A wind turbine, a roaring crowd at a football game, a jet engine running full throttle: Each of these things produces sound waves that are well below the frequencies humans can hear. But just because you can’t hear the low-frequency components of these sounds doesn’t mean they have no effect on your ears. Listening to just 90 seconds of low-frequency sound can change the way your inner ear works for minutes after the noise ends, a new study shows.

“Low-frequency sound exposure has long been thought to be innocuous, and this study suggests that it’s not,” says audiology researcher Jeffery Lichtenhan of the Washington University School of Medicine in in St. Louis, who was not involved in the new work.

Humans can generally sense sounds at frequencies between 20 and 20,000 cycles per second, or hertz (Hz)—although this range shrinks as a person ages. Prolonged exposure to loud noises within the audible range have long been known to cause hearing loss over time. But establishing the effect of sounds with frequencies under about 250 Hz has been harder. Even though they’re above the lower limit of 20 Hz, these low-frequency sounds tend to be either inaudible or barely audible, and people don’t always know when they’re exposed to them.

For the new study, neurobiologist Markus Drexl and colleagues at the Ludwig Maximilian University in Munich, Germany, asked 21 volunteers with normal hearing to sit inside soundproof booths and then played a 30-Hz sound for 90 seconds. The deep, vibrating noise, Drexl says, is about what you might hear “if you open your car windows while you’re driving fast down a highway.” Then, they used probes to record the natural activity of the ear after the noise ended, taking advantage of a phenomenon dubbed spontaneous otoacoustic emissions (SOAEs) in which the healthy human ear itself emits faint whistling sounds. “Usually they’re too faint to be heard, but with a microphone that’s more sensitive than the human ear, we can detect them,” Drexl says. Researchers know that SOAEs change when a person’s hearing changes and disappear in conjunction with hearing loss.

People’s SOAEs are normally stable over short time periods. But in the study, after 90 seconds of the low-frequency sound, participants’ SOAEs started oscillating, becoming alternately stronger and weaker. The fluctuations lasted about 3 minutes, the team reports today in Royal Society Open Science. The changes aren’t directly indicative of hearing loss, but they do mean that the ear may be temporarily more prone to damage after being exposed to low-frequency sounds, Drexl explains. “Even though we haven’t shown it yet, there’s a definite possibility that if you’re exposed to low-frequency sounds for a longer time, it might have a permanent effect,” Drexl adds.

“The unfortunate thing about our ears is that we can be doing terrible things to them with sounds that aren’t necessarily painful,” says hearing loss researcher M. Charles Liberman of Harvard Medical School in Boston. To explore the potential harm of specific sounds, such as the hotly debated question of the effect of wind turbines on hearing, Liberman says the same experiment could be repeated with conditions mimicking wind turbine noise. He’d also like to see the study expanded to look at how the ears react to noises—rather than silence—in the minutes after low-frequency sound exposure.

For older adults, being unable to identify scents is a strong predictor of death within five years, according to a study published October 1, 2014, in the journal PLOS ONE. Thirty-nine percent of study subjects who failed a simple smelling test died during that period, compared to 19 percent of those with moderate smell loss and just 10 percent of those with a healthy sense of smell.

A whole functional organ has been grown from scratch inside an animal for the first time, say researchers in Scotland.

A group of cells developed into a thymus – a critical part of the immune system – when transplanted into mice.

The findings, published in Nature Cell Biology, could pave the way to alternatives to organ transplantation.

Experts said the research was promising, but still years away from human therapies.

The thymus is found near the heart and produces a component of the immune system, called T-cells, which fight infection.

Grow your own

Scientists at the Medical Research Council centre for regenerative medicine at the University of Edinburgh started with cells from a mouse embryo.

These cells were genetically “reprogrammed” and started to transform into a type of cell found in the thymus.

These were mixed with other support-role cells and placed inside mice.

Once inside, the bunch of cells developed into a functional thymus.

It is similar to a feat last year, when lab-grown human brains reached the same level of development as a nine-week-old foetus.

The thymus is a much simpler organ and in these experiments became fully functional.

