Back in 2004, I was awakened early one morning by a loud clatter. I ran outside, only to discover that a car had smashed into the corner of my house. As I went to speak with the driver, he threw the car into reverse and sped off, striking me and running over my right foot as I fell to the ground. When his car hit me, I was wearing a computerized-vision system I had invented to give me a better view of the world. The impact and fall injured my leg and also broke my wearable computing system, which normally overwrites its memory buffers and doesn’t permanently record images. But as a result of the damage, it retained pictures of the car’s license plate and driver, who was later identified and arrested thanks to this record of the incident.

Was it blind luck (pardon the expression) that I was wearing this vision-enhancing system at the time of the accident? Not at all: I have been designing, building, and wearing some form of this gear for more than 35 years. I have found these systems to be enormously empowering. For example, when a car’s headlights shine directly into my eyes at night, I can still make out the driver’s face clearly. That’s because the computerized system combines multiple images taken with different exposures before displaying the results to me.

I’ve built dozens of these systems, which improve my vision in multiple ways. Some versions can even take in other spectral bands. If the equipment includes a camera that is sensitive to long-wavelength infrared, for example, I can detect subtle heat signatures, allowing me to see which seats in a lecture hall had just been vacated, or which cars in a parking lot most recently had their engines switched off. Other versions enhance text, making it easy to read signs that would otherwise be too far away to discern or that are printed in languages I don’t know.

Believe me, after you’ve used such eyewear for a while, you don’t want to give up all it offers. Wearing it, however, comes with a price. For one, it marks me as a nerd. For another, the early prototypes were hard to take on and off. These versions had an aluminum frame that wrapped tightly around the wearer’s head, requiring special tools to remove.

Steve Mann: My “Augmediated” Life - What I’ve learned from 35 years of wearing computerized eyewear

Japan’s Robot Suit Gets Global Safety Certificate

A robot suit that can help the elderly or disabled get around was given its global safety certificate in Japan on Wednesday, paving the way for its worldwide rollout.

The Hybrid Assistive Limb, or HAL, is a power-assisted pair of legs developed by Japanese robot maker Cyberdyne, which has also developed similar robot arms.

A quality assurance body issued the certificate based on a draft version of an international safety standard for personal robots that is expected to be approved later this year, the ministry for the economy, trade and industry said.

The metal-and-plastic exoskeleton has become the first nursing-care robot certified under the draft standard, a ministry official said.

Battery-powered HAL, which detects muscle impulses to anticipate and support the user’s body movements, is designed to help the elderly with mobility or help hospital or nursing carers to lift patients.

Cyberdyne, based in Tsukuba, northeast of Tokyo, has so far leased some 330 suits to 150 hospitals, welfare and other facilities in Japan since 2010, at 178,000 yen ($1,950) per suit per year.

"It is very significant that Japan has obtained this certification before others in the world," said Yoshiyuki Sankai, the head of Cyberdyne.

The company is unrelated to the firm of the same name responsible for the cyborg assassin played by Arnold Schwarzenegger in the 1984 film “The Terminator”.

"This is a first step forward for Japan, the great robot nation, to send our message to the world about robots of the future," said Sankai, who is also a professor at Tsukuba University.

A different version of HAL — coincidentally the name of the evil supercomputer in Stanley Kubrick’s “2001: A Space Odyssey” — has been developed for workers who need to wear heavy radiation protection as part of the clean-up at the crippled Fukushima nuclear plant.

Industrial robots have long been used in Japan, and robo-suits are gradually making inroads into hospitals and retirement homes.

But critics say the government has been slow in creating a safety framework for such robots in a country whose rapidly-ageing population is expected to enjoy ever longer lives.

Reconstructing the Past: How Recalling Memories Alters Them

Recently the neurologist and author Oliver Sacks recalled a vivid childhood memory, recounted in his autobiography, Uncle Tungsten.

During WWII he lived in London during the Blitz, and on one occasion:

"…an incendiary bomb, a thermite bomb, fell behind our house and burned with a terrible, white-hot heat. My father had a stirrup pump, and my brothers carried pails of water to him, but water seemed useless against this infernal fire—indeed, made it burn even more furiously. There was a vicious hissing and sputtering when the water hit the white-hot metal, and meanwhile the bomb was melting its own casing and throwing blobs and jets of molten metal in all directions."

Except when his autobiography came out, one of his older brothers told him he’d misremembered the event. In fact both of them had been at school when the bomb struck so they could not have witnessed the explosion.

The ‘false’ memory, it turned out, was implanted by a letter. Their elder brother had written to them, describing the frightening event, and this had lodged in his mind. Over the years the letter had gone from a third-person report to a first-person ‘memory’.

Turning the memory over in his mind, Sacks writes that he still cannot see how the memory of the bomb exploding can be false. There is no difference between this memory and others he knows to be true; it felt like he was really there.

