the researchers played soft voices to premature babies while they were asleep in their incubators a few days after birth,
including premature babies. The team's results appear in Proceedings of the National Academy of Sciences1.
all therapeutic molecules face a deadly foe#the immune system. Its macrophages are designed to spot any intruding molecules in the blood
by a rare genetic eye condition called advanced retinitis pigmentosa, which damages the light-sensitive cells that line the retina.
Retinitis pigmentosa#which affects about one in 4, 000 people in the US and about 1. 5 million people worldwide#kills the retina s photoreceptors,
Second sight plans to adapt its technology to someday assist people afflicted with age-related macular degeneration, a similar but more common disease.
cultivate a network of surgeons who can implant the device and recruit hospitals to offer it.
The Argus II is not the only retinal implant under development. Retina Implant AG takes a slightly different approach by making a prosthetic inserted beneath a portion of the retina.
The company s technology is a three-by three-millimeter microelectronic chip (0. 1-millimeter thick) containing about 1, 500 light-sensitive photodiodes,
In May the company announced the first UK patients participating its latest trial had received successfully implants.
To date surgeons have implanted Retina Implant prosthetics in 36 patients through two clinical trials over six years.
When influenza hit early and hard in the United states this year, it quietly claimed an unacknowledged victim:
but not substitute for, traditional epidemiological surveillance networks.""It is hard to think today that one can provide disease surveillance without existing systems,
says Alain-Jacques Valleron, an epidemiologist at the Pierre and Marie Curie University in Paris,
and founder of France s Sentinelles monitoring network.""The new systems depend too much on old existing ones to be able to live without them,
It is also causing more serious illness and deaths than usual, particularly among the elderly,
Traditional flu monitoring depends in part on national networks of physicians who report cases of patients with influenza-like illness (ILI)##a diffuse set of symptoms
including high fever, that is used as a proxy for flu. That estimate is refined then by testing a subset of people with these symptoms to determine how many have flu and not some other infection.
With its creation of the Sentinelles network in 1984, France was the first country to computerize its surveillance.
overseen by the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, includes some 2,
and has been extended to include surveillance for a second disease, dengue. Sources: Google Flu Trends (www. google. org/flutrends;
Its estimate for the Christmas national peak of flu is almost double the CDC s (see Fever peaks),
In 2009, Flu Trends had to tweak its algorithms after its models badly underestimated ILI in the United states at the start of the H1n1 (swine flu) pandemic###a glitch attributed to changes in people s search behaviour as a result of the exceptional nature of the pandemic (S. Cook et al.
says John Brownstein, an epidemiologist at Harvard Medical school in Boston, Massachusetts.""You need to recalibrate them every year.
Flu Near You, a system run by the Healthmap initiative co-founded by Brownstein at Boston Children s Hospital,
SLIDESHOW France's Sentinelles'network of doctors reporting cases of influenza-like illness has produced a clear picture of how the 2012-13#flu season has evolved.
#Small-molecule drug drives cancer cells to suicide Cancer researchers have pinned down a molecule that can kick-start the body s own tumour-destroying systems,
which has long been a target for cancer researchers looking for drugs that would avoid the debilitating effects of conventional therapies."
an oncologist at Pennsylvania State university in Hershey and lead author of the study, which is published today in Science Translational Medicine1.
Mice with glioblastomas that were treated with TIC10 in combination with bevacizumab#a drug used against diseases including brain tumours
This is by no means the only mechanism thought to trigger cell death in cancer. In particular, cancer researchers have been developing a number of drugs,
including TRAIL-based therapeutics, that work by activating the cellular messenger tumour protein 53 (p53).
But p53-based methods are not always effective, says El-Deiry. Most tumours have dysfunctional p53,
so in order to develop new therapeutics for cancer, one needs them to be effective in tumours with mutated p53,
The potential for TRAIL to usher in a new age in cancer therapy was identified first in the mid-1990s3.
although early clinical trials for TRAIL-based therapies showed little toxicity, they were not very successful at treating cancer,
says Andrew Thorburn, an oncologist at the University of Colorado Denver, who co-authored a review on the subject last year4."
"All the large clinical trials found no significant survival benefit to adding TRAIL-based therapeutics to standard treatments, he ads.
Many large biomedical research groups have shelved their TRAIL-based drugs L
#Europe bets on drug discovery Two sites shuttered by the pharmaceutical giant Merck, one in Scotland and one in The netherlands, will soon be humming again with the work of drug discovery.
