Why we’re building a €1 billion model of a human brain

We want to reach a unified understanding of the brain and the simulation on a supercomputer is the tool. Today you have neuroscientists working on a genetic, behavioural or cognitive level, and then you have informaticians, chemists and mathematicians. They all have their own understanding of how the brain functions and is structured. How do you get them all around the same table? We think of the project as like a CERN for the brain. The model is our way of bringing everyone, and our understanding, together.

Humans and robots work better together following cross-training

Spending a day in someone else’s shoes can help us to learn what makes them tick. Now the same approach is being used to develop a better understanding between humans and robots, to enable them to work together as a team.

Robots are increasingly being used in the manufacturing industry to perform tasks that bring them into closer contact with humans. But while a great deal of work is being done to ensure robots and humans can operate safely side-by-side, more effort is needed to make robots smart enough to work effectively with people, says Julie Shah, an assistant professor of aeronautics and astronautics at MIT and head of the Interactive Robotics Group in the Computer Science and Artificial Intelligence Laboratory (CSAIL).

“People aren’t robots, they don’t do things the same way every single time,” Shah says. “And so there is a mismatch between the way we program robots to perform tasks in exactly the same way each time and what we need them to do if they are going to work in concert with people.”

Most existing research into making robots better team players is based on the concept of interactive reward, in which a human trainer gives a positive or negative response each time a robot performs a task.

However, human studies carried out by the military have shown that simply telling people they have done well or badly at a task is a very inefficient method of encouraging them to work well as a team.

So Shah and PhD student Stefanos Nikolaidis began to investigate whether techniques that have been shown to work well in training people could also be applied to mixed teams of humans and robots. One such technique, known as cross-training, sees team members swap roles with each other on given days. “This allows people to form a better idea of how their role affects their partner and how their partner’s role affects them,” Shah says.

In a paper to be presented at the International Conference on Human-Robot Interaction in Tokyo in March, Shah and Nikolaidis will present the results of experiments they carried out with a mixed group of humans and robots, demonstrating that cross-training is an extremely effective team-building tool.

Putting Our Heads Together: Canines May Hold Clues to Human Skull Development

Man’s best friend may touch our hearts with their empathy, companionship, playfulness and loyalty, and they may also lead us to a deeper understanding of our heads.

In the article, “The Genetics of Canine Skull Shape Variation,” in the February issue of the Genetics Society of America’s journal, GENETICS, Jeffrey J. Schoenebeck, PhD, and Elaine A. Ostrander, PhD, researchers at the National Human Genome Research Institute (NHGRI), the National Institutes of Health (NIH), review progress in defining the genes and pathways that determine canine skull shape and development that have been made in the eight years since the dog genome was mapped.

The implications of this research extend beyond the interests of dog fanciers and breeders. “Dogs can serve as a model for skull growth and shape determination because the genetic conservation between dogs and humans makes it highly likely that craniofacial development is regulated similarly between both species,” Dr. Schoenebeck said. “These discoveries are important for human health and biology, especially for children born with craniofacial deformities,” Dr. Ostrander, added. In humans these deformities include Apert, Crouzon and Pfeiffer syndromes, where skull bones fuse prematurely causing facial malformations, such as wide-set bulging eyes and broad foreheads, resulting in dental, eye and other physiological problems.

Skull shape is a complex trait, involving multiple genes and their interactions. Thanks to standardized canine breeding, which documents more than 400 breeds worldwide, and their distinct morphological features, researchers can disentangle traits such as skull shape, which in many breeds is a breed-defining variation.

For example, researchers are beginning to identify which genes cause a Bulldog or a Pug to have short pushed-in faces, or brachycephaly, and those that cause Saluki’s or collies to have narrow, elongated snouts, or dolichocephaly. Between these two distinct canine cranium shapes are many variations that are also breed specific but can’t be neatly categorized as brachycephalic or dolichocephalic, such as the rounded skull of the Chihuahua or the downward pointing snout of the Bull terrier. Researchers now use genome-wide association studies (GWAS) to identify loci of interest that may be associated with these kinds of subtle differences.

The use of GWAS in determining genetic variation in dogs is in its infancy. What’s exciting said Dr. Schoenebeck is that with these studies and the tools researchers now have to map these variations “we may find new roles for genes, never before implicated in cranium development” and because similar genes and genetic pathways operate in humans, unexplained craniofacial developmental defects may become better understood.

Identifying the causative genetic mechanisms of these variations in canines offer researchers who study human cranial abnormalities “a way to figure out what sort of genetic variation matters and what doesn’t,” said Dr. Ostrander.

Drs. Schoenbeck and Ostrander clearly show there’s a lot more research to do on craniofacial development in dogs. It is also clear that the connection between us and our canine friends is in our heads as well as our hearts.

