Sound-sensing cells regenerated in ears of mice with hearing damage

One of the major causes of hearing loss in mammals is damage to the sound-sensing hair cells in the inner ear. For years, scientists have thought that these cells are not replaced once they’re lost, but new research appearing online February 20 in the journal Stem Cell Reports reveals that supporting cells in the ear can turn into hair cells in newborn mice. If the findings can be applied to older animals, they may lead to ways to help stimulate cell replacement in adults and to the design of new treatment strategies for people suffering from deafness due to hair cell loss.Whereas previous research indicated that hair cells are not replaced, this latest study found that replacement does indeed occur, but at very low levels. “The finding that newborn hair cells regenerate spontaneously is novel,” says senior author Dr. Albert Edge of Harvard Medical School and Massachusetts Eye and Ear Infirmary.The team’s previous research revealed that inhibition of the Notch signaling pathway increases hair cell differentiation and can help restore hearing to mice with noise-induced deafness. In their latest work, the investigators found that blocking the Notch pathway increases the formation of new hair cells not from remaining hair cells but from certain nearby supporting cells that express a protein called Lgr5.”By using an inhibitor of Notch signaling, we could push even more cells to differentiate into hair cells,” says Dr. Edge. “It was surprising that the Lgr5-expressing cells were the only supporting cells that differentiated under these conditions.”Combining this new knowledge about Lgr5-expressing cells with the previous finding that Notch inhibition can regenerate hair cells will allow the scientists to design new hair cell regeneration strategies to treat hearing loss and deafness.Story Source:The above story is based on materials provided by Cell Press. Note: Materials may be edited for content and length.

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Concerned about the health risk of soda?

Last week, Consumer Reports released a study on the levels of a caramel coloring agent known as 4-methylimidazole (4-MEI) in many popular, carbonated beverages. The report used phrases such as “health risk” and “potential carcinogen,” leaving many wondering whether their favorite sodas should be discarded because of a cancer risk. This is a question that toxicologists can help answer.”Our work as toxicologists is to help conduct and interpret the findings of a variety of studies that evaluate the potential hazard of natural products, environmental chemicals, and drugs to provide people with the information necessary to make informed, personal decisions,” says Lois D. Lehman-McKeeman, PhD, ATS, 2013-2014 President of the Society of Toxicology.There have been many toxicological studies of 4-MEI over the years, but focusing on the study conducted by the National Toxicology Program cited in the Consumer Reports article, there are some significant details of how the study was conducted that are important toxicologically and for understanding the results.4-MEI was administered to both mice and rats over their two-year lives through their food, so the exposure to the chemical was oral or the same as exposure would be in humans by drinking carbonated beverages. Different levels, or doses, of 4-MEI were tested. A basic tenant of toxicology is that the dose makes the poison. The level at which exposure occurs is crucial to understanding if a chemical poses a risk to health. Likewise, the greater the dose, the greater or more likely the adverse affect. The rats in the study exposed to only the highest doses of 4-MEI (not the minimal or moderate doses) experienced a higher incidence of leukemia than the control group. The mice, though, showed no such result. …

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How a ubiquitous herpesvirus sometimes leads to cancer

Oct. 10, 2013 — You might not know it, but most of us are infected with the herpesvirus known as Epstein-Barr virus (EBV). For most of us, the virus will lead at worst to a case of infectious mononucleosis, but sometimes, and especially in some parts of the world, those viruses are found in association with cancer. Now, researchers reporting in the Cell Press journal Cell Reports on October 10 have found that the difference between a relatively harmless infection and a cancer-causing one lies at least partly in the viral strain itself.Share This:The results offer some of the first evidence for the existence of distinct EBV subtypes with very different public health risks. The researchers say that vaccination or other strategies for preventing EBV infection will need to be designed with these most pathogenic, cancer-causing strains in mind.”EBV is an important but neglected pathogen,” said Henri-Jacques Delecluse of the German Cancer Research Centre in Heidelberg, Germany. “We have made an important step in recognizing that EBV is actually a family of viruses that have different properties, some of which are very likely to cause disease. So, the consequences of being infected with EBV might be different, depending on the strain one carries.”Delecluse and his colleagues made the discovery by sequencing the DNA of a viral strain dubbed M81 isolated from a Chinese patient with nasopharyngeal carcinoma (NPC). Their analyses revealed that M81 is highly similar to other viruses isolated from NPCs and profoundly different from Western strains in terms of its ability to infect and replicate within cells.The M81 strain can infect epithelial cells and multiply spontaneously at a very high level in all cells it infects, including B lymphocytes, the cells in which the viruses hide, the researchers report. It remains to be seen exactly how infected epithelial cells become cancerous.”Our results have made me radically change my strategy to address the problem of EBV-associated diseases,” Delecluse said. “The current view is that the virus is essentially the same all over the world and that local conditions explain the different consequences of EBV infection. …

