Yale researchers have devised a way to peer into the brains of two people simultaneously while are engaged in discussion. What they found will not surprise anyone who has found themselves arguing about politics or social issues.
(Illustration by Michael S. Helfenbein)
When two people agree, their brains exhibit a calm synchronicity of activity focused on sensory areas of the brain. When they disagree, however, many other regions of the brain involved in higher cognitive functions become mobilized as each individual combats the other’s argument, a Yale-led research team reports Jan. 13 in the journal Frontiers in Human Neuroscience.
“Our entire brain is a social processing network,” said senior author Joy Hirsch, the Elizabeth Mears and House Jameson Professor of Psychiatry and professor of comparative medicine and neuroscience. “However, it just takes a lot more brain real estate to disagree than to agree.”
For the study, the researchers from Yale and the University College London recruited 38 adults who were asked to say whether they agreed or disagreed with a series of statements such as “same-sex marriage is a civil right” or “marijuana should be legalized.” After matching up pairs based on their responses the researchers used an imaging technology called functional near-infrared spectroscopy to record their brain activity while they engaged in face-to-face discussions.
When the people were in agreement, brain activity was harmonious and tended to be concentrated on sensory areas of the brain such as the visual system, presumably in response to social cues from their partner. However, during disputes these areas of the brain were less active. Meanwhile, activity increased in the brain’s frontal lobes, home of higher order executive functions.
“There is a synchronicity between the brains when we agree,” Hirsch said. “But when we disagree, the neural coupling disconnects.”
Understanding how our brains function while disagreeing or agreeing is particularly important in a polarized political environment, Hirsch noted.
In discord, she said, two brains engage many emotional and cognitive resources “like a symphony orchestra playing different music.” In agreement, there “is less cognitive engagement and more social interaction between brains of the talkers, similar to a musical duet.”
The lead investigator of the paper is Alex Salama-Manteau, a former graduate student of economics at Yale and now a data scientist at Airbnb. Mark Tiede, a research scientist at the Haskins Laboratory at Yale, is second author of the paper.
For the first time, physicists from the University of Innsbruck have entangled two quantum bits distributed over several quantum objects and successfully transmitted their quantum properties. This marks an important milestone in the development of fault-tolerant quantum computers. The researchers published their report in Nature.
Image: Quantum particles lined up in a lattice form the basis for an error-tolerant quantum processor. (Credit: Harald Ritsch)
Even computers can miscalculate. Already small disturbances change stored information and corrupt results. That is why computers use methods to continuously correct such errors. In quantum computers, the vulnerability to errors can be reduced by storing quantum information in more than a single quantum particle. These logical quantum bits are less sensitive to errors. In recent years, theorists have developed many different error correction codes and optimized them for different tasks. “The most promising codes in quantum error correction are those defined on a two-dimensional lattice,” explains Thomas Monz from the Department of Experimental Physics at the University of Innsbruck. “This is due to the fact that the physical structure of current quantum computers can be very well mapped through such lattices.” With the help of the codes, logical quantum bits can be distributed over several quantum objects. The quantum physicists from Innsbruck have now succeeded for the first time in entangling two quantum bits coded in this way. The entanglement of two quantum bits is an important resource of quantum computers, giving them a performance advantage over classical computers.
A kind of quantum sewing machine
For their experiment, the physicists use an ion-trap quantum computer with ten ions. Into these ions the logical quantum bits are encoded. Using a technique that scientists refer to as ‘lattice surgery’, two logical qubits encoded on a lattice can be ‘stitched together’. “A new larger qubit is created from the qubits stitched together in this way,” explains Alexander Erhard from the Innsbruck team. In turn, a large logical qubit can be separated into two individual logical qubits by lattice surgery. In contrast to the standard operations between two logical qubits, lattice surgery only requires operations along the boundary of the encoded qubits, not on their entire surface. “This reduces the number of operations required to create entanglement between two encoded qubits,” explain the theoretical physicists Nicolai Friis and Hendrik Poulsen Nautrup.