(Image: Villemarette)

Peering into living cells — without dye nor fluophore

In the world of microscopy, this advance is almost comparable to the leap from photography to live television. Two young EPFL researchers, Yann Cotte and Fatih Toy, have designed a device that combines holographic microscopy and computational image processing to observe living biological tissues at the nanoscale. Their research is being done under the supervision of Christian Depeursinge, head of the Microvision and Microdiagnostics Group in EPFL’s School of Engineering.

Using their setup, three-dimensional images of living cells can be obtained in just a few minutes – instantaneous operation is still in the works – at an incredibly precise resolution of less than 100 nanometers, 1000 times smaller than the diameter of a human hair. And because they’re able to do this without using contrast dyes or fluorescents, the experimental results don’t run the risk of being distorted by the presence of foreign substances.

Being able to capture a living cell from every angle like this lays the groundwork for a whole new field of investigation. “We can observe in real time the reaction of a cell that is subjected to any kind of stimulus,” explains Cotte. “This opens up all kinds of new opportunities, such as studying the effects of pharmaceutical substances at the scale of the individual cell, for example.”

Watching a neuron grow

This month in Nature Photonics the researchers demonstrate the potential of their method by developing, image by image, the film of a growing neuron and the birth of a synapse, caught over the course of an hour at a rate of one image per minute. This work, which was carried out in collaboration with the Neuroenergetics and cellular dynamics laboratory in EPFL’s Brain Mind Institute, directed by Pierre Magistretti, earned them an editorial in the prestigious journal. “Because we used a low-intensity laser, the influence of the light or heat on the cell is minimal,” continues Cotte. “Our technique thus allows us to observe a cell while still keeping it alive for a long period of time.”

As the laser scans the sample, numerous images extracted by holography are captured by a digital camera, assembled by a computer and “deconvoluted” in order to eliminate noise. To develop their algorithm, the young scientists designed and built a “calibration” system in the school’s clean rooms (CMI) using a thin layer of aluminum that they pierced with 70nm-diameter “nanoholes” spaced 70nm apart.

Finally, the assembled three-dimensional image of the cell, that looks as focused as a drawing in an encyclopedia, can be virtually “sliced” to expose its internal elements, such as the nucleus, genetic material and organelles.

Toy and Cotte, who have already obtained an EPFL Innogrant, have no intention of calling a halt to their research after such a promising beginning. In a company that’s in the process of being created and in collaboration with the startup Lyncée SA, they hope to develop a system that could deliver these kinds of observations in vivo, without the need for removing tissue, using portable devices. In parallel, they will continue to design laboratory material based on these principles. Even before its official launch, the start-up they’re creating has plenty of work to do - and plenty of ambition, as well.

Old drug may point the way to new treatments for diabetes and obesity

Researchers at the University of Michigan’s Life Sciences Institute have found that amlexanox, an off-patent drug currently prescribed for the treatment of asthma and other uses, also reverses obesity, diabetes and fatty liver in mice.

The findings from the lab of Alan Saltiel, the Mary Sue Coleman director of the Life Sciences Institute, were published online Feb. 10 in the journal Nature Medicine.

"One of the reasons that diets are so ineffective in producing weight loss for some people is that their bodies adjust to the reduced calories by also reducing their metabolism, so that they are ‘defending’ their body weight," Saltiel said. "Amlexanox seems to tweak the metabolic response to excessive calorie storage in mice."

Different formulations of amlexanox are currently prescribed to treat asthma in Japan and canker sores in the United States. Saltiel is teaming up with clinical-trial specialists at U-M to test whether amlexanox will be useful for treating obesity and diabetes in humans. He is also working with medicinal chemists at U-M to develop a new compound based on the drug that optimizes its formula.

The study appears to confirm and extend the notion that the genes IKKE and TBK1 play a crucial role for maintaining metabolic balance, a discovery published by the Saltiel lab in 2009 in the journal Cell.

"Amlexanox appears to work in mice by inhibiting two genes—IKKE and TBK1—that we think together act as a sort of brake on metabolism," Saltiel said. "By releasing the brake, amlexanox seems to free the metabolic system to burn more, and possibly store less, energy."

Birds evolved ultraviolet vision several times

Ultraviolet vision evolved at least eight times in birds from a common violet sensitive ancestor finds a study published in BioMed Central’s open access journal BMC Evolutionary Biology. All of these are due to single nucleotide changes in the DNA.

Modern daytime birds either have violet sensitive or ultraviolet sensitive vision. Being ultraviolet sensitive alters visual cues used to select a mate, avoiding predators, and in finding food. Researchers from Uppsala University and the Swedish University of Agricultural Sciences sequenced the genes responsible for producing the light sensitive pigment (SWS1 opsin) from 40 species of birds, in 29 families.

