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New research suggests why the human brain and other biological networks exhibit a hierarchical structure, and the study may improve attempts to create artificial intelligence.
The study, by researchers from the University of Wyoming and the French Institute for Research in Computer Science and Automation (INRIA, in France), demonstrates that the evolution of hierarchy — a simple system of ranking — in biological networks may arise because of the costs associated with network connections.
This study also supports Ray Kurzweil’s theory of the hierarchical structure of the neocortex, presented in his 2012 book, How to Create a Mind.
The human brain has separate areas for vision, motor control, and tactile processing, for example, and each of these areas consist of sub-regions that govern different parts of the body.
Evolutionary pressure to reduce the number and cost of connections
The research findings suggest that hierarchy evolves not because it produces more efficient networks, but instead because hierarchically wired networks have fewer connections. That’s because connections in biological networks are expensive — they have to be built, maintained, etc. — so there’s an evolutionary pressure to reduce the number of connections.
In addition to shedding light on the emergence of hierarchy across the many domains in which it appears, these findings may also accelerate future research into evolving more complex, intelligent computational brains in the fields of artificial intelligence and robotics.
The research, led by Henok S. Mengistu, is described in an open-access paper in PLOS Computational Biology. The researchers also simulated the evolution of computational brain models, known as artificial neural networks, both with and without a cost for network connections. They found that hierarchical structures emerge much more frequently when a cost for connections is present.
Aside from explaining why biological networks are hierarchical, the research might also explain why many man-made systems such as the Internet and road systems are also hierarchical. “The next step is to harness and combine this knowledge to evolve large-scale, structurally organized networks in the hopes of creating better artificial intelligence and increasing our understanding of the evolution of animal intelligence, including our own,” according to the researchers.
Abstract of The Evolutionary Origins of Hierarchy
Hierarchical organization—the recursive composition of sub-modules—is ubiquitous in biological networks, including neural, metabolic, ecological, and genetic regulatory networks, and in human-made systems, such as large organizations and the Internet. To date, most research on hierarchy in networks has been limited to quantifying this property. However, an open, important question in evolutionary biology is why hierarchical organization evolves in the first place. It has recently been shown that modularity evolves because of the presence of a cost for network connections. Here we investigate whether such connection costs also tend to cause a hierarchical organization of such modules. In computational simulations, we find that networks without a connection cost do not evolve to be hierarchical, even when the task has a hierarchical structure. However, with a connection cost, networks evolve to be both modular and hierarchical, and these networks exhibit higher overall performance and evolvability (i.e. faster adaptation to new environments). Additional analyses confirm that hierarchy independently improves adaptability after controlling for modularity. Overall, our results suggest that the same force–the cost of connections–promotes the evolution of both hierarchy and modularity, and that these properties are important drivers of network performance and adaptability. In addition to shedding light on the emergence of hierarchy across the many domains in which it appears, these findings will also accelerate future research into evolving more complex, intelligent computational brains in the fields of artificial intelligence and robotics.
Boosting the transport of mitochondria (cell energy suppliers) along neuronal axons enhances the ability of mouse nerve cells to repair themselves and regrow after injury or disease, researchers at the National Institute of Neurological Disorders and Stroke report in The Journal of Cell Biology.
Neurons need large amounts of energy to extend their axons long distances through the body. This energy — in the form of adenosine triphosphate (ATP) — is provided by mitochondria.
During development, mitochondria are transported up and down growing axons to generate ATP wherever it is needed. In adults, however, mitochondria become less mobile as mature neurons produce a protein called syntaphilin that anchors the mitochondria in place.
Zu-Hang Sheng and colleagues at the National Institute of Neurological Disorders and Stroke wondered whether this decrease in mitochondrial transport might explain why adult neurons are typically unable to regrow after injury.
They initially found that when mature mouse axons are severed, nearby mitochondria are damaged and become unable to provide sufficient ATP to support injured nerve regeneration. However, when the researchers experimentally removed syntaphilin from the nerve cells (by using a genetically modified mouse), mitochondrial transport was enhanced, allowing the damaged mitochondria to be replaced by healthy mitochondria capable of producing ATP.
The Syntaphilin-deficient mature neurons therefore regained the ability to regrow after injury, just like young neurons.
“Our in vivo and in vitro studies suggest that activating an intrinsic growth program requires the coordinated modulation of mitochondrial transport and recovery of energy deficits. Such combined approaches may represent a valid therapeutic strategy to facilitate regeneration in the central and peripheral nervous systems after injury or disease,” Sheng says.
Abstract of Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits
Although neuronal regeneration is a highly energy-demanding process, axonal mitochondrial transport progressively declines with maturation. Mature neurons typically fail to regenerate after injury, thus raising a fundamental question as to whether mitochondrial transport is necessary to meet enhanced metabolic requirements during regeneration. Here, we reveal that reduced mitochondrial motility and energy deficits in injured axons are intrinsic mechanisms controlling regrowth in mature neurons. Axotomy induces acute mitochondrial depolarization and ATP depletion in injured axons. Thus, mature neuron-associated increases in mitochondria-anchoring protein syntaphilin (SNPH) and decreases in mitochondrial transport cause local energy deficits. Strikingly, enhancing mitochondrial transport via genetic manipulation facilitates regenerative capacity by replenishing healthy mitochondria in injured axons, thereby rescuing energy deficits. An in vivo sciatic nerve crush study further shows that enhanced mitochondrial transport in snph knockout mice accelerates axon regeneration. Understanding deficits in mitochondrial trafficking and energy supply in injured axons of mature neurons benefits development of new strategies to stimulate axon regeneration.
Small electrical currents appear to activate certain immune cells to jumpstart or speed wound healing and reduce infection when there’s a lack of immune cells available, such as with diabetes, University of Aberdeen (U.K.) scientists have found.