Key technology for fault tolerant quantum computers
Lattice surgery is considered one of the key techniques for the operation of future fault-tolerant quantum computers. Using lattice surgery, the physicists led by Thomas Monz and Rainer Blatt, together with the theoretical physicists Hendrik Poulsen Nautrup and Hans Briegel from the Department of Theoretical Physics at the University of Innsbruck and Nicolai Friis from the Institute of Quantum Optics and Quantum Information (IQOQI) of the Austrian Academy of Sciences in Vienna, have now demonstrated the generation of entanglement between two encoded qubits. This is the first experimental realization of non-classical correlations between topologically encoded qubits. Furthermore, the researchers were able to demonstrate for the first time the teleportation of quantum states between two encoded qubits.
The research was financially supported by the Austrian Science Fund FWF and the Research Promotion Agency FFG as well as the EU.
Reference: Entangling logical qubits with lattice surgery. Alexander Erhard, Hendrik Poulsen Nautrup, Michael Meth, Lukas Postler, Roman Stricker, Martin Ringbauer, Philipp Schindler, Hans J. Briegel, Rainer Blatt, Nicolai Friis, Thomas Monz. Nature 2020, doi: 10.1038/s41586-020-03079-6 https://www.nature.com/articles/s41586-020-03079-6
MIT study sheds light on the longstanding question of why cancer cells get their energy from fermentation.
In the 1920s, German chemist Otto Warburg discovered that cancer cells don’t metabolize sugar the same way that healthy cells usually do. Since then, scientists have tried to figure out why cancer cells use this alternative pathway, which is much less efficient.
MIT biologists have found a possible explanation for the Warburg effect, first seen in cancer cells in the 1920s and named after Otto Warburg, pictured. Credits: Image: Digital collage by Jose-Luis Olivares; cancer image courtesy of Dr. Cecil Fox, NCI; Warburg photo courtesy of NIH
MIT biologists have now found a possible answer to this longstanding question. In a study appearing in Molecular Cell, they showed that this metabolic pathway, known as fermentation, helps cells to regenerate large quantities of a molecule called NAD+, which they need to synthesize DNA and other important molecules. Their findings also account for why other types of rapidly proliferating cells, such as immune cells, switch over to fermentation.
“This has really been a hundred-year-old paradox that many people have tried to explain in different ways,” says Matthew Vander Heiden, an associate professor of biology at MIT and associate director of MIT’s Koch Institute for Integrative Cancer Research. “What we found is that under certain circumstances, cells need to do more of these electron transfer reactions, which require NAD+, in order to make molecules such as DNA.”
Vander Heiden is the senior author of the new study, and the lead authors are former MIT graduate student and postdoc Alba Luengo PhD ’18 and graduate student Zhaoqi Li.
Inefficient metabolism
Fermentation is one way that cells can convert the energy found in sugar to ATP, a chemical that cells use to store energy for all of their needs. However, mammalian cells usually break down sugar using a process called aerobic respiration, which yields much more ATP. Cells typically switch over to fermentation only when they don’t have enough oxygen available to perform aerobic respiration.
Since Warburg’s discovery, scientists have put forth many theories for why cancer cells switch to the inefficient fermentation pathway. Warburg originally proposed that cancer cells’ mitochondria, where aerobic respiration occurs, might be damaged, but this turned out not to be the case. Other explanations have focused on the possible benefits of producing ATP in a different way, but none of these theories have gained widespread support.
In this study, the MIT team decided to try to come up with a solution by asking what would happen if they suppressed cancer cells’ ability to perform fermentation. To do that, they treated the cells with a drug that forces them to divert a molecule called pyruvate from the fermentation pathway into the aerobic respiration pathway.
They saw, as others have previously shown, that blocking fermentation slows down cancer cells’ growth. Then, they tried to figure out how to restore the cells’ ability to proliferate, while still blocking fermentation. One approach they tried was to stimulate the cells to produce NAD+, a molecule that helps cells to dispose of the extra electrons that are stripped out when cells make molecules such as DNA and proteins.
Caption: MIT researchers have shown that cancer cells’ demand for NAD+ drives them to switch to a wasteful metabolic process called fermentation. Credits: Courtesy of the researchers
When the researchers treated the cells with a drug that stimulates NAD+ production, they found that the cells started rapidly proliferating again, even though they still couldn’t perform fermentation. This led the researchers to theorize that when cells are growing rapidly, they need NAD+ more than they need ATP. During aerobic respiration, cells produce a great deal of ATP and some NAD+. If cells accumulate more ATP than they can use, respiration slows and production of NAD+ also slows.
