Perfect skin: More touchy-feely robots

Robots could become a lot more 'sensitive' thanks to new artificial skins and sensor technologies developed by European scientists. 

Leading to better robotic platforms that could one day be used in industry, hospitals and even at home.

The new capabilities, and a production system for building touch-sensitivity into different robots, will improve the way robots work in unconstrained settings, as well as their ability to communicate and cooperate with each other and with humans.

The EU-funded project 'Skin-based technologies and capabilities for safe, autonomous and interactive robots' (ROBOSKIN) developed new sensor technologies and management systems which give robots an artificial sense of touch - until now an elusive quality in robotics.

According to the partners behind the research from Italy, Switzerland and the UK, it was important to create cognitive mechanisms that use tactile feedback (the sense of 'touch' or 'feel') and behaviour to make sure human-robot interaction is safe and effective for the envisaged future applications.

The artificial skin is modelled largely on real skin, which has a tiny network of nerves that sense or feel changes like hot/cold or rough/smooth.

In this case, the electronic sensors collect this so-called 'tactile data' and process it using application software which has been front-loaded to include some basic robot behaviours which can be added to over time.

'Here, we opted for programming through demonstration and robot-assisted play so the robots learn as they go along by feeling, doing and interacting,' explains project coordinator Professor Giorgio Cannata of Genoa University, Italy.

Giorgio Cannata

'We had to generate a degree of awareness in the robots to help them react to tactile events and physical contact with the outside world,' he adds.

Kaspar the friendly robot
But robot cognition is extremely complex, so ROBOSKIN started with modest ambitions in lab tests by classifying types or degrees of touch.

They created a geometric mapping using continuous contact between the test robot and the environment to build a 'body representation' - parameters by which data can be assimilated by the robot into behaviour.

KASPAR

Outside the lab, on the other hand, ROBOSKIN sensor patches were applied to common touch points (feet, cheeks, arms) located on the University of Hertfordshire's KASPAR robot, a humanoid robot designed to help autistic children communicate better.

'With our sensors, the robot could sense or detect contact and the data collected formed an important part of the contact classification we did - the distinction between, for example, wanted and unwanted touch,' explains Prof. Cannata.

ROBOSKIN scientists explored various technologies, from the more basic capacitive sensors in today's sensing technologies, to higher-performing transducers found in piezoelectric materials, and flexible organic semiconductors.

'We'll see more and more piezoelectric materials - which can act like sensors because they react to changes brought on by contact with an outside force - in the near future,' predicts Prof. Cannata.

But sensors using organic semiconductors will be the future game-changer, he suggests, as you will be able to print the chips on different organic materials like fake skin or bendable materials, and they will eventually be much cheaper to make, once scaled up.

More information: 'Skin-based technologies and capabilities for safe, autonomous and interactive robots' website.

AUTISM: Difficulty in Recognising Faces Linked to Performance in a Group of Neurons

Neuroscientists at Georgetown University Medical Center (GUMC) have discovered a brain anomaly that explains why some people diagnosed with autism cannot easily recognize faces -- a deficit linked to the impairments in social interactions considered to be the hallmark of the disorder.

They also say that the novel neuroimaging analysis technique they developed to arrive at this finding is likely to help link behavioral deficits to differences at the neural level in a range of neurological disorders.

The final manuscript published March 15 in the online journal NeuroImage: Clinical, the scientists say that in the brains of many individuals with autism, neurons in the brain area that processes faces (the fusiform face area, or FFA) are too broadly "tuned" to finely discriminate between facial features of different people.

They made this discovery using a form of functional magnetic resonance imaging (fMRI) that scans output from the blueberry-sized FFA, located behind the right ear.

"When your brain is processing faces, you want neurons to respond selectively so that each is picking up a different aspect of individual faces. The neurons need to be finely tuned to understand what is dissimilar from one face to another," says the study's senior investigator, Maximilian Riesenhuber, PhD., an associate professor of neuroscience at GUMC.

"What we found in our 15 adult participants with autism is that in those with more severe behavioral deficits, the neurons are more broadly tuned, so that one face looks more like another, as compared with the fine tuning seen in the FFA of typical adults," he says.

