Passionately Curious

Why do we move our eyes fast in the paradoxical sleep - in that sleep phase, in which most dreams take place? The secret is not yet fully aired, but we are on his track: A team at the University of Bern, in collaboration with the University of Fribourg, has identified the nerve cells behind this curious phenomenon.

REM - Rapid Eye Movement - is not only the name of a successful American rock band, but also and not least a characteristic eye movement in paradoxical sleep, so in the stage with high dream activity. This sleep phase has a peculiarity: Although the muscle tone of the sleeping person completely relaxed, the eyes suddenly move back and forth. The name “paradoxical sleep” is well deserved. Characteristic of these are signs of deep sleep (muscle atony) in connection with a brain activity, which is very similar to those in the waking state, and eye movements. This sleep phase was discovered in the 1950s by French and American researchers and consequently called rapid eye movement sleep (REM sleep), i.e. sleep with rapid eye movements. Why can this strange phenomenon be useful? For 70 years, scientists have been dreaming of getting to the bottom of the mystery. Thanks to the productive cooperation between the universities of Bern and Fribourg, this dream could now come true.

Butterfly wings arranged neurons

For several years, the team led by Franck Girard and Marco Celio at the University of Freiburg has studied neurons under the microscope, which occur in the brain stem and form a structure that is reminiscent of butterfly wings, which is why she was baptized Nucleus papilio. “These neurons are associated with multiple nerve centers, especially those responsible for eye movement, and those involved in sleep control,” explains Franck Girard. “Therefore, we asked ourselves the following question: may the nucleus papilio neurons play a role in the control of eye movements during sleep?”

Stronger together

To test this hypothesis, the Freiburg researchers turned to the research group headed by Dr. C. Gutiérrez Herrera and Prof. A. Adamantidis at the Department of Neurology at the Inselspital, University Hospital Bern, and Department for BioMedical Research of the University of Bern, who are investigating sleep in mice. “To our surprise, we found that these neurons are particularly active in the phase of paradoxical sleep,” reports Dr. Carolina Gutierrez. The researchers from Bern gathered the loop around the nucleus papilio neurons even more closely and were able to demonstrate with the help of optogenetic methods (combined optical and genetic techniques) that their artificial activation causes rapid eye movement, especially during this sleep phase. Conversely, the inhibition or elimination of these same neurons blocks the movement of the eyes.

After the “how” the “why”!

Now that it is clear that the nucleus papilio neurons play an important role in eye movement during REM sleep, it is important to find out what function this phenomenon has. Is it due to the visual experience of dreams? Does it matter in preserving memories? “Now that we are able to specifically activate the nucleus papilio ‘on demand’ in mice by optogenetic methods, we may be able to find answers to these questions,” says Antoine Adamantidis. The next step, however, will be to confirm the activation of nucleus papilio neurons during REM sleep in humans. The researchers have not yet found the key to their dreams, but they’ve come a long way.

Tucked away at the back of your brain is a phenomenal, but ignored structure. This amalgamation of neurons contains almost 50% of the cells in your brain, but only takes up 10% of the space. Even so, it remains unextolled and little considered. In the words of researcher and neurologist Jeremy Schmahmann, it’s the “Rodney Dangerfield of the brain” because “It don’t get no respect.” It’s the cerebellum.

The cerebellum in lateral and anterior views, from Anatomography maintained by Life Science Databases (LSDB)

Even though the cerebellum has so many neurons and takes up so much space, it is possible to survive without it, and a few people have. There are nine known cases of cerebellar agenesis, a condition where this structure never develops. These people live life a bit differently than the rest of us and have provided a unique view of how the cerebellum works.

Most scientists, and even regular people, know the basic function of the cerebellum. It helps coordinate motion and ensures that you remain balanced and controlled in daily life. When the motor cortex in your cerebrum tells part of your body to move, the cerebellum makes sure that motion happens in the right way.

If you wanted to scratch my head with my right arm, you’d have to do it in a very specific order. From the lift of my arm to the curl of the fingers, the motion has to be organized just right to make sure you’re not scratching the air or slapping yourself in the face. That’s what the cerebellum does. It makes sure that everything goes in order.

If you’ve ever seen someone pulled over on the side of the road, doing a sobriety test with a police officer, you’ve seen a basic test for cerebellar function.