“We hypothesized that when you make both NAD+ and ATP together, if you can’t get rid of ATP, it’s going to back up the whole system such that you also cannot make NAD+,” Li says.
Therefore, switching to a less efficient method of producing ATP, which allows the cells to generate more NAD+, actually helps them to grow faster. “If you step back and look at the pathways, what you realize is that fermentation allows you to generate NAD+ in an uncoupled way,” Luengo says.
Solving the paradox
The researchers tested this idea in other types of rapidly proliferating cells, including immune cells, and found that blocking fermentation but allowing alternative methods of NAD+ production enabled cells to continue rapidly dividing. They also observed the same phenomenon in nonmammalian cells such as yeast, which perform a different type of fermentation that produces ethanol.
“Not all proliferating cells have to do this,” Vander Heiden says. “It’s really only cells that are growing very fast. If cells are growing so fast that their demand to make stuff outstrips how much ATP they’re burning, that’s when they flip over into this type of metabolism. So, it solves, in my mind, many of the paradoxes that have existed.”
The findings suggest that drugs that force cancer cells to switch back to aerobic respiration instead of fermentation could offer a possible way to treat tumors. Drugs that inhibit NAD+ production could also have a beneficial effect, the researchers say.
The research was funded by the Ludwig Center for Molecular Oncology, the National Science Foundation, the National Institutes of Health, the Howard Hughes Medical Institute, the Medical Research Council, NHS Blood and Transplant, the Novo Nordisk Foundation, the Knut and Alice Wallenberg Foundation, Stand Up 2 Cancer, the Lustgarten Foundation, and the MIT Center for Precision Cancer Medicine.
UNIGE researchers have demonstrated that every population can protect itself against a broad range of viruses thanks to the two most diverse HLA immune genes in humans.
Do populations from different geographic regions have the same potential for defending themselves against pathogens and against viruses in particular? An analysis of human genomes, especially the HLA genes responsible for the so-called “adaptive” immune system, provide some possible answers to this question. These genes, which vary enormously between individuals, code for molecules capable of recognising the different viruses so they can trigger the appropriate immune response. In a study to be published in the journal Molecular Biology and Evolution, scientists from the University of Geneva (UNIGE), Switzerland, partnering with Cambridge University, identify the HLA variants that bind to families of viruses most effectively. The researchers show that, in spite of the great heterogeneity of HLA variants in individuals, all populations benefit from an equivalent potential when it comes to virus protection.
The human body’s first line of defence consists of recognising viruses as foreign bodies. Molecules known as human leukocyte antigens (HLAs) recognise the peptides – the small chains that make up a protein – in viruses. The HLA molecules then bind to these fragments and expose them on the surface of the cells, triggering a cascade of immune reactions designed to eliminate the virus.
The genes that code for HLA type A and type B molecules were of special interest to the researchers, since they play a primordial role in the ability to recognise the very wide range of different peptides derived from viruses that are pathogenic for humans. “These are the most polymorphic genes in our genome. We think that the existence of such a quantity of HLA genetic variants in humans is the result of natural selection, which – during our biological evolution – granted individuals better protection against the great heterogeneity of viruses. These genes enable us to constantly adapt our immunity,” explains Da Di, a researcher in the Department of Genetics and Evolution in UNIGE’s Faculty of Sciences, and the article’s first author.
Simulating immunity via computer modelling
“To simulate what happens when individuals are exposed to different viruses, we used several databases and computer tools to predict the binding strengths between HLA molecules and the peptides based on their physical and chemical properties,” reports Alicia Sanchez-Mazas, a professor in the Department of Genetics and Evolution, and the project’s leader. Two databases were used in the study: the first identified 3,000 different variants of HLA-A or HLA-B molecules. “We then created the second by randomly generating 200,000 peptides of nine amino acids – the building blocks that proteins consist of,” continues Dr Di. “This amazing number of peptides simulates the immense variety of pieces of virus possible in nature.” By modelling these binding forces, it was possible to observe that the HLA-A and HLA-B molecules distinctly recognise very different peptide families – and, it follows, potentially as many viruses. “When these binding forces are represented graphically, we can see that the peptides (grey in the figure) best recognised by the HLA-A molecules (red) form one wing of a bird; while those recognised by the HLA-B molecules (blue) form the other wing,” states José Manuel Nunes, a researcher in UNIGE’s Department of Genetics and Evolution, and co-author of the article. “Our immunity to the viruses, therefore, is like the two wings of a bird that play a joint and complementary role.”