But the hum will not be business as usual. It will be the sound of a public-private consortium placing a high-stakes wager:
is sponsored by the Europe s Innovative Medicine Initiative. The European commission s Seventh Framework Programme is contributing##80#million to the venture,
The scheme hopes to become self-sustaining by requiring milestone payments as drugs move from laboratory to clinic and from additional partnerships and screening services."
whose work at the Scripps Research Institute Molecular Screening Center in La jolla, California, led to a compound now in clinical trials for multiple sclerosis.
which some drug companies contribute both chemical analysis and screening support, but all data are publicly available.
#Synthetic vaccine could prevent future outbreaks of foot-and-mouth disease Virologists have devised a way to create an entirely synthetic vaccine for foot-and-mouth disease.
The vaccine could prevent future outbreaks of the disease, and potentially lead to new treatments for polio and other human diseases.
Bryan Charleston, head of the Livestock Viral Diseases Programme at the Pirbright Institute in Woking, UK,
and his colleagues used computer simulations to create a model of the protein shell of the virus that causes the disease,
then reconstructed it from synthetic protein components. The synthetic shell contains no genetic material and so it cannot infect the animals.
and spurred a decision to protect against future outbreaks with vaccination rather than mass slaughter.
however a vaccine made from inactivated virus caused another UK outbreak. The authors say that there is absolutely no chance that their new vaccine could revert into an infectious virus
because it contains no viral genes. Also being entirely synthetic, it cannot be contaminated with live virus during manufacturing.
It will be 6-8 years before the vaccine is available to farmers, they estimate. But if the method used to create the vaccine proves successful when scaled to commercial production,
it could also be used to create vaccines for human diseases that are caused by viruses of the same family, such as hand, foot and mouth disease,
which is ubiquitous in Southeast asia, and polio, which still blights the lives of millions of people in the developing world."
But if we could use this to move away from inactivated polio viruses in the vaccines,
because we are so close to ending this disease. JEFF J MITCHELL/REUTERSA 2001 outbreak of foot and mouth disease led to the slaughter of huge numbers of sheep and cows.
Earlier attempts to produce a synthetic vaccine for foot and mouth disease were thwarted often by peculiarities of viral geometry.
The team got around the problem by engineering the vaccine to have disulphide bonds cross-linking the protein triangles together.
says John Oxford, a virologist at St bartholomew s and the Royal London Hospital.""This really is an ace paper#they've truly given the entire issue a whole new dimension,
and Charleston that the new vaccine is unable to cause an infection or outbreak. Marvin Grubman, an animal-disease researcher at the US Department of agriculture in Orient Point, New york, says that the new vaccine"is a good piece of work,
but certainly not very novel, pointing to a foot-and-mouth vaccine his team devised that uses adenovirus to deliver empty viral shells.
That vaccine, he says, has been approved for use in the United states for cases of emergency. The authors however point out that their vaccine does not require the injection of live viruses
and that it would be suitable for preventive vaccination as well as in cases of severe outbreaks o
#Scientists map protein that creates antibiotic resistance Japanese researchers have determined the detailed molecular structure of a protein that rids cells of toxins,
but can also reduce the effectiveness of some antibiotics and cancer drugs by kicking them out of the cells they are targeting.
The discovery suggests new approaches to combat antibiotic resistance and boost the power of cancer therapies,
Geoffrey Chang, a structural biologist at the University of California, San diego, says that the findings are very similar to those for the MATE protein from Vibrio cholerae, the bacterium that causes cholera.
and represent the latest success for a'fringe'therapy in which a type of immune cell called T cells are extracted from a patient, genetically modified,
says Michel Sadelain, a researcher at the Memorial Sloan-Kettering Cancer Center in New york and an author of the study.
whether it could take on the faster-growing acute lymphoblastic leukaemia, a tenacious disease that kills more than 60%of those afflicted.#
#Carl June, an immunologist at the University of Pennsylvania in Philadelphia and a pioneer in engineering T cells to fight cancer, says that he is surprised that the method worked so well against such a swift-growing cancer.
is to move the technique out of the boutique academic cancer centres that developed it and into multicentre clinical trials."
"What needs to be done is to convince oncologists and cancer biologists that this new kind of immunotherapy can work,
he says. Oncologist Renier Brentjens, also at Memorial Sloan-Kettering Cancer Center, remembers the day that he had to tell one of the patients in the trial that the weeks of high-dose chemotherapy the 58-year-old man had endured had worked not after all."