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Antisocial texting by teens linked to bad behavior

Sep. 9, 2013 — For American teenagers, most text messaging is as harmless as passing notes, but University of Texas at Dallas researchers have discovered that engaging in antisocial texting can actually predict deviant behavior.In the Journal of Abnormal Child Psychology, scientists reported a correlation between the frequency with which adolescents text about antisocial behaviors and the likelihood that they will engage in them.”We were interested in how adolescents use electronic communication, particularly text messaging,” said Dr. Samuel Ehrenreich, post-doctoral researcher in the School of Behavioral and Brain Sciences at UT Dallas. “We examined how discussing antisocial behavior — substance abuse, property crimes, physical aggression, that sort of thing — how discussing that predicts actually engaging in this problem behavior. Basically, does talking about bad behavior predict bad behavior?”Although the idea of studying the texting habits of teens may not be new, looking directly at the messages they are sending is. Past studies relied on self-reported texting behaviors, which Ehrenreich said may be flawed due to teens providing inaccurate information about texts. They would not likely self-report texting about misbehavior. Teens also send an average of 60-100 texts per day, so they may simply forget about much of the texting they do. To circumvent these problems, free BlackBerry devices and service plans were given to 172 ninth-grade students with the understanding that their texts would be monitored.Texts were collected and stored offsite in a secure database. The participants were rated before and after the school year for rule breaking and aggressive behavior by parents, teachers and in self reports.Analysis of a sample of texts from two points in time revealed similarities in the types of antisocial messages between boys and girls. …

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New superheavy elements can be uniquely identified

Aug. 30, 2013 — An international team of researchers presents fresh evidence that confirms the existence of the superheavy chemical element 115. The experiment was conducted at the GSI Helmholtz Center for Heavy Ion Research, an accelerator laboratory located in Darmstadt. Under the lead of physicists from Lund University in Sweden, the group, which included researchers from Johannes Gutenberg University Mainz (JGU) and the Helmholtz Institute Mainz (HIM), was able to present a way to directly identify new superheavy elements.Share This:Elements beyond atomic number 104 are referred to as superheavy elements. They are produced at accelerator laboratories and generally decay after a short time. Initial reports about the discovery of an element with atomic number 115 were released from a research center in Russia in 2004. The then presented indirect evidence for the new element, however, was insufficient for an official discovery.For the new experiment, scientists at the Institute of Nuclear Chemistry at Mainz University took a sample of the exotic element americium. They deposited an americium layer on a thin foil, which was subsequently bombarded with calcium ions at the GSI facility. For the first time, the exploitation of a new detector system allowed registering photons along with the alpha-decay of the new element and its daughter products. Measured photon energies correspond to those expected for X-rays from these products and thus serve as the element’s fingerprint.”This can be regarded as one of the most important experiments in the field in recent years, because at last it is clear that even the heaviest elements’ fingerprints can be taken”, agreed Professor Dirk Rudolph from Lund University in Sweden and Professor Christoph Düllmann, professor at Mainz University and leading scientist at GSI Darmstadt and HIM. …

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Protein linked to cognitive deficits in Angelman syndrome discovered

