Month: October 2015

The world is a jumble of sights, sounds, and smells. While these signals may seem distinct and independent, they actually interact and integrate within the brain’s network of sensory neurons.

A new assistive device for blind people taps into this sensory network. It translates images into sounds, allowing visually impaired people to detect their environment without the need for hours of training or intense concentration.

The work is described in a paper published in Scientific Reports.

“Many neuroscience textbooks really only devote a few pages to multisensory interaction,” says Shinsuke Shimojo, a professor of experimental psychology at the California Institute of Technology (Caltech) and principal investigator on the study. “But 99 percent of our daily life depends on multisensory—also called multimodal—processing.”

As an example, he says, if you are talking on the phone with someone you know very well, and they are crying, you will not just hear the sound but will visualize their face in tears. “This is an example of the way sensory causality is not unidirectional—vision can influence sound, and sound can influence vision.”

Shimojo and postdoctoral scholar Noelle Stiles have exploited these crossmodal mappings to stimulate the visual cortex with auditory signals that encode information about the environment.

They explain that crossmodal mappings are ubiquitous; everyone already has them. Mappings include the intuitive matching of high pitch to elevated locations in space or the matching of noisy sounds with bright lights. Multimodal processing, like these mappings, may be the key to making sensory substitution devices more automatic.

HOW THE DEVICE WORKS

The researchers conducted trials with both sighted and blind people using a sensory substitution device, called a vOICe device, that translates images into sound.

The vOICe device is made up of a small computer connected to a camera that is attached to darkened glasses, allowing it to “see” what a human eye would. A computer algorithm scans each camera image from left to right, and for every column of pixels, generates an associated sound with a frequency and volume that depends upon the vertical location and brightness of the pixels.

A large number of bright pixels at the top of a column would translate into a loud, high-frequency sound, whereas a large number of lower dark pixels would be a quieter, lower-pitched sound. A blind person wearing this camera on a pair of glasses could then associate different sounds with features of their environment.

HEAR A SOUND, SEE A COLOR

In the trials, sighted people with no training or instruction were asked to match images to sounds; while the blind subjects were asked to feel textures and match them to sound. Tactile textures can be related to visual textures (patterns) like a topographic map—bright regions of an image translate to high tactile height relative to a page, while dark regions are flatter.

Both groups showed an intuitive ability to identify textures and images from their associated sounds. Surprisingly, the untrained (also called “naive”) group’s performance was significantly above chance, and not very different from the trained.

The intuitively identified textures used in the experiments exploited the crossmodal mappings already within the vOICe encoding algorithm.

“When we reverse the crossmodal mappings in the vOICe auditory-to-visual translation, the naive performance significantly decreased, showing that the mappings are important to the intuitive interpretation of the sound,” explains Stiles.

“We found that using this device to look at textures—patterns of light and dark—illustrated ‘intuitive’ neural connections between textures and sounds, implying that there is some preexisting crossmodality,” says Shimojo.

One common example of crossmodality is a condition called synesthesia, in which the activation of one sense leads to a different involuntary sensory experience, such as seeing a certain color when hearing a specific sound. “Now, we have discovered that crossmodal connections, preexisting in everyone, can be used to make sensory substitution intuitive with no instruction or training.”

The researchers do not exactly know yet what each sensory region of the brain is doing when processing these various signals, but they have a rough idea.

Continue on to the next page see a video that demonstrates the process and explains more about how the device works.

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NASA’s Cassini spacecraft successfully flew through the south pole geysers on Enceladus at an altitude of 30 miles on October 28th, and is now transmitting back stunning photos of the dramatic event. While the photos are amazing, the more exciting science is yet to come, according to NASA scientists, since other instruments onboard Cassini were used to take samples of the ice plumes.

A fantastic article on the NASA website chronicles the Cassini happenings:

NASA’s Cassini spacecraft has begun transmitting its latest images of Saturn’s icy, geologically active moon Enceladus, acquired during the dramatic Oct. 28 flyby in which the probe passed about 30 miles (49 kilometers) above the moon’s south polar region. The spacecraft will continue transmitting its data from the encounter for the next several days.

