IBM Research And LLNL Claim 10¹⁴ Synapse Simulation

Inspired by the function, power, and volume of the organic brain, IBMis reportedly developing TrueNorth, a novel modular, scalable, non-von Neumann, ultra-low power, cognitive computing architecture. The TrueNorth system consists of a scalable network of neurosynaptic cores, with each core containing neurons, dendrites, synapses, and axons. Also, to help the computation of TrueNorth, IBM has developed Compass, a multi-threaded, massively parallel functional simulator and a parallel compiler that maps a network of long-distance pathways in the macaque monkey brain to TrueNorth.

The research was recently presented at the Super Computing 2012 (SC12) conference in Salt Lake City.  The paper, “Compass: A scalable simulator for an architecture for Cognitive Computing" is available online.

IBM and Lawrence Livermore National Laboratory (LBNL) demonstrated near-perfect weak scaling on a 16 rack IBM Blue Gene/Q (262,144 processor cores, 256 TB memory), achieving an unprecedented scale of 256 million neurosynaptic cores containing 65 billion neurons and 16 trillion synapses running only 388× slower than real time with an average spiking rate of 8.1 Hz. By using emerging PGAS communication primitives, IBM also demonstrated 2× better real-time performance over MPI primitives on a 4 rack Blue Gene/P (16384 processor cores, 16 TB memory).

Also, since submitting the original paper, the work has continued using 96 Blue Gene/Q racks of the Lawrence Livermore National Lab Sequoia supercomputer (1,572,864 processor cores, 1.5 PB memory, 98,304 MPI processes, and 6,291,456 threads), IBM and LBNL achieved an unprecedented scale of 2.084 billion neurosynaptic cores containing 53x1010 neurons and 1.37x1014 synapses running only 1542× slower than real time. Here is PDF of IBM Research Report, RJ 10502.

As in the image above, A Network of Neurosynaptic Cores Derived from Long-distance Wiring in the Monkey Brain -Neuro-synaptic cores are locally clustered into brain-inspired regions, and each core is represented as an individual point along the ring. Arcs are drawn from a source core to a destination core with an edge color defined by the color assigned to the source core.

Nose cell transplant enables paralysed dogs to walk

Scientists have reversed paralysis in dogs after injecting them with cells grown from the lining of their nose.

The pets had all suffered spinal injuries which prevented them from using their back legs. The Cambridge University team is cautiously optimistic the technique could eventually have a role in the treatment of human patients. The study is the first to test the transplant in “real-life” injuries rather than laboratory animals.

In the study, funded by the Medical Research Council and published in the neurology journal Brain, the dogs had olfactory ensheathing cells from the lining of their nose removed. These were grown and expanded for several weeks in the laboratory.

Virtual Reality Could Spot Real-World Impairments

A virtual reality test being developed at UTSC might do a better job than pencil-and-paper tests of predicting whether a cognitive impairment will have real-world consequences.

The test developed by Konstantine Zakzanis, associate professor of psychology, and colleagues, uses a computer-game-like virtual world and asks volunteers to navigate their ways through tasks such as delivering packages or running errands around town.

“If we’re being asked to tell if people could do things like work, houseclean, and take care of their kids, we need to show that our tests predict performance in the real world,” says Zakzanis.

But standard tests don’t do that very well, he says. Although tests that ask people to do things like solve math problems, sort cards, remember names, or judge the relative positions of lines in visual two dimensional space, can detect cognitive impairments caused by circumscribed lesions following a stroke or head injury, they’re not very good at predicting who will be able to function in the real world and who won’t.

That’s a problem for cognitively impaired people who might be denied insurance benefits or workers compensation based on tests that are insensitive to demonstrating their impairment. It is akin to having a broken arm with no x-ray to prove it.