This sort of experience is probably much more common than we might like to imagine. Many memories which have the scent of authenticity may turn out to be misremembered, if not totally fictitious events, if only we could check. Without some other source with which to corroborate, it is hard verify the facts, especially for events that took place long ago.

That these sorts of distortions to memory happen is unquestioned, what fascinates is how it comes about. Does the long passage of time warp the memory, or is there some more active process that causes the change?

A study published recently sheds some light on this process and provides a model for how memories like Sack’s become distorted.

Every science writer loves a good challenge to dogma. I wish I had been in the working world in the spring of 1992, when one such intellectual overhaul happened in neuroscience. The dogma: Neurons, unlike most of the body’s cells, can’t be replenished. You’re born with just 100 billion of them and you better use them wisely. The challenge: Samuel Weiss and Brent Reynolds reported in Science that brain tissue taken from adult mice could be chemically coaxed into making new neurons.

“It left us speechless,” Weiss told the New York Times. Everybody else was pretty stunned, too. Over the next six years, other researchers confirmed that this so-called neurogenesis happens in the adult hippocampus of many animals, including tree shrews, marmosets, Old World monkeys and people. Today, more than two decades since the splashy Science report, adult neurogenesis is a bona fide subfield, with hundreds of labs studying it around the world.

But after all this time, researchers still don’t really know what it’s for. Studies have uncovered a wide variety of environmental stimuli — what you might think of as inputs — that affect neurogenesis in the dentate gyrus, a part of the hippocampus. Running and antidepressants can ramp up neurogenesis, for example, while stress, social isolation, sleep deprivation and aging can shut it down. Scientists have also looked at the outputs of neurogenesis, showing that a boost of new neurons may be important for exploratory behavior and certain kinds of learning, such as navigating a new space. But how do the inputs lead to the outputs?

“I like to think of the dentate as an association machine,” says Sam Pleasure, a neuroscientist at the University of California, San Francisco. All day long, he says, we’re walking around the world trying to associate various sensations and emotions — big dog with fangs, small screaming toddler, perilous traffic intersection — so that we can remember them later. “All these stimuli are happening and converge on this circuit, and they somehow affect how new neurons are recruited into the circuit, and that ends up coming out as the ability to form new memories.” But how it all works on the molecular level is a black box.

Two papers published in Cell Stem Cell [1 , 2]open that box a little bit. They identify molecular inhibitors — what Pleasure calls “wet blankets” — that turn off neurogenesis in certain contexts.

Opening the Black Box of Neurogenesis by Virginia Hughes

Split-Brain Patients Reveal Brain’s Flexibility

2012 Cell Imaging Competition, supported by BioTechniques

Therapeutic focus: Huntington’s disease
Description: Huntington’s stem cell derived oligodendrocyte precursors stained for phalloidin (green), vinculin (red) and DNA (blue).

Image credit: Anushree Balachandran (Genea, Australia) - High-content analysis winners

Changes in patterns of brain activity predict fear memory formation

Psychologists at the University of Amsterdam (UvA) have discovered that changes in patterns of brain activity during fearful experiences predict whether a long-term fear memory is formed. The research results have recently been published in the prestigious scientific journal ‘Nature Neuroscience’.

Researchers Renee Visser MSc, Dr Steven Scholte, Tinka Beemsterboer MSc and Prof. Merel Kindt discovered that they can predict future fear memories by looking at patterns of brain activity during fearful experiences. Up until now, there was no way of predicting fear memory. It was also, above all, unclear whether the selection of information to be stored in the long-term memory occurred at the time of fear learning or after the event.

Picture predicts pain stimulus

During magnetic resonance brain imaging (MRI), participants saw neutral pictures of faces and houses, some of which were followed by a small electric shock. In this way, the participants formed fear memories. They showed fear responses when the pictures were shown that were paired with shocks. This fear response can be measured in the brain, but is also evident from increased pupil dilation when someone sees the picture. After a few weeks, the participants returned to the lab and were shown the same images. Brain activity and pupil diameter were once again measured. The extent to which the pupil dilated when seeing the images that were previously followed by a shock, was considered an expression of the previously formed fear memory.

Pattern Analysis

In order to analyse the fMRI data, (spatial) patterns of brain activity (Multi-Voxel Pattern Analysis, or MVPA) were analysed. By correlating patterns of various stimulus presentations with each other, it is possible to measure the extent to which the representation of two stimuli is the same. It appears that images that have nothing in common, such as houses and faces, lead to increasing neural pattern similarity when they predict danger. This does not occur when they do not predict danger. This leads to the formation of stronger fear responses. The extent to which this occurs is an indication of fear memory formation: the stronger the response during learning, the stronger the fear response will be in the long term.