"And we found evidence that reduced selectivity in FFA neurons corresponded to greater behavioral deficits in everyday face recognition in our participants. This makes sense. If your neurons cannot tell different faces apart, it makes it more difficult to tell who is talking to you or understand the facial expressions that are conveyed, which limits social interaction."

Riesenhuber adds that there is huge variation in the ability of individuals diagnosed with autism to discriminate faces, and that some autistic people have no problem with facial recognition.

"But for those that do have this challenge, it can have substantial ramifications -- some researchers believe deficits in face processing are at the root of social dysfunction in autism," he says.

The neural basis for face processing
Neuroscientists have used traditional fMRI studies in the past to probe the neural bases of behavioral differences in people with autism, but these studies have produced conflicting results, says Riesenhuber.

"The fundamental problem with traditional fMRI techniques is that they can tell which parts of the brain become active during face processing, but they are poor at directly measuring neuronal selectivity," he says, "and it is this neuronal selectivity that predicts face processing performance, as shown in our previous studies."

To test their hypothesis that differences in neuronal selectivity in the FFA are foundational to differences in face processing abilities in autism, Riesenhuber and the study's lead author, neuroscientist Xiong Jiang, PhD, developed a novel brain imaging analysis technique, termed local regional heterogeneity, to estimate neuronal selectivity.

Read the full article here

Scientists Link Rare Gene Mutations to Heightened Risk of Autism

Three teams of scientists working independently to understand the biology of autism have for the first time homed in on several gene mutations that they agree sharply increase the chances that a child will develop the disorder, and have found further evidence that the risk increases with the age of the parents, particularly the father.

The gene mutations are extremely rare and together account for a tiny fraction of autism cases, suggesting that the search for therapies will be a long one, and that what is loosely known as autism may represent a broad category of related but biologically distinct conditions.

There are likely hundreds, perhaps thousands, of rare mutations that could disrupt brain development enough to result in social and developmental delays.

But experts said that the overlapping results, reported in three papers posted online Wednesday in the journal Nature, give scientists working on the genetics of autism something they have not had: a clear strategy for building a real understanding of the disease’s biological basis.

Researchers hope to find more similar, rare mutations in the next year or so that they estimate could account for 10 percent to 20 percent of all cases.

Biologists have been groping in vain for a reliable, verifiable foothold from which to investigate the underlying genetics of so-called autism spectrum disorders, including Asperger syndrome and related social difficulties that are being diagnosed at alarmingly high rates — on average, in one of 88 children, according to a government estimate released last week.

Previous studies have produced a scattering of gene findings but little consensus or confidence in how to proceed.

The new work provides a measure of both, as well as strong backing for earlier studies linking autism to the age of new fathers.

“These studies aren’t so much a breakthrough, because we knew this was coming,” said Jonathan Sebat, a geneticist at the University of California, San Diego, who was not a part of the research teams.

“But I’d say it’s a turning point. We now have a reliable way forward, and I think it’s fair to expect that we will find 20, 30, maybe more such mutations in the next year.”

Other researchers were more cautious, saying that the genetics of rare mutations was not yet well enough understood to make conclusive statements about their effect on the behavior of specific genes.

“This is a great beginning, and I’m impressed with the work, but we don’t know the cause of these rare mutations, or even their levels in the general population,” said Dr. Aravinda Chakravarti, of the Institute of Genetic Medicine at the Johns Hopkins University Medical School, who was not involved in the studies.

“I’m not saying it’s not worth it to follow up these findings, but I am saying it’s going to be a hard slog.”

The three research teams took a similar approach, analyzing genetic material taken from blood samples of families in which parents who have no signs of autism give birth to a child who develops the disorder.

This approach gives scientists the opportunity to spot the initial mutations that accompany the condition, rather than trying to work though possible genetic contributions from maternal and paternal lines.

In all three studies, the researchers focused on rare genetic glitches called de novo mutations.

De novo mutations are not inherited but occur spontaneously near or during conception. Most people have at least one and the overwhelming majority of them are harmless.

Read more here: Scientists Link Rare Gene Mutations to Heightened Risk of Autism - NYTimes.com

Autism: Researchers Continue to hunt for causes

For many families, the quest for the causes of autism has grown more urgent with the news that the estimated prevalence of autism grew by 23% from 2006 to 2008, according to a Centers for Disease Control and Prevention report out last week.

