TUNING IN TO A NEW HEARING MECHANISM
0 comentarios 11/24/2010 08:30:00 AM Publicado por Jorge Franchín
Etiquetas: Engineering
More than 30 million Americans suffer from hearing loss, and about 6 million wear hearing aids. While those devices can boost the intensity of sounds coming into the ear, they are often ineffective in loud environments such as restaurants, where you need to pick out the voice of your dining companion from background noise.
To do that, you need to be able to distinguish sounds with subtle differences. The human ear is exquisitely adapted for that task, but the underlying mechanism responsible for this selectivity has remained unclear. Now, new findings from MIT researchers reveal an entirely new mechanism by which the human ear sorts sounds, a discovery that could lead to improved, next-generation assistive hearing devices.
"We've incorporated into hearing aids everything we know about how sounds are sorted, but they're still not very effective in problematic environments such as restaurants, or anywhere there are competing speakers," says Dennis Freeman, MIT professor of electrical engineering, who is leading the research team. "If we knew how the ear sorts sounds, we could build an apparatus that sorts them the same way."
In a 2007 Proceedings of the National Academy of Sciences paper, Freeman and his associates A.J. Aranyosi and lead author Roozbeh Ghaffari showed that the tiny, gel-like tectorial membrane, located in the inner ear, coordinates with the basilar membrane to fine-tune the ear's ability to distinguish sounds. Last month, they reported in Nature Communications that a mutation in one of the proteins of the tectorial membrane interferes with that process.
It has been known for more than 50 years that sound waves entering the ear travel along the spiral-shaped, fluid-filled cochlea in the inner ear. Hair cells lining the ribbon-like basilar membrane in the cochlea translate those sound waves into electrical impulses that are sent to the brain. As sound waves travel along the basilar membrane, they "break" at different points, much as ocean waves break on the beach. The break location helps the ear to sort sounds of different frequencies.
Until recently, the role of the tectorial membrane in this process was not well understood.
In their 2007 paper, Freeman and Ghaffari showed that the tectorial membrane carries waves that move from side to side, while up-and-down waves travel along the basilar membrane. Together, the two membranes can work to activate enough hair cells so that individual sounds are detected, but not so many that sounds can't be distinguished from each other.
Made of a special gel-like material not found elsewhere in the body, the entire tectorial membrane could fit inside a one-inch segment of human hair. The tectorial membrane consists of three specialized proteins, making them the ideal targets of genetic studies of hearing.
One of those proteins is called beta-tectorin (encoded by the TectB gene), which was the focus of Ghaffari, Aranyosi and Freeman's recent Nature Communications paper. The researchers collaborated with biologist Guy Richardson of the University of Sussex and found that in mice with the TectB gene missing, sound waves did not travel as fast or as far along the tectorial membrane as waves in normal tectorial membranes. When the tectorial membrane is not functioning properly in these mice, sounds stimulate a smaller number of hair cells, making the ear less sensitive and overly selective.
Until the recent MIT studies on the tectorial membrane, researchers trying to come up with a model to explain the membrane's role didn't have a good way to test their theories, says Karl Grosh, professor of mechanical and biomedical engineering at the University of Michigan. "This is a very nice piece of work that starts to bring together the modeling and experimental results in a way that is very satisfying," he says.
Mammalian hearing systems are extremely similar across species, which leads the MIT researchers to believe that their findings in mice are applicable to human hearing as well.
Most hearing aids consist of a microphone that receives sound waves from the environment, and a loudspeaker that amplifies them and sends them into the middle and inner ear. Over the decades, refinements have been made to the basic design, but no one has been able to overcome a fundamental problem: Instead of selectively amplifying one person's voice, all sounds are amplified, including background noise.
Freeman believes that by incorporating the interactions between the tectorial membrane and basilar membrane traveling waves, this new model could improve our understanding of hearing mechanisms and lead to hearing aids with enhanced signal processing. Such a device could help tune in to a specific range of frequencies, for example, those of the person's voice that you want to listen to. Only those sounds would be amplified.
Freeman, who has hearing loss from working in a noisy factory as a teenager and side effects of a medicine he was given for rheumatic fever, worked on hearing-aid designs 25 years ago. However, he was discouraged by the fact that most new ideas for hearing-aid design did not offer significant improvements. He decided to conduct basic research in this area, hoping that understanding the ear better would naturally lead to new approaches to hearing-aid design.