"It was painful to have that conversation, says Brentjens.""He tells me now it was the worst news he has heard ever in his life.
Another month in the hospital on intensive chemotherapy drugs did nothing to help. By the time the man started the trial,
The treatment had driven his cancer into remission#as it did for the other four patients in the trial
#so he became eligible for a bone-marrow transplant. A hundred days later, he is doing well,
Four of the five patients were well enough to receive transplants; the remaining patient relapsed and was ineligible.
and faces an untested path to regulatory approval, says Steven Rosenberg, head of the tumour immunology section at the National Cancer Institute in Bethesda, Maryland.
And Sadelein says that he is an investigator on a trial with the Dana-Farber Cancer Institute in Boston
#Gene-analysis firms reach for the cloud For Chaim Jalas at the Center for Rare Jewish Genetic disorders in New york,
and identify mutations that might be causing the undiagnosed diseases that afflict his clients families.
And the cloud-based interfaces let him collaborate with doctors in Israel without worrying about repeatedly transferring data on slow Internet connections."
which will be touting for customers at a meeting of the American College of Medical Genetics and Genomics in Phoenix, Arizona, on 19-23 march.
as ever more affordable sequencing moves from academia into the clinic (see Nature 494,290-291; 2013).
) Doctors will increasingly want to use sequen#cing data to guide decisions about patient care, but might not necessarily want to invest in staff
and finds those most likely to cause disease. Personalis, down the road in Menlo Park, offers sequencing services and interpretation for clinicians and pharmaceutical and biotechnology companies.
to explore the variants roles in disease. The company will outsource the sequencing to Illumina,
and hospitals to analyse data. But one of the biggest questions will be how deeply analysis companies can reach into medical settings,
where privacy concerns are paramount. Hospitals can be fined if patient privacy is compromised, and clinical geneticists may be uneasy about uploading data to the cloud."
"It s your licence and your lab that go on the line when it comes to reporting a clinical result,
That is a large part of why many hospitals have chosen so far to build their own analysis infrastructure,
diseases and scavengers#but acknowledge that it might have been caused by behavioural changes, such as the birds learning to avoid cars.
but it would require surgery and would cover only a small fraction of the brain.
#Distinctive virus behind mystery horse disease For almost 100 years, veterinarians have puzzled over the cause of Theiler's disease,
a mysterious type of equine hepatitis that is linked to blood products and causes liver failure in up to 90%of afflicted animals.
A team of US scientists has discovered now that the disease is caused by a virus that shares just 35%of its amino acid sequences with its closest-known relative.
The team named it Theiler's disease-associated virus (TDAV), and published the discovery in the Proceedings of the National Academy of Sciences1.
Led by Amy Kistler at the Novartis Institutes for Biomedical Research in Emeryville California, the team responded to an outbreak of Theiler's disease at a farm in
which eight horses had developed suddenly hepatitis after being injected with an antitoxin to prevent them from developing botulism.
The researchers used next-generation sequencing to analyse RNA samples from the antitoxin and from two of the horses,
and assembled the complete genome of the new virus. The virus was found in every one of the eight horses,
and one later showed rising levels of liver enzymes that suggested liver disease. Although the researchers did not purify the virus before injecting it into the horses, Pablo Murcia, a virologist from the University of Glasgow,
It is also possible that there is another unknown virus behind Theiler's disease. After all, human hepatitis can be caused by at least five viruses. TDAV belongs to the family Flaviviridae,
which includes the viruses behind yellow fever, dengue fever and hepatitis C. It is associated most closely with a genus of newly discovered viruses called Pegivirus,
and is the first of these to be linked convincingly to disease.""The challenges in culturing pegiviruses mean that we re only now getting an understanding of how widely distributed and significant they are,
says James wood, who studies animal infections at the University of Cambridge, UK. He hints that some studies on new pegiviruses may be published in the future u
#Obama to announce $2 billion plan to get US cars off gasoline An article by Scientific American.
This afternoon, President Barack Obama will ask Congress to direct our cars, trucks and buses to a realm that doesn t include gas stations.
and transmit thought commands collected from a brain implant. The researchers say that the wireless BCI is able to stream thought commands via its radio at a rate of 48 megabits per second, about the speed of a home Internet connection.