In most cases, however, scientists can't tell parents what caused their child's autism, says Thomas Insel, director of the National Institutes of Mental Health. In large part, the causes of autism — which is likely not one disease, but a group of conditions with related symptoms — remain a mystery.

For years, scientists had only a few clues about the condition, noticing that autism is about four times as common in boys as in girls, for example.

Recently, scientists have found a number of risk factors for autism, many of which point toward problems that develop very early in life, such as during pregnancy or delivery, or even during the process of creating eggs and sperm, says Craig Newschaffer, a professor at Philadelphia's Drexel University.

To better understand causes of autism, researchers at four major universities are following 1,200 mothers of autistic children through a project called the EARLI study, or the Early Autism Risk Longitudinal Investigation.

Because researchers know that these moms are at high risk of having a second autistic child, they closely follow the women's subsequent pregnancies, testing blood, urine, hair, even vacuuming dust from the women's homes, says Newschaffer, one of the study's lead researchers.

Researchers ask pregnant women to keep lists of any illnesses, since infections during pregnancy are suspected of playing a role in autism.

Doctors can confidently reassure parents that one thing doesn't cause autism — vaccines, says Paul Offit, chief of infectious diseases at Children's Hospital of Philadelphia. Nearly two dozen studies have failed to find a link between autism and vaccines, whether given alone or in combination.

Researchers have clues to other causes:

Genes. About 15% to 20% of autistic children have a genetic mutation that causes their disorder, Insel says. Certain genetic disorders, such as Fragile X syndrome and Rett syndrome, are well-known for increasing the risk of autism.

Even when genes are the main contributor to autism, however, it's possible that most children have a unique mutation or set of mutations, says David Amaral, research director of the University of California-Davis MIND Institute.

Family history. If parents have one child with autism, the risk of having a second child diagnosed with the disorder is nearly 20%, according to a landmark study from U.C.-Davis. Among those with two autistic children, the risk of having a third is 32%, study author Sally Ozonoff says.

Environmental pollution. One California study published last year found that babies whose mothers lived near a highway while pregnant were more likely to be diagnosed as autistic.

Older parents. Both older father and mothers are at higher risk of having autistic children, Newschaffer says. Research from Israel and the Harvard School of Public Health also suggests that infertility treatments, which are more often used among older patients, are linked to a higher risk of autism.

Prematurity and low birthweight. An October study in Pediatrics found that, among babies born weighing less than about 4½ pounds, 5% had been diagnosed as autistic by age 21.

Medications. Many studies now show that a seizure treatment called valproic acid can increase the risk of autism in children exposed before birth. A single study published last year found a higher risk among children exposed prenatally to antidepressants. Using prenatal vitamins is also linked to a lower risk of autism.

Closely spaced pregnancies. In a 2011 study, children who were born less than one year after an older sibling were three times as likely to be diagnosed with autism, compared with children born three years after their mom's last pregnancy.

Talkbox: visual language for autistic children

Talkbox Presentation

The number of children diagnosed as autistic has been growing.

The reasons as to why are unclear: is the disease simply more prevalent than it was, are newer definitions of the condition including a wider spectrum of children, or both?

As numbers rise, and technology advances, designers have been looking for ways to help autistic children communicate.

The focus has been especially on those with severe speech impairment. For instance, therapists have been experimenting with iPad applications that focus on improving communication, behaviour modeling and activity planning.

Most communication systems that have been developed in the past are text or voice based.

This is where Talkbox, a new concept that is being developed, seeks to change the current methods of communication, delivering a personalized visual language to the kids using it.

Talkbox’s aim is to facilitate an autistic child to interact and communicate with others in a language that they know and understand.

To do this, Talkbox will take the repetitive behaviors seen in autistic patients and create an organized “connection list” as well as a time or place based dictionary and vocabulary.

The concept features a speech processing engine that works with a system that finds and recognizes different objects.

It uses a multitouch screen for animation playback, and a simple button to take pictures of things and people that surround the child.

A panel displays photos of people a child may need to communicate with, and the child can communicate from Talkbox to a smartphone via the Internet, and the phones can be used to respond by accessing the vocabulary online.

The images taken by the child can be printed out to serve as what Talkbox calls “story makers,” to help the child connect the images they see.