Stanford/Yale study gives insight into subtle genomic differences among our own cells

Stanford University School of Medicine scientists have demonstrated, in a study conducted jointly with researchers at Yale University, that induced-pluripotent stem cells — the embryonic-stem-cell lookalikes whose discovery a few years ago won this year’s Nobel Prize in medicine — are not as genetically unstable as was thought.

The new study, published online Nov. 18 in Nature, showed that what seemed to be changes in iPS cells’ genetic makeup — presumed to be inflicted either in the course of their generation from adult cells or during their propagation and maintenance in laboratory culture dishes — instead are often accurate reflections of existing but previously undetected genetic variations among the cells comprising our bodies.

That’s good news for researchers hoping to use the cells to study disease or, someday, for regenerative medicine. But it raises the question of whether and to what extent we humans are really walking mosaics whose constituent cells differ genetically from one to the next in possibly significant respects, said Alexander Urban, PhD, assistant professor of psychiatry and behavioral sciences. Urban shared senior authorship of the study with bioinformatics professor Mark Gerstein, PhD, and neurobiology professor Flora Vaccarino, MD, both of Yale.

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Breakthrough nanoparticle halts multiple sclerosis

In a breakthrough for nanotechnology and multiple sclerosis, a biodegradable nanoparticle turns out to be the perfect vehicle to stealthily deliver an antigen that tricks the immune system into stopping its attack on myelin and halt a model of relapsing remitting multiple sclerosis (MS) in mice, according to new Northwestern Medicine research.

The new nanotechnology also can be applied to a variety of immune-mediated diseases including Type 1 diabetes, food allergies and airway allergies such as asthma.

In MS, the immune system attacks the myelin membrane that insulates nerves cells in the brain, spinal cord and optic nerve. When the insulation is destroyed, electrical signals can’t be effectively conducted, resulting in symptoms that range from mild limb numbness to paralysis or blindness. About 80 percent of MS patients are diagnosed with the relapsing remitting form of the disease.

The Northwestern nanotechnology does not suppress the entire immune system as do current therapies for MS, which make patients more susceptible to everyday infections and higher rates of cancer. Rather, when the nanoparticles are attached to myelin antigens and injected into the mice, the immune system is reset to normal. The immune system stops recognizing myelin as an alien invader and halts its attack on it.

"This is a highly significant breakthrough in translational immunotherapy," said Stephen Miller, a corresponding author of the study and the Judy Gugenheim Research Professor of Microbiology-Immunology at Northwestern University Feinberg School of Medicine. "The beauty of this new technology is it can be used in many immune-related diseases. We simply change the antigen that’s delivered."

"The holy grail is to develop a therapy that is specific to the pathological immune response, in this case the body attacking myelin," Miller added. "Our approach resets the immune system so it no longer attacks myelin but leaves the function of the normal immune system intact."

The nanoparticle, made from an easily produced and already FDA-approved substance, was developed by Lonnie Shea, professor of chemical and biological engineering at Northwestern’s McCormick School of Engineering and Applied Science.

"This is a major breakthrough in nanotechnology, showing you can use it to regulate the immune system," said Shea, also a corresponding author. The paper was published Nov. 18 in the journal Nature Biotechnology.

Medical vital-sign monitoring reduced to the size of a postage stamp

Electrical engineers at Oregon State University have developed new technology to monitor medical vital signs, with sophisticated sensors so small and cheap they could fit onto a bandage, be manufactured in high volumes and cost less than a quarter.

A patent is being processed for the monitoring system and it’s now ready for clinical trials, researchers say. When commercialized, it could be used as a disposable electronic sensor, with many potential applications due to its powerful performance, small size, and low cost.

Heart monitoring is one obvious candidate, since the system could gather data on some components of an EKG, such as pulse rate and atrial fibrillation. Its ability to measure EEG brain signals could find use in nursing care for patients with dementia, and recordings of physical activity could improve weight loss programs. Measurements of perspiration and temperature could provide data on infection or disease onset.