When diversity means equality
The authors also investigated the variability of HLA molecules in terms of different populations, some of whom have a limited number of variants due to weaker genetic mixing. This suggests that certain populations would potentially be less well protected against some families of viruses. However, by analysing the variants of 123 global populations, the researchers found that each population systematically had molecules capable of recognising very different virus families. “This indicates that even in populations that have reduced genetic variability (such as native populations in Australia that have very few alleles for HLA genes), there are molecules in the immune system capable of countering viruses from very different families. This gives them a protective potential equivalent to other populations,” concludes Professor Sanchez-Mazas.
NASA has extended the Juno mission to explore Jupiter through September 2025, expanding the science goals to include the overall Jovian system, made up of the planet and its rings and moons. In addition to continuing to explore our Solar System’s largest planet, NASA’s planetary orbiter will rendezvous with three of the most intriguing Jovian moons.
“Since its first orbit in 2016, Juno has delivered one revelation after another about the inner workings of this massive gas giant,” said Southwest Research Institute’s Scott Bolton, Juno principal investigator. “With the extended mission, we will answer fundamental questions that arose during Juno’s prime mission while reaching beyond the planet to explore Jupiter’s ring system and largest satellites.”
Proposed in 2003 and launched in 2011, Juno arrived at Jupiter on July 4, 2016. The prime mission operations will be completed in July 2021. The extended mission includes 42 additional orbits including close passes of Jupiter’s north polar cyclones and flybys of the Galilean moons Ganymede, Europa and Io, as well as the first extensive exploration of Jupiter’s ring system.
The extended mission represents an efficient advance for NASA’s Solar System exploration strategy. The data Juno collects will complement the goals of the next generation of missions to the Jovian system — NASA’s Europa Clipper and ESA’s JUpiter ICy moons Explorer (JUICE). Juno’s investigation of Jupiter’s volcanic moon Io addresses many science goals identified by the National Academy of Sciences for a future Io explorer mission.
The extended mission’s science campaigns expand on discoveries Juno has already made about Jupiter’s interior structure, internal magnetic field, magnetosphere and atmosphere, including its deep atmosphere, polar cyclones and auroras.
“With this extension, Juno becomes its own follow-on mission,” said Steve Levin, Juno project scientist at NASA’s Jet Propulsion Laboratory (JPL). “Close-up observations of the poles, radio occultations, satellite flybys, and focused magnetic field studies combine to make a new mission, the next logical step in our exploration of the Jovian system.”
For example, scientists will target Jupiter’s enigmatic “Great Blue Spot,” an isolated patch near the planet’s equator exhibiting an intense magnetic field, deploying high spatial resolution magnetic surveys during six flybys. As Juno’s orbit evolves, multiple flybys of Ganymede (2), Europa (3), and Io (11) are planned en route to multiple passages through Jupiter’s tenuous rings.
The natural evolution of Juno’s polar orbit around the gas giant provides new science opportunities that the extended mission capitalizes on.
“The mission designers have done an amazing job crafting an extended mission that conserves the mission’s single most valuable resource — fuel,” said Ed Hirst, Juno project manager from NASA JPL. “Gravity assists from multiple satellite flybys steer our spacecraft through the Jovian system while providing a wealth of science opportunities.”
JPL, a division of Caltech in Pasadena, California, manages the Juno mission for the principal investigator, Dr. Scott J. Bolton, of the Southwest Research Institute in San Antonio. Juno is part of NASA’s New Frontiers Program, which is managed at NASA’s Marshall Space Flight Center in Huntsville, Alabama, for the agency’s Science Mission Directorate in Washington. Lockheed Martin Space in Denver built and operates the spacecraft.
Promising as a highly sensitive oscillator toward 5G communication.
Liwen Sang, independent scientist at International Center for Materials Nanoarchitectonics, National Institute for Materials Science (also JST PRESTO researcher) developed a MEMS resonator that stably operates even under high temperatures by regulating the strain caused by the heat from gallium nitride (GaN).
