JHU Engineers Develop Drive-thru Type Test to Detect Viral Infections in Bacteria (Medicine)

The pandemic has made clear the threat that some viruses pose to people. But viruses can also infect life-sustaining bacteria and a Johns Hopkins University-led team has developed a test to determine if bacteria are sick, similar to the one used to test humans for COVID-19.

“If there was a COVID-like pandemic occurring in important bacterial populations it would be difficult to tell, because before this study, we lacked the affordable and accurate tools necessary to study viral infections in uncultured bacterial populations,” said study corresponding author Sarah Preheim, a Johns Hopkins assistant professor of environmental health and engineering.

The findings were published today in Nature Microbiology.

Sick bacteria are stymied in their function as decomposers and as part of the foundation of the food web in the Chesapeake Bay and other waterways. Determining viral infections in bacteria traditionally relies on culturing both bacteria and virus, which misses 99% of bacteria found in the environment because they cannot be grown in culture, Preheim says, adding that tests of viral infections in uncultured bacteria are expensive and difficult to apply widely, not unlike the early stages of COVID-19 testing.

The key to making a test of viral infections for uncultured bacteria faster and more affordable was to isolate single bacterial cells in a small bubble (i.e. an emulsion droplet) and fuse the genes of the virus and bacteria together once inside.

“The fused genes act like name tags for the bacteria and viruses,” said lead author Eric Sakowski, a former postdoctoral researcher in Preheim’s laboratory who is now an assistant professor at Mount St. Mary’s University. “By fusing the genes together, we are able to identify which bacteria are infected, as well as the variant of the virus that is causing the infection.”

The resulting test provides a novel way to screen for viral infections in a subset of bacterial populations. The test allows researchers to identify a link between environmental conditions and infections in Actinobacteria, one of the most abundant bacterial groups in the Chesapeake Bay and one that plays a crucial role in decomposing organic matter, making nutrients available to plants and photosynthetic algae.

Though the researchers developed this tool studying the Chesapeake Bay, they say their approach could be widely applied across aquatic ecosystems, shedding light on viral ecology and helping predict – and even prevent – devastating environmental impacts.

“This testing tool allows us to track viral infections more easily, so we can monitor these infections to see when they are most likely to have important environmental consequences,” Preheim said.

Sakowski said the new test could someday also affect how we treat bacterial infections.

“Viruses show potential for treating infections caused by antibiotic-resistant bacteria,” he said. “Knowing which viruses most effectively infect bacteria will be critical to this type of treatment.”

Preheim’s team also included Johns Hopkins doctoral student Keith Arora-Williams, and Funing Tian, Ahmed A. Zayed, Olivier Zablocki, and Matthew B. Sullivan, all from the Ohio State University.

Support was provided by the National Science Foundation and the Gordon E. and Betty I. Moore Foundation.


Reference: Sakowski, E.G., Arora-Williams, K., Tian, F. et al. Interaction dynamics and virus–host range for estuarine actinophages captured by epicPCR. Nat Microbiol (2021). https://www.nature.com/articles/s41564-021-00873-4 https://doi.org/10.1038/s41564-021-00873-4


Provided by Johns Hopkins University

Smaller Plates Help Reduce Food Waste in Campus Dining Halls (Food)

Food waste is a major problem in the U.S., and young adults are among the worst culprits. Many of them attend college or university and live on campus, making dining halls a prime target for waste reduction efforts. And a simple intervention can make a big difference, a University of Illinois study shows.

Shifting from round to oval plates with a smaller surface area can significantly reduce food waste in dining halls, says Brenna Ellison, associate professor in the Department of Agricultural and Consumer Economics (ACE) and co-author on the study.

“Americans waste about 31% of the food that is available at the retail and consumer levels,” Ellison says. “All-you-can-eat settings [common in dining halls] are extra challenging, because there’s not the normal incentives to try to reduce waste on your own. When you pay a fixed amount of money to go and eat, you want to get your money’s worth.”