Braingate was among the first to place implants in the brains of paralyzed people and show that electrical signals emitted by neurons inside the cortex could be recorded,
#MIT's multifunctional fiber implant could revolutionize neural prosthetics Today cutting edge neural implants can passively read brain activity,
these fiber based neural implants are much more flexible than the current industry standard, multielectrode arrays and hooked eedlestyle stimulators.
so harder implants that don bend with their surrounding biological environment can easily shift and move to a different area than they were implanted,
The most exciting thing about these new fibers is undoubtedly the ability to bundle together different functionalities in the same implant,
to have an implant with electrodes paired with drug delivery pumps that could sense an oncoming epileptic seizure
what theye created to build whatever kind of neural implants they can dream up. And people say we aren living in the future
simulate lesion dynamics or implement network analysis functions from a library of graph theoretic measures. Within the immersive mixed/virtual reality space of Brainx3 users can explore and analysis dynamical activity patterns of brain networks
or for discovering of signaling pathways associated to brain function and/or dysfunction or as a tool for virtual neurosurgery.
Knowledge of brain activity in these various states is clinically relevant for assessing levels of consciousness in patients with severe brain injury y
which could revolutionize drug discovery and personalized medicine. In a laboratory first, Duke researchers have grown human skeletal muscle that contracts
and study diseases in functioning human muscle outside of the human body. The study was led by Nenad Bursac, associate professor of biomedical engineering at Duke university
and those that make taking muscle biopsies difficult. Bursac and Madden started with a small sample of human cells that had progressed already beyond stem cells
To see if the muscle could be used as a proxy for medical tests, Bursac and Madden studied its response to a variety of drugs,
showing the lab-grown muscle was giving a truly human response. ne of our goals is to use this method to provide personalized medicine to patients,
said Bursac. e can take a biopsy from each patient, grow many new muscles to use as test samples
Bursac group is also trying to grow contracting human muscles using induced pluripotent stem cells instead of biopsied cells. here are a some diseases, like Duchenne Muscular dystrophy for example,
that make taking muscle biopsies difficult, said Bursac. f we could grow working, testable muscles from induced pluripotent stem cells,
and William Krauss, professor of biomedical engineering, medicine and nursing at Duke university. The research was supported by NIH Grants R01ar055226 and R01ar065873 from the National Institute of Arthritis and Musculoskeletal and Skin disease and UH2TR000505 from the NIH Common Fund for the Microphysiological Systems Initiative.
Bioengineered human myobundles mimic clinical responses of skeletal muscle to drugs Existing in vitro models of human skeletal muscle cannot recapitulate the organization and function of native muscle
myobundles undergo dose-dependent hypertrophy or toxic myopathy similar to clinical outcomes. Human myobundles provide an enabling platform for predictive drug
and toxicology screening and development of novel therapeutics for muscle-related disorders. ioengineered human myobundles mimic clinical responses of skeletal muscle to drugsby Lauran Madden, Mark Juhas, William
#Researchers Identify Important Control Mechanisms for Walking Even after complete spinal paralysis, the human spinal cord is able to trigger activity in the leg muscles using electrical pulses from an implanted stimulator.
Now, as part of a joint international project, a team of young researchers at the Center for Medical Physics and Biomedical engineering at Meduni Vienna has succeeded in identifying the mechanisms the spinal cord uses to control this muscle activity.
even if the neural pathways from the brain are interrupted physically as the result of a spinal cord injury.
This is the first time throughout the world that the spinal-cord activation patterns for walking have been decoded Paraplegics still have neural connections (so-called locomotion centers) below the site of the injury
explains study author Simon Danner, from the Center for Medical Physics and Biomedical engineering of Meduni Vienna.
New possibilities for rehabilitation following spinal paralysis These new findings relating to the basic patterns for triggering
and the resulting paralysis by stimulating them electrically. This opens the way to new therapeutic options for helping paraplegics to at least partially regain lost rhythmic movements.
Exactly how the neural networks need to be stimulated depends upon the patient individual injury profile and is the subject of further studies.
To help with this, the scientists at Meduni Vienna have developed a unique, noninvasive method for stimulating the spinal cord,
which involves attaching electrodes to the surface of the skin. his method allows easy access to the neural connections in the spinal cord below a spinal injury
#Genetic Brain disorders Converge at the Synapse Several genetic disorders cause intellectual disability and autism. Historically, these genetic brain diseases were viewed as untreatable.
However, in recent years neuroscientists have shown in animal models that it is possible to reverse the debilitating effects of these gene mutations.
a treatment developed for one genetic cause of autism and intellectual disability might be useful for many others.