But people with cerebellar agenesis have let us see a lot more of what the cerebellum does, and it’s not just motor coordination. Before the development of fMRI, and even today when we have that technology, one of the best ways to learn about how a portion of the brain works is to find people who are missing that portion, or in whom it has become damaged. One of the people who lives without a cerebellum is Jonathan Keleher, a 36 year-old man from Boston.

Jonathan was born without a cerebellum, it just never developed. On an X-ray, there’s a black space where his should be. At first, his family didn’t realize this, but signs started to appear after a few months. Babies have “developmental milestones” that they hit pretty regularly. These are things like sitting up on their own, walking, and talking. Most babies hit these milestones at about the same time, give or take a few weeks. When Jonathan missed all of them, his family started rushing him to experts to figure out the problem.

Finally, at five years old, a brain scan revealed what was wrong. There was a black space where his cerebellum should be.

The cerebellum should be in that big black portion on the bottom right, but there’s nothing but air. Photo from Feng Yu, et. al https://academic.oup.com/brain/article/138/6/e353/269537

That’s when physicians and researchers got to work, studying Jonathan’s development and helping him to be as normal as possible. Today, thirty years later, he’s not without symptoms, but his brain has adapted remarkably well. Even so, it’s given us some insight into what this part of the brain does.

People with cerebellar agenesis are clumsy. Most can walk (though they may need a cane), but fine motor skills like writing, typing, and speaking are a challenge. Their speech is never quite perfect and their handwriting is always a bit off. Their reaction times are slow and they can’t drive cars or ride bikes, there’s just too much going on. This is how Jonathan lives. He can write slowly, type fairly well, and has learned to speak in a slightly stilted manner. But motor changes aren’t the only pathology seen in Jonathan and those others who live without cerebella, they also demonstrate emotional, social, and intellectual changes.

People with cerebellar agenesis have trouble developing deep, complex relationships like most of us form with our spouses, best friends, and partners. They lack emotional nuance and complexity, and so are unable to form these bonds. This shows the role the cerebellum must play in emotional coordination. It’s not just a motor center.

These people also struggle to “read a room” like most of us can. They have difficulty adapting in social situations, both the simple and the complex. The cerebellum clearly has some role in coordinating social stimuli as well as motor. We’re not yet sure how deep this effect is, but there is certainly some.

People who were born with cerebellar agenesis tend to adapt to it fairly well. The brain is plastic, it’s adaptable. fMRI imaging has shown that Jonathan’s other brain areas help make up for his lack of a cerebellum. The role of this part of the brain is distributed to many others so these people can continue to live complete, functional lives. Even so, these other structures never accomplish the job quite as well as the cerebellum can. The cerebellum is specially designed to carry out these functions. Other brain structures can technically do it, but they’re not as effective. It’s like putting a linebacker in to play wide receiver in a football game. They know the basics, understand the rules, and can probably run the routes, but even a great linebacker like Brian Urlacher would never have been as good a wide receiver as Jerry Rice. He doesn’t have the same abilities.

That’s similar to how Jonathan’s brain has developed. It has passed cerebellar roles on to parts that aren’t refined and bred to carry them out. In his brain, many roles are filled passably, but most of the work of the cerebellum remains poorly executed.

A rearview of the cerebellum, from the book, Tumors of the Cerebellum via the Internet Archive.

What would happen if your cerebellum disappeared today?

That wouldn’t be good.

Unlike Jonathan and those other adults with cerebellar agenesis, your brain hasn’t developed to give these roles to other areas. The responsibilities haven’t been redistributed. So your brain function wouldn’t adapt, there would just be things missing.

That means you wouldn’t be able to walk, speak, eat, think clearly, or feel emotions, at least not in a complex way. Sure, you could still feel happy, sad, or angry, but you’d lose the emotional warmth of a summer’s day, or the melancholy of late winter. Essential parts of the human experience would just disappear.

So, life without the cerebellum. It is possible, and it’s not too bad all-in-all. But, if you have to pick a part of your brain to lose today, you should probably choose something else.

Track a Killer

Killer T cells are important disease-fighting members of the immune system. Experiments in the lab show how they rapidly kill one cell after the other with a unique cocktail of chemicals fired out in deadly packages called cytotoxic granules. But like an athlete that shines in training but chokes in the big games, T cells seem to work much more slowly in their natural environment. To understand how they function in the body, researchers genetically modified mice to add a fluorescent tag (green, with the structures that support T cells labelled red) onto a protein in the granules, and used microscopy to observe the T cells in action as they fought off invaders. Getting a glimpse at this process could answer questions about how they interact with other cells in the body, and might provide clues on how to enhance their behaviour to better tackle threats like cancer and viruses.