"We're really trying to figure out the algorithm by which sounds are sorted, because if we could figure that out, we could put it into a machine," says Freeman, who is a member of MIT's Research Laboratory of Electronics and the Harvard-MIT Division of Health Sciences and Technology. His group's recent tectorial membrane research was funded by the National Institutes of Health.
Next, the researchers are continuing their studies of tectorial membrane protein mutations to see if tectorial membrane traveling waves play similar roles in other genetic disorders of hearing.
(Photo: MIT)
NEW GUIDE CAN PREDICT CANCER PATIENTS SURVIVAL
University of Manchester scientists have helped develop a new way of predicting how long terminally ill cancer patients have to live.
The research, funded by Cancer Research UK and presented today (Tuesday) at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool, is based on blood tests, white cell blood count, pulse rate and patient symptoms and can predict survival at least as well as a doctor.
Professor Chris Todd, in the School of Nursing, Midwifery and Social Work, said that the prediction model differed from previous scales in that it could help to give a more accurate picture of whether patients might have only two weeks or two months left to live, independently of a doctor's estimate.
The scale could help families, carers and nurses make plans with cancer patients who are close to the end of their life.
The study, carried out with colleagues at St George's University of London, looked at 18 palliative care services, including hospices, hospital support teams and community service and more than 1,000 patients with advanced cancer who were no longer receiving treatment.
A combination of markers like blood tests, pulse rate, weight loss, tiredness, breathlessness and white blood cell count were used to produce two versions of the scale.
Dr Paddy Stone, lead author based at St George's University of London, said: "These scales can provide valuable information for patients, carers and health professionals. It is important to remember that these results do not provide a definitive model for predicting how long someone will live, but it will give everyone concerned a clearer idea of what it is likely to happen.
"This study provides a solid starting point for improving accuracy in survival predictions which can continue to be refined and improved."
Manchester's Professor Todd said: "An instrument like this will also help us identify which patients could take part in studies aimed at improving the quality of life for people receiving end-of-life care. We are already looking at how to improve the prediction models and how to make them readily available to clinicians through, for example, iPhones and other mobile devices."
Scientists claim that one form of the scale, which does not require a blood test, provides a prediction of survival as good as a doctor's estimate, while another version using a blood test is better than a clinician's prognosis.
The model could also be adapted to a patient who may not be able to respond to questions about their health.
Mike Hobday, head of campaigns at Macmillan Cancer Support, said: "This scale could prove useful to patients, families and clinicians who are wondering whether to begin discussions around palliative care arrangements.
"All too often this conversation is left until it is too late to make arrangements while patients wait to know what their future is. Having the conversation at an earlier point, alongside ensuring a 24 hour community nursing service is in place will vastly improve the chances of the 57% of people with a cancer diagnosis who want to die at home being able to do so."
SOY MAY STOP PROSTATE CANCER SPREAD
Northwestern Medicine researchers at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University have found that a new, nontoxic drug made from a chemical in soy could prevent the movement of cancer cells from the prostate to the rest of the body.
These findings will be presented at the Ninth Annual American Association for Cancer Research Frontiers in Cancer Prevention Research Conference.
Genistein, a natural chemical found in soy, is being used in the lab of Raymond Bergan, M.D., the director of experimental therapeutics at the Lurie Cancer Center, to inhibit prostate cancer cells from becoming metastatic and spreading to other parts of the body. So far the cancer therapy drug has worked in preclinical animal studies and now shows benefits in humans with prostate cancer.
A recent phase II randomized study of 38 men with localized prostate cancer found that genistein, when given once a day as a pill, one month prior to surgery, had beneficial effects on prostate cancer cells.
Researchers examined the cancer cells from the subjects' prostates after surgery and found that genistein increased the expression of genes that suppress the invasion of cancer cells and decreased the expression of genes that enhance invasion.
"The first step is to see if the drug has the effect that you want on the cells and the prostate, and the answer is 'yes, it does,'" said Bergan, a professor of hematology and oncology at Northwestern University Feinberg School of Medicine and a physician at Northwestern Memorial Hospital.
The next step is to conduct another phase II study to see if the drug can stop the cancer cells from moving out of the prostate and into the rest of the body, Bergan said. If confirmed, Bergan said this could be the first therapy for any cancer that is non-toxic and targets and inhibits cancer cell movement.
"All therapies designed to stop cancer cell movement that have been tested to date in humans have basically failed have because they have been ineffective or toxic," Bergan said. "If this drug can effectively stop prostate cancer from moving in the body, theoretically, a similar therapy could have the same effect on the cells of other cancers."