In a paper published today in the online edition of Nature Neuroscience, a research team led by Mark Bear,
the Picower Professor of Neuroscience in MIT Picower Institute for Learning and Memory, showed that two very different genetic causes of autism
and intellectual disability disrupt protein synthesis at synapses, and that a treatment developed for one disease produced a cognitive benefit in the other.
The research was performed by postdoc and lead author Di Tian, graduate student Laura Stoppel, and research scientist Arnold Heynen, in collaboration with scientists at Cold Spring Harbor Laboratory and Roche pharmaceuticals.
Researching the role of fragile X syndrome One heritable cause of intellectual disability and autism is fragile X syndrome,
which arises when a single gene on the X chromosome, called FMR1, is turned off during brain development.
that too much protein synthesis downstream of mglur5 activation gives rise to many of the psychiatric and neurological symptoms of fragile X. Bear lab tested this idea in mice,
Different genes, same consequences Another cause of autism and intellectual disability is the loss of a series of genes on human chromosome 16,
Some of the 27 affected genes play a role in protein synthesis regulation, leading Bear and colleagues to wonder if 16p11.2 microdeletion syndrome and fragile X syndrome affect synapses in the same way.
similar to fragile X. Restoring brain function after disease onset These findings encouraged the MIT researchers to attempt to improve memory function in the 16p11.2 mice with the same approach that has worked in fragile X mice.
The implication, according to Bear, is that ome cognitive aspects of this disease, previously believed to be an intractable consequence of altered early brain development,
Current research indicates that well over 100 distinct gene mutations can manifest as intellectual disability and autism.
as they indicate not only that drug therapies might be effective to improve cognition and behavior in affected individuals,
Studies at other institutions have identified mutations in the gene for Syngap associated with autism and intellectual disability.
All three of the disability-associated mutations showed similar effects: Compared to normal neurons, there was less Syngap in synapses
Biomedical Research, the UCSF Diabetes Center Obesity Pilot program, and the National institutes of health b
#New ALS Gene and Signaling Pathways Identified Using advanced DNA sequencing methods, researchers have identified a new gene that is associated with sporadic amyotrophic lateral sclerosis (ALS),
or Lou Gehrig disease. ALS is a devastating neurodegenerative disorder that results in the loss of all voluntary movement
and is fatal in the majority of cases. The next-generation genetic sequencing of the exomes (protein-coding portions) of 2, 874 ALS patients and 6,
inflammation (a reaction to injury or infection) and autophagy (a cellular process involved in the removal of damaged cellular components.
The study, conducted by an international ALS consortium that includes scientists and clinicians from Columbia University Medical center (CUMC), Biogen idec,
especially since the inflammatory and autophagy pathways have been implicated previously in the disease, said Lucie Bruijn, Phd,
Chief Scientist for The ALS Association. he fact that TBK1 accounts for one percent of ALS adds significantly to our growing understanding of the genetic underpinnings of the disease.
LS is an incredibly diverse disease, caused by dozens of different genetic mutations, which wee only beginning to discover.
the better we can deciphernd influencehe pathways that lead to disease. The other co-leaders of the study are Richard M. Myers, Phd, president and scientific director of Hudsonalpha,
and Tim Harris, Phd, DSC, Senior vice president, Technology and Translational Sciences, Biogen idec. hese findings demonstrate the power of exome sequencing in the search for rare variants that predispose individuals to disease and in identifying potential
focused collaborations with the best academic scientists to advance our understanding of the molecular pathology of disease.
especially in the context of precision medicine and whole-genome sequencing.""Industry and academia often do things together,
The combination of those groups with a large number of the clinical collaborators who have been seeing patients with this disease for many years and providing clinical information
TBK1 mutations appeared in about 1 percent of the ALS patients large proportion in the context of a complex disease with multiple genetic components, according to Dr. Goldstein.
may actually be a major player in the disease. emarkably, the TBK1 protein and optineurin, which is encoded by the OPTN gene,
and mouse models with mutations in TBK1 or OPTN to study ALS disease mechanisms and to screen for drug candidates.
Several compounds that affect TBK1 signaling have already been developed for use in cancer, where the gene is thought to play a role in tumor-cell survival. his is a great example of the potential of precision medicine,
said Tom Maniatis, Phd, the Isidore S. Edelman Professor, chair of biochemistry and molecular biophysics,
and director of Columbia university-wide precision medicine initiative. t now seems clear that future ALS treatments will not be equally effective for all patients because of the disease genetic diversity.
as candidate therapies become available, we hope to be able to use the genetic data from each ALS patient to direct that person to the most appropriate clinical trials and,
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