Written by Anthony Lewis

Image from work by Praneeth Chitirala and Hsin-Fang Chang, and colleagues

Cellular Neurophysiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, Homburg, Germany

Image originally published under a Creative Commons Licence (BY 4.0)

Published in eLife, July 2020

Wildfire smoke: How you can protect your lungs

During a wildfire, people throughout the surrounding area may suffer the effects of the smoke. Talk with your doctor about how to prepare for this smoke, especially if you or someone in the family fits into one of these categories: works outdoors; is under age 18 or over age 65; or has asthma, COPD or other lung diseases, chronic heart disease, or diabetes. Monitor your breathing and exposure to the smoke.

GIF credit: Eleanor Lutz

General Recommendations

Stay indoors: People living close to the fire-stricken areas should remain indoors, unless prompted by local officials to evacuate, and avoid breathing smoke, ashes and other pollution in the area.

Don’t count on a dust mask: Ordinary dust masks, designed to filter out large particles, and cloth facial coverings will not help. They still allow the more dangerous smaller particles to pass through. Special, more expensive dust masks with an N-95 or N-100 filter will filter out the damaging fine particles, but may not fit properly and are difficult for people with lung disease to use.

If you have lung disease, consult with your doctor before using a N95 mask. These masks can make it more difficult for anyone to breathe and should only be used if you must go outside.

Due to the COVID19 pandemic, N95 masks may not be readily available due to shortages and because they are needed for frontline health care workers.

Take precautions for kids: Extra precaution should be taken for children, who are more susceptible to smoke.  Their lungs are still developing and they breathe in more air (and consequently more pollution) for their size than adults. Masks should not be used for children because they will likely not fit properly.

Roll up your car windows: When driving your car in smoky areas, keep your windows and vents closed, and operate on “recirculate” setting, including when using air conditioning.

Protect the air in your home: Stay inside as much as possible, with doors, windows and fireplace dampers shut and preferably with clean air circulating through air conditioners and air cleaners. Use air conditioners on the recirculation setting to keep from pulling outside air into the room. Air cleaning devices that have HEPA filters can provide added protection from the soot and smoke. Place damp towels under the doors and other places where the outside air may leak in.

Prepare to evacuate if directed. Listen to your local or state officials and protect yourself and your family.

Don’t exercise outside: If you live close to or in the surrounding area, don’t exercise outdoors, especially if you smell smoke or notice eye or throat irritation.

If You Have Lung Disease, Chronic Heart Disease or Diabetes

Check in with your doctor: People with asthma or other lung diseases, cardiovascular diseases or diabetes should check with their physician regarding any changes in medication that may be needed to cope with the smoky conditions.

Keep an eye on symptoms: Higher levels of smoke in some areas can make breathing more difficult. If you are experiencing symptoms, please try to contact your physician. If you cannot, asthma patients can follow the asthma action plan and COPD patients can follow the COPD action plan developed with their physician. Use your peak flow meter if prescribed. Do not hesitate to take your medication, and avail yourself of the full spectrum of medications your doctor has prescribed to you.

Ask about your oxygen use: People using oxygen should not adjust their levels of intake before consulting a physician. (Call your doctor BEFORE you take any action.)

Know when to seek medical attention: If symptoms are not relieved by the usual medicines, seek medical attention. Symptoms to watch for: wheezing, shortness of breath, difficulty taking a full breath, chest heaviness, lightheadedness, and dizziness. If you have any concerns or questions please contact your physician.

Watch for breathing issues after exposure: If you develop a persistent cough or difficult or painful breathing, call your physician. The first symptoms can appear as late as 24 to 48 hours after exposure. Smoke can remain in areas for many days after the fires have ended.

Clean Up

Residents and volunteers should use caution during clean-up because the process involves ashes and other sources of pollution.

Avoid dust and soot: People with lung or heart problems should avoid clean-up activities and areas where dust or soot is present.

Reduce dust and soot: Thoroughly wet dusty and sooty area prior to clean-up. This will help to reduce the amount of particles becoming airborne.

Cover your face: Wear an appropriate dust mask during clean-up, a HEPA-filtered one or an N-95.