Generating a phylogenetic tree from these sequences shows that there have been at least 14 shifts between violet and ultraviolet sensitive colour vision and back. An ancestor of Passeriformes (perching birds including larks, swallows, blackbirds, finches, birds of paradise, and crows) and Psittaciformes (parrots and allies) changed from the ancestral violet sensitive colour vision to ultraviolet and, in some cases passerines have reverted back to violet vision.

Anders Ödeen and Olle Håstad, who performed this research commented, “There are two different amino acid alterations that can each change bird colour vision from violet to ultraviolet. One particular single nucleotide change has occurred at least 11 separate times. In general during evolution once a colour shift has occurred all species from this ancestor keep it meaning that the rest of the eye and physiology, must also evolved to ‘cement’ in the new colour sensitivity.”

(Image: webexhibits.org)

Breakthrough: New lenses cure colour blindness

Scientists have developed glasses with purple-tinged lenses that enhance reds and greens, allowing those with the most common form of the condition to see them properly.

One tester of the Oxy-Iso lenses has told how he “shivered with excitement” after putting on the glasses for the first time. Dr Daniel Bor, an academic from the University of Sussex, said: “The main thing I have problems with is when people use red and green on graphs in seminars and I can’t tell the difference between them.

"And there’s my occasionally weird dress sense, which my wife puts me right on. But putting on the glasses for the first time was really quite an exciting moment. I was with my daughter in the gym and suddenly her lips stood out.

"She was wearing a red-orange jumper and suddenly it stood out from the surroundings."

The glasses, which were originally developed for medical use, are the brainchild of US scientist Mark Changizi. The lenses filter out bands of light that interfere with the ability to distinguish various shades of red and green.

Dr Changizi, of Idaho firm 2AI Labs, said: “It makes it so they can suddenly see red-green differences in the world which were originally too small for them to notice.”

Wearing the glasses, Dr Bor managed to pass the colour blindness test used in schools around the world. However, they were not without their drawbacks. He said: “My daughter’s baby monitor has a yellow light on it and normally I can see that. But with the glasses on, it was completely invisible.

"Without the glasses, nothing is invisible. It was a bit disturbing that some things disappeared out of my vision.

"I wouldn’t wear them all the time but if I was going to an art gallery or a flower show, I’d take them with me. I’d really welcome them then."

The glasses only work for red-green colour blindness. This is the most common form and although rare in women, it affects up to 8 per cent of men. You can pick up a pair on Amazon from $297.

Experimental gene therapy treatment for duchenne muscular dystrophy offers hope for youngster

Jacob Rutt is a bright 11-year-old who likes to draw detailed maps in his spare time. But the budding geographer has a hard time with physical skills most children take for granted ― running and climbing trees are beyond him, and even walking can be difficult. He was diagnosed with a form of muscular dystrophy known as Duchenne when he was two years old.

The disease affects about 1 in 3,500 newborns ― mostly boys ― worldwide. It usually becomes apparent in early childhood, as weakened skeletal muscles cause delays in milestones such as sitting and walking. Children usually become wheelchair-dependent during their teens. As heart muscle is increasingly affected, the disease becomes life threatening and many patients die from heart failure in their 20s.

Today, Jacob is one of 51 children participating in a nationwide clinical trial for a new type treatment that could offer help to those suffering from devastating neuromuscular disease. Clinical researchers at UC Davis Medical Center and a handful other research centers around the nation are testing a high-tech drug designed to fix the underlying genetic defect causing the progressive muscular decline that is seen in children with Duchenne.

“This type of genetic therapy is the most exciting treatment approach I have witnessed in my career for Duchenne muscular dystrophy,” said Craig McDonald, professor and chair of the Department of Physical Medicine Rehabilitation at UC Davis, as well as principal investigator of the national clinical trial that Jacob is participating in. “We are hopeful that it will delay many of the disease’s manifestations and ultimately improve life expectancy for patients.”

My gray matter might be waning. Then again, it might not be. But I swear that I can feel memories — as I’m making them — slide off a neuron and into a tangle of plaque. I steel myself for those moments to come when I won’t remember what just went into my head.

I’m not losing track of my car keys, which is pretty standard in aging minds. Nor have I ever forgotten to turn off the oven after use, common in menopausal women. I can always find my car in the parking lot, although lots of “normal” folk can’t.

Rather, I suddenly can’t remember the name of someone with whom I’ve worked for years. I cover by saying “sir” or “madam” like the Southerner I am, even though I live in Vermont and grown people here don’t use such terms. Better to think I’m quirky than losing my faculties. Sometimes I’ll send myself an e-mail to-do reminder and then, seconds later, find myself thrilled to see a new entry pop into my inbox. Oops, it’s from me. Worse yet, a massage therapist kicked me out of her practice for missing three appointments. I didn’t recall making any of them. There must another Nancy.

Am I losing track of me?

Waiting for the Forgetting to Begin by Nancy Stearns Bercaw