The creators of this system see this as a way to let children interact directly with others by building stories.

Talkbox uses this “visual vocabulary” to connect the child to others, but also to help the parents of autistic children form a new sort of community.

They can upload videos and images of the new vocabulary to the Talkbox website to help connect to and learn from each other.

Read more at DesignBuzz 

Gardening in the Brain: Cells Called Microglia Prune the Connections Between Neurons

Microglia (green) in a mouse brain. The nuclei of all cells in the brain are labelled blue. (Credit: EMBL/R. Paolicelli)

Gardeners know that some trees require regular pruning: some of their branches have to be cut so that others can grow stronger.

The same is true of the developing brain: cells called microglia prune the connections between neurons, shaping how the brain is wired, scientists at the European Molecular Biology Laboratory (EMBL) in Monterotondo, Italy, discovered. Published online in Science, the findings could one day help understand neurodevelopmental disorders like autism.

"We're very excited, because our data shows microglia are critical to get the connectivity right in the brain," says Cornelius Gross, who led the work: "they 'eat up' synapses to make space for the most effective contacts between neurons to grow strong."

Microglia are related to the white blood cells that engulf pathogens and cellular debris, and scientists knew already that microglia perform that same clean-up task when the brain is injured, 'swallowing up' dead and dying neurons.

Looking at the developing mouse brain under the microscope, Gross and colleagues found proteins from synapses -- the connections between neurons -- inside microglia, indicating that microglia are able to engulf synapses too.

To probe further, the scientists introduced a mutation that reduced the number of microglia in the developing mouse brain.

"What we saw was similar to what others have seen in at least some cases of autism in humans: many more connections between neurons," Gross says. "So we should be aware that changes in how microglia work might be a major factor in neurodevelopmental disorders that have altered brain wiring."

The microglia-limiting mutation the EMBL scientists used has only temporary effects, so eventually the number of microglia increases and the mouse brain establishes the right connections.

However, this happens later in development than it normally would, and Gross and colleagues would now like to find out if that delay has long-term consequences.

Does it affect the behaviour of the mice behaviour, for example? At the same time, Gross and colleagues plan to investigate what microglia do in the healthy adult brain, where their role is essentially unknown.

Testosterone reduces the empathetic responses in Women

Testosterone - Lauded by some and viewed with suspicion by others, few people have a completely neutral view of the hormone that separates boys from girls.

According to the extreme male brain theory of autism, the organising effects of testosterone on the brain in utero, and its ongoing shaping of social behaviors throughout life, explains why men exhibit more aggressive, risk-taking behaviour than women do.

It may also account for the social intelligence deficits of people with autism and the skewed gender ratio of the disorder.

A new study shows that even a little bit of testosterone administered under the tongue can cause a woman to show less empathy — to behave, in other words, more like a man.

This is especially true, researchers say, when a woman has been exposed to higher-than-average levels of testosterone as a fetus.

The 2D:4D Finger Test
One increasingly accepted marker of fetal androgen exposure is the 2D:4D ratio, comparing the length of the index finger to that of the ring finger on the right hand. In women, the ring finger is typically longer than the index finger, whereas in men, or in individuals with high fetal testosterone exposure, the two fingers are of nearly identical length.

Exposure to lower testosterone levels in utero, as inferred by a higher 2D:4D ratio, may protect men from prostate cancer. Researchers have also reported lower 2D:4D ratios in children with autism and in their parents and siblings.

In the study, researchers administered a single 0.5 mg dose of testosterone to 16 young women between 20 and 25 years of age in one session, and a single dose of placebo in a second session 48 hours later. The women experienced a ten-fold increase in blood testosterone levels 15 minutes after intake, with the levels returning to baseline in about an hour and a half.

During that time, the participants took a test of cognitive empathy called Reading the Mind in the Eyes, which asks them to infer the emotions expressed in a photograph of a pair of eyes. Interestingly, 75 percent of the women in the study achieved lower scores on the test after testosterone than after placebo.

When the researchers compared the women's 2D:4D ratios, as computed from scans of their right hands, they found something even more interesting: the women with the lowest 2D:4D ratios (highest fetal testosterone exposure) showed the most significant decrease in empathy as measured by the test.

This may not be not a slam-dunk for the extreme male brain theory, but the results jibe with other studies that have found a continuum of social cognition abilities.