Structurally it contained the two main regions – the cortex and medulla – and it also produced T-cells.

Prof Clare Blackburn, part of the research team, said it was “tremendously exciting” when the team realised what they had achieved.

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A diet of junk food not only makes rats fat, but also reduces their appetite for novel foods, a preference that normally drives them to seek a balanced diet, reports a study published in the open-access journal Frontiers in Psychology.

By artificially activating circuits in the brain, scientists have turned negative memories into positive ones.

They gave mice bad memories of a place, then made them good – or vice versa – without ever returning to that place.

Neurons storing the “place” memory were re-activated in a different emotional context, modifying the association.

Although unlikely to be applied in humans with traumatic memories, the work sheds new light on the details of how emotional memories form and change.

Incremental progress

“Emotion is intimately associated with memories of past events and episodes, and yet the ‘valence’ – the emotional value of the memories – is malleable,” said the study’s senior author Prof Susumu Tonegawa, from the Riken-MIT Center for Neural Circuit Genetics in Massachusetts, US.

He offered examples of a mugging, or a blissful holiday, which might make you fearful of a particular street, or fond of a beach.

We all know that these sorts of emotional associations can be changed by a new, contrasting experience. Your favourite seaside memories, for example, might be soured by news of a shark attack.

Therapists already use this malleability in their efforts to treat trauma victims or people with depression, attempting to replace negative associations with positive ones.

Prof Tonegawa’s team has unpicked some of the networks that make this happen inside the brain.

Two years ago, they showed they could label the cells storing a new, fearful memory in a mouse’s brain, and turn them on again at a later date to cause fearful behaviour.

Then in 2013, they labelled a memory of a place and later reactivated it, while giving the mice small electric shocks. This created a false, fearful association with the original place.

Now they have managed to actually switch the emotional, fearful – or cheerful – content of a memory, from one extreme to the other.

Re-wired connections

Male mice were given a negative experience, consisting of small electric shocks, in a particular room, and the neurons working to store that memory were labelled using “optogenetics”.

Optogenetics: switches for brain cells

• Developed in flies, and then mice, during the early 2000s
• Now used in neuroscience labs all over the world
• Allows researchers to control neurons (brain cells) with coloured light
• Involves genetic installation of light-sensitive ion channels, which change the flow of electrical charge and activate or silence neurons
• To deliver the light, a thin optical fibre can be implanted into the brain
• Much more precise than older techniques, such as stimulating parts of the brain with electric current
• Used in this study to turn specific neurons on, but a range of channels that respond to different colours of light can be used to switch neurons both on and off
• Hotly tipped for a Nobel Prize in the future

This is a technique that effectively installs a switch in those neurons, allowing them to be turned on again at will. The trigger used to stimulate them is a beam of blue light, sent into the brain by an optical fibre.

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A team of researchers has found a part of the brain that controls how motivated mice are to exercise, according to a new study.

The researchers created genetically modified mice that lacked neurons in the dorsal medial portion of a region of the brain called the habenula.

The major difference was that the mice didn’t like to run on mouse wheels, which normal mice love to do, the researchers reported in a paper they published in the Journal of Neuroscience. “They were physically capable of running, but appeared unmotivated to do it,” Eric Turner, the study’s lead scientist and a brain researcher at Seattle Children’s Research Institute, said in a statement. The mice also had “minor” differences in their gait and balance, compared to normal mice.

Why mess with mouse habenulas? The team was seeking a target for future antidepressant drugs. They knew that some strong science indicates that exercise can help people with depression. What if a future drug could mimic the emotional effects of exercise on the brain?

Of course, there’s a lot of work scientists will have to do before they know whether it’s a good idea to target this brain area for depression. There’s the straightforward issue of checking, with replicating studies, whether this brain region really is responsible for making mice want to exercise. Then scientists will have to see if the analogous region in human brains works similarly. They’ll also want to study whether targeting this brain region improves depression. (What if it just makes you want to exercise, without resolving your depression?) Lastly, it’s always a challenge to design drugs that are safe and effective, even if you’ve got all your targets lined up.

