• Passings: Robert E. Sandlin and Robert J. Briskey
  • Researchers Developing Middle-Ear Microphone for Cochlear Implants
  • Williams Sound Partners with Audio Induction Loop System Manufacturer
  • Location Discovered of Genes That May Be Responsible for Age-Related High Frequency Hearing Loss
  • AG Bell Launches Internet Resource on Hearing Loss for Families, Individuals, and Professionals
  • UCSF Researchers Show How Selective Hearing Works in the Brain
  • Neuromonics Clinical Summary Details Results of Effective Tinnitus Treatment
William Demant Reports Solid First-Quarter Growth

William Demant Holding Group, the parent company of Oticon, Bernafon, Sonic, and other brands, issued its first-quarter 2012 report to stockholders, discussing hearing aid trends and its market outlook in various countries.

Unit sales for hearing aids saw positive development in the first quarter of the year and are in line with Demant’s expectations of a rise in revenue of 5% to 9%, and an expected increase in operating profits (EBIT).

The company also indicated that its growth was driven by stable development in the increase in the elderly population and, to a minor degree, by “macro-economic trends.”

The American hearing aid market saw growth of 4% to 5% in the first 3 months of the year, which is a slight increase on the historic growth rate. The demand by both the private sector and Veterans Affairs (VA) contributed to the positive trend.

The European division also saw positive unit growth in most major markets, although there were periodic fluctuations from country to country. The fluctuations are partly due to a number of countries in southern and central Europe being affected by harsh winter weather in February. In overall terms, growth in Europe was slightly below growth in the United States.

For Japan, the company sees a growth rate of 2% to 4% for the year, corresponding to historic growth rates and rebounding from last year’s earthquake and tsunami.

The company also reports that its recently introduced Oticon Intigai, an IIC instrument (Invisible Inside the Canal) has received a very good reception, as well as new Bernafon and Sonic offerings.

In this column last month HR reported that US hearing aid net unit volume grew by 5.3% in the first quarter of 2012, with private-sector (ie, excluding VA activity) units increasing by 5.4%.

Emory Researchers Experimenting with Regenerating Hair Cells

Mature sensory hair cells are red, while immature hair cells are green. The arrows indicate locations where hair cells are usually not found

Researchers at Emory University School of Medicine in Atlanta have shown that introducing a gene called Atoh1 into the cochleae of young mice can induce the formation of extra sensory hair cells. Their results show the potential of a gene therapy approach to regenerating sensory hair cells to treat hearing loss, but the research also demonstrates its current limitations.

The extra hair cells produce electrical signals like normal hair cells and connect with neurons. However, after the mice are 2 weeks old, which is before puberty, inducing Atoh1 has little effect. This suggests that an analogous treatment in adult humans would also not be effective by itself. The findings were published May 9 in the Journal of Neuroscience.

“We’ve shown that hair cell regeneration is possible in principle,” says Ping Chen, PhD, associate professor of cell biology at Emory University School of Medicine. “In this paper, we have identified which cells are capable of becoming hair cells under the influence of Atoh1, and we show that there are strong age-dependent limitations on the effects of Atoh1 by itself.”

The first author of the paper, Michael Kelly, and his coworkers engineered mice to turn on the Atoh1 gene in the inner ear in response to the antibiotic doxycycline. Previous experimenters had used a virus to introduce Atoh1 into the cochleae of animals. This approach resembles gene therapy, but has the disadvantage of being slightly different each time, Chen says. In contrast, the mice have the Atoh1 gene turned on in specific cells along the lining of the inner ear, called the cochlear epithelium, but only when fed doxycycline.

Young mice given doxycycline for 2 days had extra sensory hair cells in parts of the cochlea where developing hair cells usually appear and also additional locations (see image).

The extra hair cells could generate electrical signals, although those signals weren’t as strong as mature hair cells. Also, the extra hair cells appeared to attract neuronal fibers, which suggests that those signals could connect to the rest of the nervous system.

“They can generate electrical signals, but we don’t know if they can really function in the context of hearing.” Chen says. “For that to happen, the hair cells’ signals need to be coordinated and integrated.”

Although doxycycline could turn on Atoh1 all over the surface of the cochlea, extra sensory hair cells did not appear everywhere. When they removed cochleae from the mice and grew them in culture dishes, her team was able to provoke even more hair cells to grow when they added a drug that inhibits the Notch pathway.

Manipulating the Notch pathway affects several aspects of embryonic development and in some contexts appears to cause cancer, so the approach needs to be refined further. Chen says that it may be possible to unlock the age-related limits on hair cell regeneration by supplying additional genes or drugs in combination with Atoh1, and the results with the Notch drug provide an example.

“Our future goals are to develop approaches to stimulate hair cell formation in older animals, and to examine functional recovery after Atoh1 induction,” she says.

The National Institute on Deafness and Other Communication Disorders, the National Basic Research Program of China, and the Natural Science Foundation of China supported the research.

UK Researchers Identify Key Cellular Mechanisms for Onset of Tinnitus

Researchers at the University of Leicester’s Department of Cell Physiology and Pharmacology have identified a cellular mechanism that could underlie the development of tinnitus following exposure to loud noises. The discovery could lead to novel tinnitus treatments, and investigations into potential drugs to prevent tinnitus are currently under way.

University of Leicester researcher Dr Martine Hamann, who led the study published in the journal Hearing Research, said in the press statement, “We need to know the implications of acoustic overexposure, not only in terms of hearing loss but also what’s happening in the brain and central nervous system. It’s believed that tinnitus results from changes in excitability in cells in the brain— cells become more reactive, in this case more reactive to an unknown sound.”

Hamann and her team, including PhD student Nadia Pilati, looked at cells in an area of the brain called the dorsal cochlear nucleus— the relay carrying signals from nerve cells in the ear to the parts of the brain that decode and make sense of sounds. Following exposure to loud noises, some of the nerve cells (neurons) in the dorsal cochlear nucleus start to fire erratically, and this uncontrolled activity eventually leads to tinnitus.

“We showed that exposure to loud sound triggers hearing loss a few days after the exposure to the sound,” Hamann said. “It also triggers this uncontrolled activity in the neurons of the dorsal cochlear nucleus. This is all happening very quickly, in a matter of days.”

In a key breakthrough in collaboration with GlaxoSmithKline (GSK), the team also discovered the specific cellular mechanism that leads to the neurons’ overactivity. Malfunctions in specific potassium channels that help regulate the nerve cells’ electrical activity mean the neurons cannot return to an equilibrium resting state.

Ordinarily, these cells only fire regularly and therefore regularly return to a rest state. However, if the potassium channels are not working properly, the cells cannot return to a rest state and instead fire continuously in random bursts, creating the sensation of constant noise when none exists.

“In normal conditions, the channel helps to drag down the cellular electrical activity to its resting state and this allows the cell to function with a regular pattern,” Hamann explained. “After exposure to loud sound, the channel is functioning less and therefore the cell is constantly active, being unable to reach its resting state and displaying those irregular bursts.”

Although many researchers have investigated the mechanisms underlying tinnitus, this is reportedly the first time that cellular bursting activity has been characterized and linked to specific potassium channels. Identifying the potassium channels involved in the early stages of tinnitus opens up new possibilities for preventing tinnitus with early drug treatments.

Hamann’s team is currently investigating potential drugs that could regulate the damaged cells, preventing their erratic firing and returning them to a resting state. If suitable drug compounds are discovered, they could be given to patients who have been exposed to loud noises to protect them against the onset of tinnitus.

These investigations are still in the preliminary stages, however, and any drug treatment is years away.

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