“Cassini’s stunning images are providing us a quick look at Enceladus from this ultra-close flyby, but some of the most exciting science is yet to come,” said Linda Spilker, the mission’s project scientist at NASA’s Jet Propulsion Laboratory in Pasadena, California.

Researchers will soon begin studying data from Cassini’s gas analyzer and dust detector instruments, which directly sampled the moon’s plume of gas and dust-sized icy particles during the flyby. Those analyses are likely to take several weeks, but should provide important insights about the composition of the global ocean beneath Enceladus’ surface and any hydrothermal activity occurring on the ocean floor. The potential for such activity in this small ocean world has made Enceladus a prime target for future exploration in search of habitable environments in the solar system beyond Earth

You can see more of the “raw” images from Cassini on the mission website at: http://saturn.jpl.nasa.gov/mission/flybys/enceladus20151028, and you can learn more from the excellent article on the NASA website as well.

 

Source: NASA.com – “Saturn’s Geyser Moon Shines in Close Flyby Views“

Featured Photo Credit: NASA/JPL-Caltech/Space Science Institute

Robert Lustig, University of California, San Francisco

Children are manifesting increased rates of adult diseases like hypertension or high triglycerides. And they are getting diseases that used to be unheard of in children, like Type 2 diabetes and fatty liver disease. So why is this happening?

Everyone assumes this is the result of the obesity epidemic – too many calories in, too few out. Children and adults are getting fat, so they’re getting sick. And it is generally assumed that no one specific food causes it, because “a calorie is a calorie”.

I’ve been studying the role that sugar plays in contributing to chronic disease for years, and my research group at the University of California, San Francisco has just published research in the journal Obesity that challenges this assumption. If calories come from sugar, they just aren’t the same.

Diabetes is increasing faster than obesity

It’s clear that the cause of rising rates of health conditions like Type 2 diabetes isn’t as simple as people just eating too many calories.

Obesity is increasing globally at 1% per year, while diabetes is increasing globally at 4% per year. If diabetes were just a subset of obesity, how can you explain its more rapid increase?

And certain countries are obese without being diabetic (such as Iceland, Mongolia and Micronesia), while other countries are diabetic without being obese (India, Pakistan and China, for instance). Twelve percent of people in China have diabetes, but the obesity rate is much lower. The US is the fattest nation on Earth and our diabetes prevalence is 9.3%.

While 80% of the obese population in the US is metabolically ill (meaning they have conditions like diabetes, hypertension, lipid problems and heart disease), 20% is not. Conversely, 40% of the normal weight population has metabolic syndrome.

If normal weight people have these conditions, how then are they related to obesity? Indeed, we now know that obesity is a marker rather than a cause for these diseases.

Epidemiological studies have found a correlation between added sugar consumption and health conditions like cardiovascular disease. So could cutting excess sugar out of our diets reverse metabolic syndrome?

What happens when you stop feeding kids added sugar?

Our group at UCSF studied 43 Latino and African-American children with obesity and metabolic syndrome over a 10-day period. We started by assessing their metabolic status – insulin and glucose levels, as well as blood fats and other markers for disease, like lactate and free fatty acids – on their home diet.

For the next nine days, each child ate an individual tailored diet. We catered their meals to provide same number of calories and protein and fat content as their usual home diet. We gave them the same percentage of carbohydrate, but we substituted starch for sugar. The big difference: this special diet had no added sugar. This means their diet had no sugar from sugarcane or high fructose corn syrup. The kids consumed foods such as fruits and other whole foods that naturally contain some sugar. These foods also have fiber, which reduces the rate of sugar absorption, so they don’t affect the body the same way that added sugar does.

We took chicken teriyaki out. We put turkey hot dogs in. We took sweetened yogurt out. We put baked potato chips in. We took donuts out. We put bagels in. We gave them unhealthy processed food, just with no added sugar. Each child was given a scale to take home, and if their weight was declining, we made them eat more. Then we studied them again.

The children had eaten the same number of calories and had not lost any weight, and yet every aspect of their metabolic health improved. With added sugar cut out of their diet for 10 days, blood pressure, triglycerides, low-density lipoprotein (LDL, or “bad cholesterol”), insulin sensitivity and glucose tolerance all improved. And remember, we weren’t giving them just leafy greens and tofu – we fed the kids processed foods, just ones without sugar.