High-precision synchronization is required for the fifth generation mobile communication system (5G) with a high speed and large capacity. To that end, a high-performance frequency reference oscillator which can balance the temporal stability and temporal resolution is necessary as a timing device to generate signals on a fixed cycle. The conventional quartz resonator as the oscillator has the poor integration capability and its application is limited. Although a micro-electromechanical system (MEMS)*1 resonator can achieve a high temporal resolution with small phase noise and superior integration capability, the silicon (Si)-based MEMS suffers from a bad stability at higher temperatures.
In the present study, a high-quality GaN epitaxial film was fabricated on a Si substrate using metal organic chemical vapor deposition (MOCVD)*2 to fabricate the GaN resonator. The strain engineering was proposed to improve the temporal performance. The strain was achieved through utilizing the lattice mismatch and thermal mismatch between GaN and Si substrate. Therefore, GaN was directly grown on Si without any strain-removal layer. By optimizing the temperature decrease method during MOCVD growth, there was no crack observed on GaN and its crystalline quality is comparable to that obtained by the conventional method of using a superlattice strain-removal layer.
The developed GaN-based MEMS resonator was verified to operate stably even at 600K. It showed a high temporal resolution and good temporal stability with little frequency shift when the temperature was increased. This is because the internal thermal strain compensated the frequency shift and reduce the energy dissipation. Since the device is small, highly sensitive and can be integrated with CMOS technology, it is promising for the application to 5G communication, IoT timing device, on-vehicle applications, and advanced driver assistance system.
The research was supported by JST’s Strategic Basic Research Program, Precursory Research for Embryonic Science and Technology(PRESTO). This result was presented at the IEEE International Electron Devices Meeting (IEDM2020) held online on December 12-18, 2020, titled “Self-Temperature-Compensated GaN MEMS Resonators through Strain Engineering up to 600 K.”
(1) Micro-electro mechanical systems (MEMS)
A device where mechanical components, sensors, actuators, and electrical circuit are integrated on a substrate, such as semiconductor, glass, or organic material through microfabrication technology. For the main component, three-dimensional shape and movable structures are built through etching.
(2) Metal organic chemical vapor deposition (MOCVD)
A useful crystal growth method to build a wafer for compound semiconductors. Organometallic compounds of the Group III and Group V are simultaneously provided to the heated crystalline surface of the substrate to achieve epitaxial growth.
Some organisms evolve an internal switch that can remain hidden for generations until stress flicks it on.
Computer simulations of cells evolving over tens of thousands of generations reveal why some organisms retain a disused switch mechanism that turns on under severe stress, changing some of their characteristics. Maintaining this “hidden” switch is one means for organisms to maintain a high degree of gene expression stability under normal conditions.
Tomato hornworm larvae are green in warmer regions, making camouflage easier, but black in cooler temperatures so that they can absorb more sunlight. This phenomenon, found in some organisms, is called phenotypic switching. Normally hidden, this switching is activated in response to dangerous genetic or environmental changes.
Scientists have typically studied this process by investigating the changes undergone by organisms under different circumstances over many generations. Several years ago, for example, a team bred generations of tobacco hornworm larvae to observe and induce color changes similar to those that occurred in their tomato hornworm relatives.
“Computer simulations, when built on reasonable assumptions and conducted under careful control, are a very powerful tool to mimic the real situation,” says KAUST computational bioscientist Xin Gao. “This helps scientists observe and understand principles that are otherwise very difficult, or impossible, to observe by wet-lab experiments.”
Gao and KAUST research scientist Hiroyuki Kuwahara designed a computer simulation of the evolution of 1,000 asexual microorganisms. Each organism was given a gene circuit model for regulating the expression of a specific protein X.
The simulation evolved the population over 90,000 generations. The original founding population had identical nonswitching gene circuits and evolved over 30,000 generations, collectively called the ancient population, under stable conditions. The next 30,000 generations, called the intermediate population, were exposed to fluctuating environments that switched every 20 generations. The final 30,000 generations, the derived population, were exposed to a stable environment.
The individuals in the ancient and derived populations, who evolved in stable environments, both had gene expression levels that were optimized for stability. But they were different: the ancient population’s stability did not involve phenotypic switching, while the derived population’s did. The difference, explains Kuwahara, stems from the intermediate population, in which switching was favored in order to deal with the fluctuating conditions.