Ellison’s research team previously worked with University Housing at Illinois on an educational campaign to reduce waste.

“It wasn’t as successful as we expected it to be,” she says. “So University Housing wanted to see if changing the plates would be a more successful way to reduce waste.”

Thurman Etchison, assistant director of dining­–facilities and equipment operations at U of I, says a 2016 waste study in campus dining hallsshowed about 3.3 ounces (93.5 grams) of wasted food per meal served. That amounted to 14,875 pounds (6,747 kilograms) per week across six residential dining hall locations.

“When we think about food waste in our setting, it is important to note it is not just the resources to produce the food that are wasted,” Etchison says. “There is a great deal of energy, water and labor that go into the refrigeration, preparation, transportation, and serving of this food that is wasted as well. If that were not enough, there is also the wasted energy, labor, and water that go into disposing of that food. The food we waste costs us more per pound than the food that is eaten.”

Ellison and co-authors Rachel Richardson, former graduate student in ACE, and Melissa Pflugh Prescott, assistant professor in the Department of Food Science and Human Nutrition, conducted the plate study in two University Housing dining halls on the U of I campus; both the round and oval plates were tested in each location, making sure to use the same menu for both plate types.

The researchers approached diners after they selected their food, and asked to take a picture of the plate and weigh the food. Diners then filled out a short survey, and when they were done eating and brought their tray to the dish return, the researchers again took a picture and weighed the remaining food.

The study included more than 1200 observations, and the researchers found significant reductions in food selection, consumption, and waste when diners used the oval plates. Overall, food waste went down from 15.8% of food selected for round plates to 11.8% for oval plates. That amounts to nearly 20 grams (0.7 oz) less food waste per plate, which adds up to a lot for a dining hall that serves thousands of meals, Ellison notes. 

The researchers did not weigh plates for any diners who went back for seconds, Ellison says. They did ask diners if they went back for seconds on the survey. Using this information, they estimated the potential effects of seconds and found it would not significantly change the results.

Ellison concludes that changing plate type is a viable strategy to reduce food waste, though dining hall managers need to weigh the cost of purchasing new plates against the potential savings. Combining the direct-nudge approach of smaller plates with an education campaign may be even more effective, she notes.

The Department of Agricultural and Consumer Economics and the Department of Food Science and Human Nutrition are in the College of Agricultural, Consumer and Environmental SciencesUniversity of Illinois.

The paper, “Impact of plate shape and size on individual food waste in a university dining hall,” is published in Resources, Conservation & Recycling. Authors include Rachel Richardson, Melissa Pflugh Prescott, and Brenna Ellison. [https://doi.org/10.1016/j.resconrec.2020.105293]

This research was supported by funding from the National Institute of Food and Agriculture, U.S. Department of Agriculture, under award number ILLU-470–334.


Provided by Illinois College of Agricultural, Consumer & Environmental Sciences

New Radiology Research Shows Promising Results for Focused Ultrasound Treatment of Alzheimer’s (Medicine)

West Virginia University scientists used MRI scans to show what happens when ultrasound waves target a specific area of Alzheimer’s patient’s brains. They concluded that this treatment may induce an immunological healing response, a potential breakthrough for a disease that accounts for up to 80% of all dementia cases.

Rashi Mehta, a researcher with the WVU School of Medicine and Rockefeller Neuroscience Institute, led the study that appears in the journal Radiology.

“Focused ultrasound is an innovative technique and new way of approaching brain diseases, including Alzheimer’s disease,” said Mehta, an associate professor in the Departments of Radiology, Neuroscience and Neuroradiology. “Novel techniques are needed for Alzheimer’s disease since traditional approaches have not proven effective.”

In 2018, WVU launched a first-of-its-kind clinical trial to explore the use of focused ultrasound to open the blood-brain barrier in early-stage Alzheimer’s patients.

“The blood-brain barrier has long presented a challenge in treating the most pressing neurological disorders,” said Ali Rezai, the executive chair of RNI and principal investigator of the clinical trial. “The ability to noninvasively and reversibly open the blood-brain barrier in deep brain areas, such as the hippocampus, offers a new potential in developing treatments for Alzheimer’s disease.”