Further studies are needed to see if this will also work in adults, and if the benefits are short-term or long-term.

Sugar is like alcohol

This study demonstrates that a calorie is not a calorie, and that sugar is a primary contributor to metabolic syndrome, unrelated to calories or weight gain. By removing added sugar, we improved metabolic health.

Sugar may not be the only contributor to chronic disease, but it is far and away the easiest one to avoid. Kids could improve their metabolic health – even while continuing to eat processed food – just by dumping the sugar. Can you imagine how much healthier they’d be if they ate real food?

The naysayers will say, “But sugar is natural. Sugar has been with us for thousands of years. Sugar is food, and how can food be toxic?”

Webster’s Dictionary defines food as:

material consisting essentially of protein, carbohydrate, and fat used in the body of an organism to sustain growth, repair, and vital processes and to furnish energy.

Sugar by itself furnishes energy, and that’s about it. In that sense, sugar is like alcohol. It’s got calories, but it’s not nutrition. There’s no biochemical reaction that requires it. And at high doses, alcohol can fry your liver.

Same with sugar. Fructose, the sweet molecule in sugar, contains calories that you can burn for energy, but it’s not nutrition, because there’s no biochemical reaction that requires it. In excess, it can fry your liver, just like alcohol. And this makes sense, because where do you get alcohol from? Fermentation of sugar.

Too much sugar causes diabetes, heart disease, fatty liver disease and tooth decay. When consumed in excess, it’s a toxin. And it’s addictive – just like alcohol. That’s why children are getting the diseases of alcohol – Type 2 diabetes and fatty liver disease – without alcohol. But our research suggests we could turn this around in 10 days – if we chose to.

Robert Lustig, Professor of Pediatrics , University of California, San Francisco

This article was originally published on The Conversation. Read the original article.

Featured Photo Credit: By Uwe Hermann (http://hermann-uwe.de/photoblog/sugar) [CC BY-SA 3.0], via Wikimedia Commons

In the war against Alzheimer’s disease, one of the big villains is a protein called amyloid beta—”Abeta” for short.

In a diseased brain, sticky strands of the protein clump into plaques that kill nerve cells and choke the gaps between them. Under a microscope the plaques look sinister, even to the untrained eye—scattershot black blotches, splattered across healthy tissue.

Scientists, knowing the damage Abeta can cause, have searched for therapies that clear the protein from the brains of Alzheimer’s patients. So far, all clinical trials of this approach have failed. Though two trials are still ongoing, for now Alzheimer’s remains a disease with no prevention, treatment, or cure.

Now Carmela Abraham, Boston University professor of biochemistry and medicine, and colleagues have discovered a new way to attack Abeta. Instead of clearing it from the brain, the scientists have found a compound that prevents the body from making it in the first place.

The work, funded by the Alzheimer’s Association and the Cure Alzheimer’s Fund, may eventually lead to a novel treatment for this deadly disease.

“Alzheimer’s is now the number six killer of adults in the United States. Deaths from breast cancer and heart disease keep dropping, but Alzheimer’s increases every year,” says Abraham. “Caring for Alzheimer’s patients costs over $200 billion per year. The estimate for 2050 is $1.1 trillion, which means it will completely break the health care system. We have to find a drug.”

The brain creates Abeta with enzymes that chop a larger protein, called the amyloid precursor protein (APP), into smaller bits. Sometimes, for reasons scientists don’t quite understand, two APP proteins join together in a process called dimerization, which ultimately leads to increased Abeta.

Abraham wondered: if scientists could stop dimerization, would that stop Abeta in its tracks? She decided to try.

Continue reading to learn the astonishing discovery she made.

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Darren Saunders, UNSW Australia

New research about the risk of cancer from exposure to common chemicals is usually accompanied by headlines screaming “X causes cancer!” So when a new study on the topic was published in Carcinogenesis last week, I cringed in anticipation.

Cancer is caused by a combination of genetic and environmental influences – a kind of genetic lottery where the odds are stacked by environmental and lifestyle factors.