These findings may lead to greater insights into the formation of emotional memory. As a result, it is possible to conduct experimental research into the mechanisms that strengthen, weaken or even erase fear memory in a more direct fashion, without having to wait until the fear memory is expressed.

Parkin protects from neuronal cell death

Parkinson’s disease is the most common movement disorder and the second most common neurodegenerative disease after Alzheimer’s disease. It is characterized by the loss of dopamin-producing neurons in the substantia nigra, a region in the midbrain, which is implicated in motor control. The typical clinical signs include resting tremor, muscle rigidity, slowness of movements, and impaired balance. In about 10% of cases Parkinson’s disease is caused by mutations in specific genes, one of them is called parkin.

“Parkinson-associated genes are particularly interesting for researchers, since insights into the function and dysfunction of these genes allow conclusions on the pathomechanisms underlying Parkinson’s disease”, says Dr. Konstanze Winklhofer of the Adolf Butenandt Institute at the LMU Munich, who is also affiliated with the German Center for Neurodegenerative Diseases (DZNE). Winklhofer and her colleagues had previously observed that parkin can protect neurons from cell death under various stress conditions. In the course of this project, it became obvious that a loss of parkin function impairs the activity and integrity of mitochondria, which serve as the cellular power stations. In their latest publication, Winklhofer and coworkers uncovered the molecular mechanism that accounts for parkin’s neuroprotective action.

“We discovered a novel signaling pathway that is responsible for the neuroprotective activity of parkin,” Winklhofer reports. The central player of this pathway is a protein called NEMO, which is activated by the enzymatic attachment of a linear chain of ubiquitin molecules. This reaction is promoted by parkin, thereby enabling NEMO to activate a signal cascade, which ultimately leads to the expression of a specific set of genes. Winklhofer’s team identified one essential gene targeted by this pathway, which turned out to code for the mitochondrial protein OPA1. OPA1 maintains the integrity of mitochondria and prevents stress-induced neuronal cell death.

“These findings suggest that strategies to activate this signal pathway or to enhance the synthesis of OPA1 in cells exposed to stress could be of therapeutic benefit,” Winklhofer points out.

The newly identified signal pathway may also be relevant in the context of other neurological conditions that are characterized by the loss of specific neurons. Konstanze Winklhofer and her group are already engaged in further projects designed to determine whether other molecules regulated by this pathway might provide targets for therapeutic interventions.

New chemical probe provides tool to investigate role of malignant brain tumor domains

In an article published as the cover story of the March 2013 issue of Nature Chemical Biology, Lindsey James, PhD, research assistant professor in the lab of Stephen Frye, Fred Eshelman Distinguished Professor in the UNC School of Pharmacy and member of the UNC Lineberger Comprehensive Cancer Center, announced the discovery of a chemical probe that can be used to investigate the L3MBTL3 methyl-lysine reader domain. The probe, named UNC1215, will provide researchers with a powerful tool to investigate the function of malignant brain tumor (MBT) domain proteins in biology and disease.

“Before this there were no known chemical probes for the more than 200 domains in the human genome that recognize methyl lysine. In that regard, it is a first in class compound. The goal is to use the chemical probe to understand the biology of the proteins that it targets,” said Dr. James.

Chromatin regulatory pathways play a fundamental role in gene expression and disease development, especially in the case of cancer. While many chemical probes work through the inhibition of enzyme activity, L3MBTL3 functions as a mediator of protein-to-protein interactions, which have been historically difficult to target with small, drug-like molecules.The researchers found three to four further disease subtypes within TN tumors, with more than 75 percent of the tumors falling into the basal-like subtype. Further research is needed to identify the distinct biomarkers shared by the expanded subtypes of TN cancers. The ultimate goal will be to target the individual biomarkers of these subtypes and create therapies that target their individual biology, according to Dr. Perou.

“Many people believe that protein-protein interactions are difficult to target. Often they have a large surface area, so it is hard for small molecules to go in and intervene,” said Dr. James.

Almost 40 percent of the genes that drive cancer can be mapped to dysfunction within signaling pathways. In the last five years, chemical probe development has allowed researchers to make fundamental observations of the role of these pathways in cancer development, as well as pointing to potential targets for new therapies. Each of the complex interactions within the signaling pathways represents a potential point where a therapy can be applied, and the probes allow researchers to interact with these processes at the molecular level and observe the overall effect of their perturbation on the disease state.

In a 2008 Nature Chemical Biology commentary, Dr. Frye outlined the qualities that make a good chemical probe. To Frye, a good chemical probe must be highly selective to enable specific questions to be asked and it must function as well in a cell as in the test tube, providing clear quantitative data with a well understood mechanism of action in either situation. It also must be available to all academic researchers without restrictions on its use, a criteria that the L3MBTL3 probe fulfills through the Frye lab’s commitment to provide researchers with the probe free of charge on request and UNC1215 is already available through commercial vendors as well.