Do not disturb: If exposure to asbestos or other hazardous materials is suspected, do not disturb the area. Dust masks do not protect against asbestos.

Information Source: American Lung Association. GIF credit: webstockreview (top). 

United States smoke model from September 15th, 2020 (Erick Adame):

Phosphine Detected In The Atmosphere of Venus - An Indicator of Possible Life?

Astronomers detected signs of a smelly, toxic gas that microbes can make in the planet’s clouds.

Chemical signs of the gas phosphine have been spotted in observations of the Venusian atmosphere, researchers report September 14 in Nature Astronomy. Examining the atmosphere in millimeter wavelengths of light showed that the planet’s clouds appear to contain up to 20 parts per billion of phosphine — enough that something must be actively producing it, the researchers say.

If the discovery holds up, and if no other explanations for the gas are found, then the hellish planet next door could be the first to yield signs of extraterrestrial life — though those are very big ifs!

The presence of phosphine is seen by many astrobiologists as a “biosignature” i.e. an indicator of the possible presence of life. The detection was made by the Atacama (ALMA) array located in Chile and the James Clerk Maxwell telescope located in Hawaii. The research team includes members from the University of Manchester, the Massachusetts Institute of Technology, and Cardiff University. A paper will appear in the 14 September issue of Nature Astronomy.

A virtual reality experience may not be enough to induce an identity shift in people, according to new research published in the journal Cyberpsychology, Behavior, and Social Networking.

“I am interested in how interactive technologies, such as video games and virtual reality systems, can be used to influence people’s beliefs and behaviors,” said study author Jorge Peña, an associate professor and director of the Virtual Interaction & Communication Technology (VICTR) lab at the University of California, Davis.

“Thus, I became interested in the identity shift effect, which predicts that presenting the self in online public venues (e.g., social media, blogs, etc.) influences people to behave in line with their public persona.”

In the study, 228 college students completed an assessment of personality and then returned to the lab about one week later, where they were randomly assigned to portray either an extraverted or introverted person while answering questions in a virtual reality classroom. Some participants completed the task in an empty virtual classroom, while others completed the task in a virtual classroom that was full of virtual students.

After their virtual reality experience, the participants again provided ratings of their personality. Based on previous research, Peña and his colleagues expected that people’s identities would shift based on whether they were assigned to act as extraverts or not.

But the participants did not regard themselves as more extraverted after portraying themselves as extraverts in the virtual reality environment.

“Identity shift is an interesting phenomenon that describes how people change based on how they present themselves in public. However, we found no evidence for this phenomenon in a preregistered study that placed people in virtual reality rooms that were either empty or full of people,” Peña told PsyPost.

“More studies are needed to determine the strength of the identity shift effect. Some experimental conditions such as providing individuals with feedback about their online performance seem more reliable in comparison to asking people to portray extraverted or introverted versions of the self.”

The study, “Examining Identity Shift Effects in Virtual Reality“, was authored by Jorge Peña and Dillon Hill.

The coronavirus is mutating — does it matter?

By Ewen Callaway (Nature). Animation: Closed’ and ‘open’ conformations of the spike protein on SARS-CoV-2, which binds to receptors on human cells. A common mutation (circled) seems to make the protein favour open conformations, which might mean the virus can enter cells more easily. Source: Structural data from K. Shen & J. Luban.

When COVID-19 spread around the globe this year, David Montefiori wondered how the deadly virus behind the pandemic might be changing as it passed from person to person. Montefiori is a virologist who has spent much of his career studying how chance mutations in HIV help it to evade the immune system. The same thing might happen with SARS-CoV-2, he thought.

In March, Montefiori, who directs an AIDS-vaccine research laboratory at Duke University in Durham, North Carolina, contacted Bette Korber, an expert in HIV evolution and a long-time collaborator. Korber, a computational biologist at the Los Alamos National Laboratory (LANL) in Sante Fe, New Mexico, had already started scouring thousands of coronavirus genetic sequences for mutations that might have changed the virus’s properties as it made its way around the world.