There are valid concerns over chemical exposure and cancer risk. The World Health Organization (WHO) and International Agency for Research on Cancer (IARC) estimate toxic environmental exposure to known carcinogens accounts for between 7% and 19% of cancer cases. With around 14 million new cases of cancer diagnosed worldwide annually, this accounts for a huge personal and financial cost.

The reporting of this kind of study is often framed in a way that fuels chemophobia, an “irrational” fear of chemicals. It’s perfect fodder for the likes of blogger Food Babe and the echo chamber of alternative health blogs.

Compound Interest, CC BY-NC-ND

In this latest case, the Daily Mail didn’t disappoint, with its headline claiming chemicals in fried potatoes, handwash and sunscreen could lead to cancer if combined. The Daily Mail’s hyperbolic contribution to classifying things as either causing or curing cancer (or both) is legendary, spawning the Kill or Cure website.

Everything gives you cancer?

The IARC classifies chemicals on a scale of decreasing carcingogenic certainty. The widely used weedkiller glyphosate, for example, was recently classified in Group 2: possibly/probably carcinogenic to humans.

For context, this places it in the same category as burning wood in your fireplace and shift work. There is a possible link to lymphoma with very high glyphosate exposure (for farmers spraying huge quantities of the stuff) but the data are limited and conflicting.

This review of the cancer risk associated with 50 common ingredients from random recipes in a cookbook is a brilliant demonstration of the difficulties faced in weighing evidence for cancer risk. While lots of studies claim a link between various foods and either increased cancer risk, or a protective effect, in many cases the evidence is unconvincing.

Sensationalist reporting of medical research often leaves a lot to be desired, but the blame doesn’t always lay at the feet of journalists and bloggers. A recent case study of reporting around a study into pancreatic cancer risk and red meat consumption showed that most journalists simply regurgitated information in the accompanying press release.

Does this study tell us anything new?

The latest study represents a big effort by an international team of more than 200 cancer biologists and toxicologists involved in the Halifax Project. It is not a primary research study, but reviews the available literature on the carcinogenic potential of low-dose environmental exposure to chemical mixtures.

Data on 85 chemicals – with varying levels of evidence – were included in the review. In some cases, only a single study was available, so the evidence is severely limited in some aspects.

The Halifax Project study puts forward an interesting hypothesis – that exposure to low doses and mixtures of chemicals might synergise to cause cancer. The authors go on to suggest that World Health Organization efforts to assess chemical safety should be realigned with our current understanding of cancer biology.

Probably the most telling (under)statement in the whole paper is that:

[the hypothesis] needs to be rigorously pursued before the merits of this hypothesis can be further advanced.

A new framework for understanding chemical risk in cancer?

For me, the most interesting outcome of this study is the recommendation to change research and regulatory strategy when assessing chemical risk to use an “adverse outcome pathway concept” model.

In other words, the carcinogenic potential of low-dose chemical exposure should be interpreted in the context of the “hallmarks of cancer”. This concept provides a mechanistic framework for understanding cancer biology, describing characteristic features of tumours such as sustained growth, new blood vessel formation, and so on.

Missing the forest for the trees

The hallmarks concept has been a galvanising force in cancer biology. Its great strength is as an organising principle for rationalising the complexity of cancer. It is only valid as a whole.

To assess the cancer-causing potential of chemical agents against each of the individual hallmarks in isolation completely misses the point. Effects on a single individual feature in isolation do not necessarily translate into transforming a normal cell into a cancer cell. Even then, there are huge challenges in translating lab-based findings on the effects of individual chemicals or mixtures of chemicals to whole body in real world.

What can we do?

The authors of this study admit their suggestion for expanding the evaluation of chemical risk is “not a trivial undertaking” and it would be hugely expensive. In the face of limited funding and time, it’s valid to question whether this approach will provide a return on the investment.

Environmental chemical exposure is a valid concern, but the evidence does not support hyperbolic claims that we are swimming around in a soup of cancer-causing chemicals. Lifestyle changes such as giving up smoking, maintaining a healthy weight and avoiding too much alcohol are far more achievable ways to reduce cancer risk.

Darren Saunders, Senior Lecturer, UNSW Australia

This article was originally published on The Conversation. Read the original article.

Featured Photo Credit: F Mira/Flickr, CC BY-SA