The simulations suggest that populations of organisms maintain their switching machinery over a long period of environmental stability by gradually evolving low-threshold switches, which easily switch in fluctuating circumstances, to high-threshold switches when the environment is more stable.
This is easier, says Kuwahara, than reverting to a nonswitching state through small mutational shifts. “Instead, we end up with a type of ‘hidden’ phenotypic switching that acts like an evolutionary capacitor, storing genetic variations and releasing alternative phenotypes in the event of substantial perturbations,” Kuwahara says.
The team next plans to use computer simulations to study more complex biological systems while also interactively collaborating with researchers conducting wet-lab experiments. Their aim is to develop theoretical frameworks that can be experimentally validated.
Improved neuronal glucose uptake plus healthier eating might have anti-aging effects.
Researchers from Tokyo Metropolitan University have discovered that fruit flies with genetic modifications to enhance glucose uptake have significantly longer lifespans. Looking at the brain cells of aging flies, they found that better glucose uptake compensates for age-related deterioration in motor functions, and led to longer life. The effect was more pronounced when coupled with dietary restrictions. This suggests healthier eating plus improved glucose uptake in the brain might lead to enhanced lifespans.
The brain is a particularly power-hungry part of our bodies, consuming 20% of the oxygen we take in and 25% of the glucose. That’s why it’s so important that it can stay powered, using the glucose to produce adenosine triphosphate (ATP), the “energy courier” of the body. This chemical process, known as glycolysis, happens in both the intracellular fluid and a part of cells known as the mitochondria. But as we get older, our brain cells become less adept at making ATP, something that broadly correlates with less glucose availability. That might suggest that more food for more glucose might actually be a good thing. On the other hand, it is known that a healthier diet actually leads to longer life. Unravelling the mystery surrounding these two contradictory pieces of knowledge might lead to a better understanding of healthier, longer lifespans.
A team led by Associate Professor Kanae Ando studied this problem using Drosophila fruit flies. Firstly, they confirmed that brain cells in older flies tended to have lower levels of ATP, and lower uptake of glucose. They specifically tied this down to lower amounts of the enzymes needed for glycolysis. To counteract this effect, they genetically modified flies to produce more of a glucose-transporting protein called hGut3. Amazingly, this increase in glucose uptake was all that was required to significantly improve the amount of ATP in cells. More specifically, they found that more hGut3 led to less decrease in the production of the enzymes, counteracting the decline with age. Though this did not lead to an improvement in age-related damage to mitochondria, they also suffered less deterioration in locomotor functions.
Graphical abstract by Ando et al.
But that’s not all. In a further twist, the team put the flies with enhanced glucose uptake under dietary restrictions, to see how the effects interact. Now, the flies had even longer lifespans. Curiously, the increased glucose uptake did not actually improve the levels of glucose in brain cells. The results point to the importance of not just how much glucose there is, but how efficiently it is used once taken into cells to make the energy the brain needs.
Though the anti-aging benefits of a restricted diet have been shown in many species, the team were able to combine this with improved glucose uptake to leverage the benefits of both for even longer lifespans in a model organism. Further study may provide vital clues to how we might keep our brains healthier for longer.
This work was supported by a research award from the Japan Foundation for Aging and Health, a JSPS KAKENHI Grant-in-Aid for Scientific Research on Challenging Research (Exploratory) (19K21593), NIG-JOINT (71A2018, 25A2019), a Grant-in-Aid for JSPS Research Fellows (18J21936) and Research Funding for Longevity Science (19-7) from the National Center for Geriatrics and Gerontology, Japan.
Why the way we experience and interact with the world is entirely mind-made
Saltatory conduction is the process through which the brain receives information from the five sense organs, which include the eyes, ears, nose, tongue, and skin. When sense receptors in the sense organs are stimulated, electrochemical impulses travel via a process of neurotransmission from the peripheral nervous system to the central nervous system. Once received by the central nervous system, these electrochemical messages culminate in the brain where they are transformed into coherent information that can be acted upon.
Saltatory conduction was first identified in 1939 by Japanese born American biophysicist Ichiji Tasaki, and scientific understanding of the process has increased significantly since that time. However, although the mechanisms of this fundamental biological process are well documented, it appears that some important implications of saltatory conduction have been overlooked in the scientific literature – particularly in terms of how it can advance understanding of how we perceive reality.