And of course, if you can measure pulse rate and skin responses, why not a lie detector?

“Current technology allows you to measure these body signals using bulky, power-consuming, costly instruments,” said Patrick Chiang, an associate professor in the OSU School of Electrical Engineering and Computer Science.

“What we’ve enabled is the integration of these large components onto a single microchip, achieving significant improvements in power consumption,” Chiang said. “We can now make important biomedical measurements more portable, routine, convenient and affordable than ever before.”

The much higher cost and larger size of conventional body data monitoring precludes many possible uses, Chiang said. Compared to other technologies, the new system-on-a-chip cuts the size, weight, power consumption and cost by about 10 times.

New algorithm greatly improves speed and accuracy of thought-controlled computer cursor

When a paralyzed person imagines moving a limb, cells in the part of the brain that controls movement still activate as if trying to make the immobile limb work again. Despite neurological injury or disease that has severed the pathway between brain and muscle, the region where the signals originate remains intact and functional.

In recent years, neuroscientists and neuroengineers working in prosthetics have begun to develop brain-implantable sensors that can measure signals from individual neurons, and after passing those signals through a mathematical decode algorithm, can use them to control computer cursors with thoughts. The work is part of a field known as neural prosthetics.

A team of Stanford researchers have now developed an algorithm, known as ReFIT, that vastly improves the speed and accuracy of neural prosthetics that control computer cursors. The results were published November 18 in the journal Nature Neuroscience in a paper by Krishna Shenoy, a professor of electrical engineering, bioengineering and neurobiology at Stanford, and a team led by research associate Dr. Vikash Gilja and bioengineering doctoral candidate Paul Nuyujukian.

In side-by-side demonstrations with rhesus monkeys, cursors controlled by the ReFIT algorithm doubled the performance of existing systems and approached performance of the real arm. Better yet, more than four years after implantation, the new system is still going strong, while previous systems have seen a steady decline in performance over time.

"These findings could lead to greatly improved prosthetic system performance and robustness in paralyzed people, which we are actively pursuing as part of the FDA Phase-I BrainGate2 clinical trial here at Stanford," said Shenoy.

Optogenetics illuminates pathways of motivation through brain

Whether you are an apple tree or an antelope, survival depends on using your energy efficiently. In a difficult or dangerous situation, the key question is whether exerting effort — sending out roots in search of nutrients in a drought or running at top speed from a predator — will be worth the energy.

In a paper published online Nov. 18 in Nature, Karl Deisseroth, MD, PhD, a professor of bioengineering and of psychiatry and behavioral sciences at Stanford University, and postdoctoral scholar Melissa Warden, PhD, describe how they have isolated the neurons that carry these split-second decisions to act from the higher brain to the brain stem. In doing so, they have provided insight into the causes of severe brain disorders such as depression.

In organisms as complex as humans, the neural mechanisms that help answer the question, “Is it worth my effort?” can fail, leading to debilitating mental illnesses. Major depressive disorder, for instance, which affects nearly 20 percent of people at some point in life, is correlated with underperformance in the parts of the brain involved in motivation. But researchers have struggled to work out the exact cause and effect.

“It’s challenging because we do not have a fundamental understanding of the circuitry that controls this sort of behavioral pattern selection. We don’t understand what the brain is doing wrong when these behaviors become dysfunctional, or even what the brain is supposed to be doing when things are working right,” Deisseroth said. “This is the level of the mystery we face in this field.”

Clinicians refer to this slowing down of motivation in depressed patients as “psychomotor retardation.” According to Deisseroth, who is also a practicing psychiatrist, patients may experience this symptom mentally, finding it hard to envision the positive results of an action, or, he said, they may feel physically heavy, like their limbs just do not want to move.

“This is one of the most debilitating aspects of depression, and motivation to take action is something that we can model in animals. That’s the exciting opportunity for us as researchers,” said Deisseroth, who also holds the D.H. Chen Professorship.

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