The lack of running the team documented in the mice may be related to depression, or whatever its murine counterpart might be. The dorsal medial habenula-lacking mice didn’t like sugar water as much as normal mice do, which is a measure of mouse depression. However, dorsal medial habenula-lacking mice did perform the same as normal mice in the forced-swim test, which is another common, if weird, test for hopelessness and depression in mice.

The scientists performed one additional set of experiments that indicate the dorsal medial habenula might be a good target for antidepressants. They hooked mice up to a setup that allowed the mice to turn up or turn down their own dorsal medial habenula. (These are different mice from the mice who lacked dorsal medial habenulas altogether, of course.) The brain-controlling mice always chose to turn their dorsal medial habenulas up, suggesting it’s rewarding to do so. Now if only you could ask the mice exactly what that felt like.

Last week two American aid workers who had contracted Ebola while working in west Africa were released from a U.S. hospital and pronounced “recovered.” They had been flown to Emory University Hospital in Atlanta from Liberia earlier this month to receive care in the hospital’s specialized infectious disease unit. Kent Brantly, a physician with the humanitarian group Samaritan’s Purse, and missionary Nancy Writebol, of SIM USA, beat the strain of the disease they had contracted, which kills 52 percent of its victims. Bruce Ribner, medical director of the hospital’s Infectious Disease Unit, sat down with Scientific American to explain how the two Americans were cared for, the lessons that could be applied to help patients across Africa and why the hysteria over flying the two individuals back to the U.S. was unfounded.
 
[An edited transcript of the interview follows.]
 
Are Brantly and Writebol now immune to the Zaire strain of Ebola?
In general, patients who have recovered from Ebola virus infection do develop a very robust immunity to the virus. They develop antibodies against the virus and they also develop cell-mediated immunity—the lymphocytes important to form viral control of pathogens. In general, the finding is it’s basically like being immunized—it would be unusual to get infection with the same strain.
 
Will that immunity afford them protection against other strains of Ebola?
We are still evaluating that in our two patients. Cross-protection is not quite as robust. There are five strains of Ebola viruses. Even though that data is not great, the feeling is there is potential for being infected if you go to a different part of Africa and get exposed to a different strain.
 
You said “still evaluating.” Are you still caring for Brantly and Writebol?
We are going to be following those two patients as outpatients, and as part of our evaluation they have agreed to undergo additional testing so we can better understand immunity to Ebola virus. We are meeting with them periodically.
 
What sort of lessons has Emory learned from caring for these two people that would be transferrable to patients in west Africa?
We are not being critical of our colleagues in west Africa. They suffer from a terrible lack of infrastructure and the sort of testing that everyone in our society takes for granted, such as the ability to do a complete blood count—measuring your red blood cells, your white blood cells and your platelets—which is done as part of any standard checkup here. The facility in Liberia where our two patients were didn’t even have this simple thing, which everyone assumes is done as part of your annual physical.
 
What we found in general is that among our Ebola patients, because of the amount of fluid they lost through diarrhea and vomiting, they had a lot of electrolyte abnormalities. And so replacing that with standard fluids [used in hospital settings] without monitoring will not do a very good job of replacing things like sodium and potassium. In both of our patients we found those levels to be very low. One of the messages we will be sending back to our colleagues is even if you don’t have the equipment to measure these levels, do be aware this is occurring when patients are having a lot of body fluid loss.
 
Our two patients also gained an enormous amount of fluid in their tissues, what we call edema. In Ebola virus disease there is damage to the liver and the liver no longer makes sufficient amount of protein; the proteins in the blood are very low and there is an enormous amount of fluid leakage out into the tissues. So one of the takeaway messages is to pay closer attention to that and perhaps early on try to replace some of these proteins that patients’ livers lack.
 
Considering how limited resources are in some of these facilities, could health care workers really act on this information?
I think the world is becoming aware that issues like this are not going to go away. The developed countries of the world will have to do our part to assist our colleagues with less developed infrastructure to care for sick people. I think one of the messages that is going out from many sources is we really have to help countries such as the ones involved in this outbreak to develop their medical infrastructure. Hopefully in five years they will have this infrastructure.

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