Fewer Synapses, More Efficient Learning: Molecular Glue Wires the Brain

Yale University researchers have found that a single molecule not only connects brain cells but also changes how we learn. The findings, reported in the December 9 issue of the journal Neuron, may help researchers discover ways to improve memory and could lead to new therapies to correct neurological disorders.


The junctions between brain cells over which nerve pulses pass -- called synapses -- are crucial for regulating learning and memory and how we think. Aberrations in the structure and function of synapses have been linked to mental retardation and autism, while synapses are lost in the aging brains of Alzheimer's patients.

However, the mechanisms that organize synapses in the living brain remain a puzzle. Yale scientists identified one critical piece of this puzzle, a molecule called SynCAM 1 that spans across synaptic junctions.

"We hypothesized that this molecule might promote new synapses in the developing brain, but were surprised that it also impacts the maintenance and function of these structures," said Thomas Biederer, associate professor of molecular biophysics and biochemistry and senior author of the study. "We can now define how this molecule supports the brain's ability to wire itself."

The Yale team focused on SynCAM 1, an adhesion molecule that helps to hold synaptic junctions together. They found that when the SynCAM 1 gene was activated in mice, more synaptic connections formed. Mice without the molecule produced fewer synapses.

When we learn, new synapses can form. However, the strength of synaptic connections also changes during learning, based on the amount of stimuli received -- a quality scientists termed "plasticity." Together with a group in Germany led by Valentin Stein, the team was surprised to find that SynCAM 1 controls an important form of synaptic plasticity.

Unexpectedly, Biederer and colleagues also found that mice with high amounts of SynCAM 1 are unable to learn while mice lacking SynCAM 1 -- and having fewer synapses -- learn better. Apparently an excess of the molecule can be damaging. This builds on recent theories suggesting that having too many connections isn't always better and that the balance of synaptic activity is crucial for proper learning and memory.

"Synapses are dynamic structures. It appears that SynCAM 1 ties synapses together; some of this molecule is needed to promote contact but too much glues down the synapse and inhibits its function. It may act a bit like a sculptor who helps give synapses their shape." Biederer also said that the molecule is almost identical in mice and man, and likely has the same roles in human brains.

Journal Reference:

1. Elissa M. Robbins, Alexander J. Krupp, Karen Perez De Arce, Ananda K. Ghosh, Adam I. Fogel, Antony Boucard, Thomas C. Südhof, Valentin Stein, Thomas Biederer. SynCAM 1 adhesion dynamically regulates synapse number and impacts plasticity and learning. Neuron, 2010; 68 (5): 894-906 DOI: 10.1016/j.neuron.2010.11.003

Estrogen, Puberty and Autism | Neurodiversity

Estrogen, Puberty and Autism Neurodiversity

To what degree have high and low-fat diets influenced human evolution? If low fat delays puberty and results in more brain growth, might this be because more synapses are useful for finding more fat?

When there is more fat in diets and puberty rates drop, for a woman there is a greater number of children produced over a single lifetime. Less fat in diet, fewer children produced. This seems like an evolutionary process.

Do thin males with less fat have less estrogen, reach puberty later, have bigger brains and exhibit more neotenous features?

Should autistic males be on extremely low-fat diets so that they reach puberty later, thus allowing more time for their brains to mature?

Is the degree of brain synapse pruning that occurs in infancy related to the estrogen levels in the mother or the child? High mother testosterone levels encourage higher rates of autism, which may be directly related to less pervasive synapse pruning. Is it possible that a high mother estrogen level results in low male baby estrogen levels that prolong or diminish the testosterone prunings?

In other words, the Simon Baron-Cohen research regarding mother testosterone levels and autism may be related to mother estrogen levels. If low estrogen at puberty translates to delayed puberty, delayed testosterone surges and increased brain growth, then the same process may be engaged during the first testosterone surges that compel a diminution of the right cerebral hemisphere during infancy. Low estrogen levels as an embryo, infant and toddler may have a direct impact on cerebral lateralization and synapse production.

Another interesting article 'Introduction to Neotenty' Here ............

The Recent Rise in Autism and Asthma: Graphs

The rise in the number of reported cases of Autism from 1992 - 2008

The prevalence in the number of reported cases of Asthma around the World