Aug. 1, 2013 — A team of neuroscientists has identified a protein in laboratory mice linked to impairments similar to those afflicted with Angelman syndrome (AS) — a condition associated with symptoms that include autism, intellectual disability, and motor abnormalities.The findings appear in the journal Cell Reports.”By isolating a protein that contributes to cognitive deficits in Angelman syndrome, these findings mark a step forward in not only addressing AS, but perhaps other developmental disorders as well,” said Eric Klann, a professor in New York University’s Center for Neural Science and one of the study’s co-authors.The study’s researchers also included: Shelly Buffington and Matthew Rasband of the Baylor College of Medicine; Jerry Lingrel of the Department of Molecular Genetics, Biochemistry, and Microbiology at the University of Cincinnati; and Hanoch Kaphzan, Akila Ramaraj, and Emanuela Santini of NYU’s Center for Neural Science.Previous research has shown that AS model mice display brain dysfunctions that match neurological abnormalities observed in humans, including cognitive deficits such as long-term memory. A previous study by Klann and his colleagues pointed to a potential cause for the condition — overexpression of a subunit of a protein termed Na/K-ATPase in AS model mice.In the Cell Reports study, the authors hypothesized that if they could decrease expression of this subunit, they could improve cognitive function of AS model mice.To do this, they ran different populations of mice through cognitive and memory tests — including a water maze to examine spatial memory and a fear conditioning paradigm to examine associative memory. They examined behaviors of the following types of mice: normal mice, AS model mice, mice that had reduced levels of the Na/K-ATPase, and AS model mice in which expression of the subunit of Na/K-ATPase was reduced.In the water maze test, the mice needed to elevate themselves onto a platform in a specific location to get out of the water. The AS mice took longer to learn this task, but AS mice with reduced levels of the Na/K-ATPase subunit learned the task as fast as normal mice. In the second test, the researchers removed the maze’s platform and measured how long the mice searched for the platform in this part of the maze in order to measure their memory of the platform location. The normal mice and the AS model mice with diminished expression of the Na/K-ATPase subunit searched the correct area of the maze in the same amount of time. However, other AS model mice had no memory of the platform location.In a second experiment, the researchers placed the mice in a staging area where they received a mild electric foot shock. Later, they were returned to the same staging area — a process that tested whether or not they could recall being at this location. Scientists typically measure recall in this commonly used experiment by gauging “freezing behavior” — that is, freezing when returned to an area in which they’d previously received a foot shock.Here, the results were consistent with the maze findings — the normal mice and the AS model mice with diminished expression of the Na/K-ATPase subunit exhibited freezing behavior upon the return to the staging area where they’d earlier received the foot shock, demonstrating the ability to recall a previous incident. …

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New cause of life-threatening disease identified

The groundbreaking results have been published in Cell Reports. The research is supported by the Lundbeck Foundation, the Novo Nordisk Foundation and the Danish Heart Association (in Danish), among others. Need to cite this story in your essay, paper, or report? Use one of the following formats: APA MLA Note: If no author is given, the source is cited instead.Include this item in your blog or web site:close

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Scientists find potential new clues for identifying breast cancer risk

June 4, 2013 — New research provides critical insights into how normal breast precursor cells may be genetically vulnerable to develop into cancer. The research is published June 4th in the inaugural issue of Stem Cell Reports, an open-access journal from the International Society of Stem Cell Research (ISSCR) published by Cell Press. Scientists discovered that a particular class of normal breast precursor cells have extremely short chromosome ends (known as telomeres). As a result, these cells would be expected to be prone to acquiring mutations that lead to cancer if they managed to stay alive. These findings suggest new indicators for identifying women at higher risk for breast cancer and provide insights into potential new strategies to detect, treat, and prevent the disease.Dr. David Gilley’s laboratory at the Indiana University School of Medicine in Indianapolis and Dr. Connie Eaves’ laboratory at the BC Cancer Agency’s Terry Fox Laboratory in Vancouver, Canada, collaborated to determine how telomeres are regulated in different types of normal breast cells. Their studies revealed that a subset of normal breast precursor cells, called luminal progenitors, have dangerously short telomeres and display a correspondingly high level DNA damage response localized at their chromosome ends. This shows how a normal process of tissue development produces a cell type that is predisposed to acquire cancer-causing mutations.”This is the first report of a particular normal human precursor cell type that shows such telomere malfunction,” says Dr. Eaves. …

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