Compared with HIV, SARS-CoV-2 is changing much more slowly as it spreads. But one mutation stood out to Korber. It was in the gene encoding the spike protein, which helps virus particles to penetrate cells. Korber saw the mutation appearing again and again in samples from people with COVID-19. At the 614th amino-acid position of the spike protein, the amino acid aspartate (D, in biochemical shorthand) was regularly being replaced by glycine (G) because of a copying fault that altered a single nucleotide in the virus’s 29,903-letter RNA code. Virologists were calling it the D614G mutation.

n April, Korber, Montefiori and others warned in a preprint posted to the bioRxiv server that “D614G is increasing in frequency at an alarming rate”1. It had rapidly become the dominant SARS-CoV-2 lineage in Europe and had then taken hold in the United States, Canada and Australia. D614G represented a “more transmissible form of SARS-CoV-2”, the paper declared, one that had emerged as a product of natural selection.

These assertions dismayed many scientists. It wasn’t clear that the D614G viral lineage was more transmissible, or that its rise indicated anything unusual, they said. But alarm spread fast across the media. Although many news stories included researchers’ caveats, some headlines declared that the virus was mutating to become more dangerous. In retrospect, Montefiori says he and his colleagues regret describing the variant’s rise as “alarming”. The word was scrubbed from the peer-reviewed version of the paper, published in Cell in July2.

The work sparked a frenzy of interest in D614G. Even those who were sceptical that the mutation had changed the virus’s properties agreed that it was intriguing, because of its meteoric rise and ubiquity. For months, that lineage has been found in almost all sequenced samples of SARS-CoV-2 (see ‘Global spread’). “This variant now is the pandemic. As a result, its properties matter,” wrote Nathan Grubaugh, a viral epidemiologist at the Yale School of Public Health in New Haven, Connecticut, and two colleagues in a Cell essay on Korber and Montefiori’s findings3.

So far, the upshot of this work is less clear than Montefiori and Korber’s preprint suggested. Some experiments suggest that viruses carrying the variant infect cells more easily. Other work has revealed possible good news: the variant might mean that vaccines can target SARS-CoV-2 more easily. But many scientists say there remains no solid proof that D614G has a significant effect on the spread of the virus, or that a process of natural selection explains its rise. “The jury’s out,” says Timothy Sheahan, a coronavirologist at the University of North Carolina at Chapel Hill. “This mutation might mean something, or it might not.”

Researchers still have more questions than answers about coronavirus mutations, and no one has yet found any change in SARS-CoV-2 that should raise public-health concerns, Sheahan, Grubaugh and others say. But studying mutations in detail could be important for controlling the pandemic. It might also help to pre-empt the most worrying of mutations: those that could help the virus to evade immune systems, vaccines or antibody therapies.

How to Give A.I. a Pinch of Consciousness

A.I. researchers are turning to neuroscience to build smarter, more powerful neural networks

By Chris Baraniuk (One Zero Medium). Image: Engineered Arts prosthetic expert Mike Humphrey checks on Fred, a recently completed Mesmer robot that was built at the company’s headquarters in Penryn on May 9, 2018, in Cornwall, England. Photo: Matt Cardy/Stringer/Getty Images.

In 1998, an engineer in Sony’s computer science lab in Japan filmed a lost-looking robot moving trepidatiously around an enclosure. The robot was tasked with two objectives: avoid obstacles and find objects in the pen. It was able to do so because of its ability to learn the contours of the enclosure and the locations of the sought-after objects.

But whenever the robot encountered an obstacle it didn’t expect, something interesting happened: Its cognitive processes momentarily became chaotic. The robot was grappling with new, unexpected data that didn’t match its predictions about the enclosure. The researchers who set up the experiment argued that the robot’s “self-consciousness” arose in this moment of incoherence. Rather than carrying on as usual, it had to turn its attention inward, so to speak, to decide how to deal with the conflict.

This idea about self-consciousness — that it asserts itself in specific contexts, such as when we are confronted with information that forces us to reassess our environment and then make an executive decision about what to do next — is an old one, dating back to the work of the German philosopher Martin Heidegger in the early 20th century. Now, A.I. researchers are increasingly influenced by neuroscience and are investigating whether neural networks can and should achieve the same higher levels of cognition that occur in the human brain.

Far from the “stupid” robots of today, which don’t have any real understanding of where they are or what they experience, the hope is that a level of awareness analogous to consciousness in humans could make future A.I.s much more intelligent. They could learn by themselves, for example, how to select and focus on data in order to acquire new skills that they assimilate and go on to perform with ease. But giving machines the power to think like this also brings with it risks — and ethical uncertainties.

