe for the animals. rugs aimed at treating a disease should be able to reverse an already existing defect as well as block future damage,
Other researchers working on the study came from Johns Hopkins, the University at Buffalo, the University of Tokyo
Grants from the National institutes of health, the Stanley Foundation, the RUSK Foundation, the S-R Foundation, the National Alliance for Research on Schizophrenia and Depression, Johns Hopkins Medicine Brain science Institute, the Maryland
Stem Cell Research Fund, the Japan Society for the Promotion of Science, PREST, and the Howard hughes medical institute supported the work a
#DNA sequencing reveals six new forms of blindness Scientists have discovered six new forms of inherited blindness,
each one resulting from mutations in a different gene important in eye development and vision.
The research, carried out by experts from the University of Leeds School of medicine over the past three years, focuses on identifying new genes which,
when mutated, cause these blinding disorders. Pinpointing the exact cause gives clinicians the ability to offer their patients more information about how their condition will progress,
which multiple members were blind from birth due to conditions such as Leber congenital amaurosis, cone-rod dystrophy,
is driving a diagnostic revolution in inherited eye diseases. s the cost of sequencing comes down,
Inglehearn adds. his still doesn lead us straight to the mutations that cause the condition,
the greater understanding of the biology of vision gained from such studies also informs the search for new forms of therapy,
Inglehearn says. ince new therapies are often specific to particular forms of inherited blindness, it is essential for each patient to know which condition they have,
helping to test the new therapies and potentially benefiting from them themselves. A grant from the National Eye Research Centre, together with funding from other sources, supported the research s
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