In a lab experiment, the scientists exposed healing macrophages (white blood cells that eat things that don’t belong), taken from human blood, to electrical fields of strength similar to that generated in injured skin. When the voltage was applied, the macrophages moved in a directed manner to Candida albicans fungus cells (representing damaged skin) to facilitate healing (engulfing and digesting extracellular particles). (This process is called “phagocytosis,” in which macrophages clean the wound site, limit infection, and allow the repair process to proceed.)
The electric fields enhanced the uptake and clearance of a variety of targets known to promote inflammation and impair healing in addition to Candida albicans, including latex beads and expended white blood cells.*
“These findings raise the prospect that EF-based therapies could be extended beyond tissue repair and ultimately, be exploited to modulate the function of macrophages in other inflammatory diseases where these cells are dysregulated,” the researchers note in a report appearing in the June 2016 issue of the Journal of Leukocyte Biology.
“This new work identifies previously unappreciated opportunities to tune immune system function with electrical fields and has potentially wide-reaching implications for wound repair for a variety of diseases where macrophages play a role, including infectious disease, cancer and even obesity,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology.
The research extends previous research reported by KurzweilAI (New evidence that electrical stimulation accelerates wound healing).
* The experiments also showed that electric fields selectively augmented the production of protein modulators associated with the healing process, enhancing cytokine (growth factor) production and phagocytic activity essential for clearance of infection and for tissue repair and confirming that macrophages are tuned to respond to naturally generated electrical signals in a manner that boosts their healing ability.
Abstract of Electric fields are novel determinants of human macrophage functions
Macrophages are key cells in inflammation and repair, and their activity requires close regulation. The characterization of cues coordinating macrophage function has focused on biologic and soluble mediators, with little known about their responses to physical stimuli, such as the electrical fields that are generated naturally in injured tissue and which accelerate wound healing. To address this gap in understanding, we tested how properties of human monocyte-derived macrophages are regulated by applied electrical fields, similar in strengths to those established naturally. With the use of live-cell video microscopy, we show that macrophage migration is directed anodally by electrical fields as low as 5 mV/mm and is electrical field strength dependent, with effects peaking ∼300 mV/mm. Monocytes, as macrophage precursors, migrate in the opposite, cathodal direction. Strikingly, we show for the first time that electrical fields significantly enhance macrophage phagocytic uptake of a variety of targets, including carboxylate beads, apoptotic neutrophils, and the nominal opportunist pathogen Candida albicans, which engage different classes of surface receptors. These electrical field-induced functional changes are accompanied by clustering of phagocytic receptors, enhanced PI3K and ERK activation, mobilization of intracellular calcium, and actin polarization. Electrical fields also modulate cytokine production selectively and can augment some effects of conventional polarizing stimuli on cytokine secretion. Taken together, electrical signals have been identified as major contributors to the coordination and regulation of important human macrophage functions, including those essential for microbial clearance and healing. Our results open up a new area of research into effects of naturally occurring and clinically applied electrical fields in conditions where macrophage activity is critical.
Finnish researchers have developed a method for building highly efficient miniaturized micro-supercapacitor energy storage directly inside a silicon microcircuit chip, making it possible to power autonomous sensor networks, wearable electronics, and mobile internet-of-things (IoT) devices.
Supercapacitors function similar to standard batteries, but store electrostatic energy instead of chemical energy.
The researchers at VTT Technical Research Centre of Finland have developed a hybrid nano-electrode that’s only a few nanometers thick. It consists of porous silicon coated with a titanium nitride layer formed by atomic layer deposition.
The nano-electrode design features the highest-ever conductive surface-to-volume ratio. That combined with an ionic liquid (in a microchannel formed in between two electrodes), results in an extremely small form factor and efficient energy storage. That design makes it possible for a silicon-based micro-supercapacitor to achieve higher energy storage (energy density) and faster charge/discharge (power density) than the leading carbon- and graphene-based supercapacitors, according to the researchers.
The micro-supercapacitor can store 0.2 joule (55 microwatts of power for one hour) on a one-square-centimeter silicon chip. This design also leaves the surface of the chip available for active integrated microcircuits and sensors.
Micro-supercapacitors can also be integrated directly with active microelectronic devices to store electrical energy generated by thermal, light, and vibration energy harvesters to supply electrical energy (see, for example, Wireless device converts ‘lost’ microwave energy into electric power).
An open-access paper on the research has been published in Nano Energy journal.Abstract of Conformal titanium nitride in a porous silicon matrix: A nanomaterial for in-chip supercapacitors
Today’s supercapacitor energy storages are typically discrete devices aimed for printed boards and power applications. The development of autonomous sensor networks and wearable electronics and the miniaturization of mobile devices would benefit substantially from solutions in which the energy storage is integrated with the active device. Nanostructures based on porous silicon (PS) provide a route towards integration due to the very high inherent surface area to volume ratio and compatibility with microelectronics fabrication processes. Unfortunately, pristine PS has limited wettability and poor chemical stability in electrolytes and the high resistance of the PS matrix severely limits the power efficiency. In this work, we demonstrate that excellent wettability and electro-chemical properties in aqueous and organic electrolytes can be obtained by coating the PS matrix with an ultra-thin layer of titanium nitride by atomic layer deposition. Our approach leads to very high specific capacitance (15 F cm−3), energy density (1.3 mWh cm−3), power density (up to 214 W cm−3) and excellent stability (more than 13,000 cycles). Furthermore, we show that the PS–TiN nanomaterial can be integrated inside a silicon chip monolithically by combining MEMS and nanofabrication techniques. This leads to realization of in-chip supercapacitor, i.e., it opens a new way to exploit the otherwise inactive volume of a silicon chip to store energy.