“I don’t design consciousness,” says Jun Tani, PhD, co-designer of the 1998 experiment and now a professor in the Cognitive Neurorobotics Research Unit at the Okinawa Institute of Technology. He tells OneZero that to describe what his robots experience as “consciousness” is to use a metaphor. That is, the bots aren’t actually cogitating in a way we would recognize, they’re just exhibiting behavior that is structurally similar. And yet he is fascinated by parallels between machine minds and human minds. So much so that he has tried simulating the neural responses associated with autism via a robot.

One of the world’s foremost A.I. experts, Yoshua Bengio, founder of Mila, the Quebec Artificial Intelligence Institute, is likewise fascinated by consciousness in A.I. He uses the analogy of driving to describe the switch between conscious and unconscious actions.

“It starts by conscious control when you learn how to drive and then, after some practice, most of the work is done at an unconscious level and you can have a conversation while driving,” he explains via email.

That higher, attentive level of processing is not always necessary — or even desirable — but it seems to be crucial for humans to learn new skills or adapt to unexpected challenges. A.I. systems and robots could potentially avoid the stupidity that currently plagues them if only they could gain the same ability to prioritize, focus, and resolve a problem.

Inspired in part by what we think we know about human consciousness, Bengio and his colleagues have spent several years working on the principle of “attention mechanisms” for A.I. systems. These systems are able to learn what data is relevant and therefore what to focus on in order to complete a given task.

“Research on consciousness,” Bengio adds, “is still considered somewhat taboo in A.I.” Because consciousness is such a difficult phenomenon to understand, even for neuroscientists, it has mostly been discussed by philosophers until now, he says.

Knowledge about the human brain and the human experience of consciousness is increasingly relevant to the pursuit of more advanced systems and has already led to some fascinating crossovers. Take, for example, the work by Newton Howard, PhD, professor of computational neurosciences and neurosurgery at the University of Oxford. He and colleagues have designed an operating system inspired by the human brain.

Rather than rely on one approach to solving problems, it can choose the best data processing technique for the task in question — a bit like how different parts of the brain handle different sorts of information.

He’s also experimenting with a system that can gather data from various sensors and sources in order to automatically build knowledge on various topics. “When it’s deployed, it’s like a child,” he says. “It’s eager to learn.”

All of this work, loosely inspired by what we know about human brains, may push the boundaries of what A.I. can accomplish today. And yet some argue it might not get us much closer to a truly conscious machine mind that has a sense of a self, a detached “soul” that inhabits its body (or chipset), with free will to boot.

The philosopher Daniel Dennett, who has spent much of his life thinking about what consciousness is and is not, argues that we won’t see machines develop this level of consciousness anytime soon — not even within 50 years. He and others have pointed out that the A.I.s we are able to build today seem to have no semblance of the reflective thinking or awareness that we assume are crucial for consciousness.

It’s in the search for a system that does possess these attributes, though, that a profound crossover between neuroscience and A.I. research might happen. At the moment, consciousness remains one of the great mysteries of science. No one knows to what activity in the brain it is tied, exactly, though scientists are gradually working out that certain neural connections seem to be associated with it. Some researchers have found oscillations in brain activity that appear to be related to specific states of consciousness — signatures, if you like, of wakefulness.

By replicating such activity in a machine, we could perhaps enable it to experience conscious thought, suggests Camilo Miguel Signorelli, a research assistant in computer science at the University of Oxford.

He mentions the liquid “wetware” brain of the robot in Ex Machina, a gel-based container of neural activity. “I had to get away from circuitry, I needed something that could arrange and rearrange on a molecular level,” explains Oscar Isaac’s character, who has created a conscious cyborg.

“That would be an ideal system for an experiment,” says Signorelli, since a fluid, highly plastic brain might be configured to experience consciousness-forming neural oscillations — akin to the waves of activity we see in human brains.

This, it must be said, is highly speculative. And yet it raises the question of whether completely different hardware might be necessary for consciousness (as we experience it) to arise in a machine. Even if we do one day successfully confirm the presence of consciousness in a computer, Signorelli says that we will probably have no real power over it.

“Probably we will get another animal, humanlike consciousness but we can’t control this consciousness,” he says.

As some have argued, that could make such an A.I. dangerous and unpredictable. But a conscious machine that proves to be harmless could still raise ethical quandaries. What if it felt pain, despair, or a terrible state of confusion?