More specifically, saltatory conduction provides evidence indicating that the reality we perceive and experience on a day-to-day basis is far less real or concrete than collective opinion might suggest. The reason for this is that without exception, our sense of movement, touch, taste, pain, pleasure, sight, sound, and so forth are the product of the brain filtering, transforming and organising electrochemical information into a working three-dimensional mental construction.
For example, when we look at a tree, what we see is the brain’s interpretation of electrochemical signals that were transmitted by sensory receptors in the eyes. Consequently, our perception of the tree isn’t “direct” but is the end product of a biophysical process involving receiving, transforming, transmitting and then retransforming information. The same applies if we reach out and touch the tree – we experience the brain’s reconstruction, based on input from electrochemical signals, of how it interprets the tree should feel to the hand.
A good way to understand this principle is to consider how information is processed using Voiceover Internet Protocol that underlies web-based video calling platforms such as Messenger, Skype and WhatsApp. In such instances, a caller’s camera and microphone capture analogue video and audio signals which are then compressed and transformed into digital numeric packets. These data packets are then transmitted over a digital network before being decompressed and transformed back to analogue video images and audio sounds by the recipient’s video conferencing system. However, at no point can it be said that the two callers’ interaction with each other is unmodified and direct, as their video call is subject to various stages of data transformation and transportation.
A similar type of “data transformation” process occurs during saltatory conduction such that in reality, we never directly touch, smell, see, hear, or taste sensory phenomena. Consequently, although we have the impression of living in and moving through a physical world, we never truly go anywhere or do anything because at any given time, our experience of life corresponds to the mental projection of the brain. In other words, the manner by which we experience and interact with the world is entirely mind-made – we project a reality and then relate to it entirely within the realm of the mind.
Consider the analogy of a dream whereby the dreamer is invariably under the impression that what they are experiencing is real. For example, when dreaming, individuals can have the sensation of coming or going, pleasure or pain, and fast or slow. In fact, an individual can experience a dream as being real to the extent that it causes them to wake up screaming if the dream is sufficiently frightening. However, although the dream may appear real, in truth it has no material existence and unfolds completely within the expanse of the mind. In a dream, nothing really comes or goes, there is no here or there, no near or far, no up or down, and no fast or slow.
However, it’s not correct to assert that what we experience during dreamt or waking reality is unreal, because regardless of whether a phenomenon or situation exists in material absolute terms or is just a fabrication of the mind, we still undergo an authentic experience. Indeed, the extent to which a given experience is designated as authentic or meaningful is highly subjective and varies according to context and how the mind has been conditioned.
Nevertheless, it appears that as part of some fundamental biological processes such as saltatory conduction, there exists evidence suggesting a need to re-examine the accuracy of certain widely accepted scientific assumptions concerning the underlying nature of mind and matter. Perhaps through fostering a better understanding of the inseparability between mind and matter in this manner, new psychological and technological approaches will emerge that better enable humans to harness resources and benefit from both their psychological and physical world.
References: (1) Shonin, E., & Van Gordon, W. (2014). Dream or reality? Philosophy Now, 104, 54 (2) Soeng, M. (1995). Heart Sutra: Ancient Buddhist Wisdom in the Light of Quantum Reality. Cumberland: Primary Point Press. (3) Van Gordon, W., Sapthiang, S., Barrows, P., & Shonin, E. (2020). Understanding and practicing emptiness. Mindfulness, Advance Online Publication, DOI: 10.1007/s12671-020-01586-1 (4) Van Gordon, W., Shonin, E., Dunn, T., Sapthiang, S., Kotera, Y., Garcia-Campayo, J., & Sheffield, D. (2019). Exploring emptiness and its effects on non-attachment, mystical experiences, and psycho-spiritual wellbeing: A quantitative and qualitative study of advanced meditators. Explore: The Journal of Science and Healing, 15, 261-272. (5) Vogel, H. (2009). Nervous System: Cambridge Illustrated Surgical Pathology. New York: Cambridge University Press. (6) Wireless Research Centre (n.d.). How Voice and Video Call Works? Available from: https://danenet.wicip.org/2019/04/23/how-voice-and-video-call-works/
Copyright of this article totally belongs to Dr. William Van Gordon, who is a Chartered Psychologist and Associate Professor of Contemplative Psychology at the University of Derby (UK). This article is republished here from psychology today under common creative licenses
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