“The risk of mistakenly creating suffering in a conscious machine is something that we need to avoid,” says Andrea Luppi, a PhD student at the University of Cambridge who studies human brain activity and consciousness.

Bright light at night interrupts the body’s normal day-night cycles, called circadian rhythms, and can trigger insomnia. In fact, circadian rhythms play a major role in health. Disrupted day-night cycles have even been linked to increased incidence of diseases like cancer, heart disease, obesity, depressive disorders and type 2 diabetes in people who work night shifts. Therefore, understanding how human eyes sense light could lead to “smart” lights that can prevent depression, foster sleep at night, and maintain healthy circadian rhythms.

In a Science study, researchers at the Salk Institute report the discovery of three cell types in the eye that detect light and align the brain’s circadian rhythm to our ambient light. The study marks the first direct assessment in humans of light responses from these cells, called intrinsically photosensitive retinal ganglion cells (ipRGCs)—and the implications for health are substantial.

“We have become mostly an indoor species, and we are removed from the natural cycle of daylight during the day and near-complete darkness at night,” says Salk Professor Satchidananda Panda, senior author of the paper. “Understanding how ipRGCs respond to the quality, quantity, duration, and sequence of light will help us design better lighting for neonatal ICUs, ICUs, childcare centers, schools, factories, offices, hospitals, retirement homes and even the space station.”

This new understanding of ipRGCs may also fuel future research into developing therapeutic lighting that can treat depression, insomnia, Attention Deficit and Hyperactivity Disorder (ADHD), migraine pain, and even sleep problems among patients with Alzheimer’s disease.

“It’s also going to open a number of avenues to try new drugs or work on particular diseases that are specific to humans,” says Ludovic Mure, a postdoctoral researcher in the Panda lab and first author of the new study.

While ipRGCs had been identified before in mouse retinas, these cells had never been reported in humans. For the new study, the Salk team used a new method developed by study co-authors Anne Hanneken of Scripps Research Institute and Frans Vinberg of John A. Moran Eye Center of the University of Utah to keep retina samples healthy and functional after donors passed away. The researchers then placed these samples on an electrode grid to study how they reacted to light.

They found that a small group of cells began firing after just a 30-second pulse of light. After the light was turned off, some of these cells took several seconds to stop firing. The researchers tested several colors of light, and found that these “intrinsically photosensitive” cells were most sensitive to blue light—the type used in popular cool-white LED lights and in many of our devices, such as smartphones and laptops.

Follow-up experiments revealed three distinct types of ipRGCs. Type 1 responded to light relatively quickly but took a long time to turn off. Type 2 took longer to turn on and also very long to turn off. Type 3 responded only when a light was very bright, but they turned on faster and then switched off as soon as the light was gone. Understanding how each ipRGC type functions may allow researchers to better design lighting or even therapeutics that can turn the cell activity on or off.

The new study actually helps explain a phenomenon reported in past studies of some blind people. These people, despite not being able to see, are still able to align their sleep-wake cycle and circadian rhythms to a day-night cycle. Thus, they must be sensing light somehow.

Now it appears that ipRGCs are the cells responsible for sending that light signal to the brain, even in people who lack the rod and cone cells needed to relay an image to the brain.

It also appears that, in people with functional rods and cones, ipRGCs actually work closely with these other visual cells. The new study suggests that ipRGCs can combine their own light sensitively with light detected by the rods and cones to add brightness and contrast information to what we see.

“This adds another dimension to designing better televisions, computer monitors and smartphone screens in which changing the proportion of blue light can trick the brain into seeing an image as bright or dim,” says Panda.

Panda says the next step in this research will be to study the net output of these cells under different light colors, intensity and duration—for example, comparing how they react to short pulses of light versus a longer duration of a few minutes. The team is also interested in how the cells react to sequences of light, such as a blue light that turns orange or vice versa, which would mimic some of the variety of light we encounter in nature at dawn and dusk.

Binge-Drinkers’ Brains Have to Work Harder to Feel Empathy for Others

Many colourful stars are packed close together in this image of the globular cluster NGC 1805, taken by the NASA/ESA Hubble Space Telescope. This tight grouping of thousands of stars is located near the edge of the Large Magellanic Cloud, a satellite galaxy of our own Milky Way. The stars orbit closely to one another, like bees swarming around a hive. In the dense centre of one of these clusters, stars are 100 to 1000 times closer together than the nearest stars are to our Sun, making planetary systems around them unlikely.