The ultrasound targeted the hippocampus in particular because it plays a large role in learning and memory.

Mehta used MRI with contrast-enhancement dye to observe the changes that took place in the brains of three early-stage Alzheimer’s patients—ages 61, 72 and 73—who underwent the ultrasound treatment.

She observed that the dye moved along the course of draining veins following the procedure.

“This imaging pattern was unexpected and enhances our understanding of brain physiology,” she said. “The glymphatic system, which is a fluid-movement and waste-clearance system that’s unique to the brain, has been studied in animals, but there is controversy about whether this system truly exists in humans. The imaging pattern that we discuss in the paper offers evidence not only to support that the system does likely exist in humans but that focused ultrasound may modulate fluid movement patterns and immunological responses along this system.”

Mehta and her colleagues’ analysis of the MRI scans suggests that an immunological healing response may occur around the draining veins following the procedure.

Her research team included Rezai; RNI researchers Jeffrey Carpenter, Marc Haut, Manish Ranjan, Umer Najib, Paul Lockman, Peng Wang and Pierre-Francois D’haese; and Rupal Mehta from the Rush University Alzheimer’s Disease Center.

“This observation may be an important clue in understanding the physiological mechanism by which the focused ultrasound procedure modifies brain amyloid levels and might be used to treat patients with Alzheimer’s disease and other brain disorders,” she said.

Why are amyloid levels important? Unusually high amounts of this protein tend to clump together in the brains of Alzheimer’s patients, forming plaques between nerve cells and sabotaging their function. The ongoing clinical trial aims to assess whether focused ultrasound can reduce amyloid plaques in patients with Alzheimer’s disease.

This project did not involve any medications. The ultrasound itself was enough to elicit a probable immunological response. In the future, however, the treatment may make it easier to medicate the brain with more precision, even in people who don’t have Alzheimer’s disease.

“The blood brain barrier limits our ability to deliver drugs and therapeutic agents directly to the brain,” Mehta said. “Therefore, opening this barrier in patients would allow focal delivery of medications in select brain regions targeted by the procedure.”

The clinical trial—sponsored by INSIGHTEC, the manufacturer of the ultrasound device—continues.

As Mehta and her team enroll more participants, they plan to examine the treatment’s long-term effects. They want to know whether it is safe and effective for slowing—or even reversing—the progression of Alzheimer’s dementia.

So far, the results are promising. The treatment has not harmed any of the participants who have completed it.

“We are thankful to the patients who have volunteered for this trial,” Mehta said. “They are brave to undergo this procedure, which if proven effective may benefit patients with Alzheimer’s disease in the future.”

Alzheimer’s disease is the nation’s most common form of dementia, and it’s on the rise. The Alzheimer’s Association reports that 5.8 million Americans age 65 and older had Alzheimer’s dementia in 2020. By 2050, that number could rise to 13.8 million.

The focused ultrasound team at RNI is committed to improving the lives of patients with Alzheimer’s disease by pioneering advances using a truly integrated approach and the latest technologies. 

Research reported in this publication was supported by the National Institute of General Medical Sciences, a division of the National Institutes of Health, under Award Number 5U54GM104942-04. This publication does not necessarily reflect the views of NIGMS or NIH.

Featured image: In 2018, WVU launched a first-of-its-kind clinical trial to explore the use of focused ultrasound to open the blood-brain barrier in early-stage Alzheimer’s patients. Since then, WVU researchers have been investigating the treatment’s effects on the brain. A new study by Rashi Mehta—a researcher with the School of Medicine and Rockefeller Neuroscience Institute—finds that focused ultrasound may induce an immunological healing effect in the brains of Alzheimer’s patients. (WVU Photo/Caylie Silveira)


Reference:

Title: Blood-brain barrier opening with MRI-guided focused ultrasound elicits meningeal venous permeability in humans with early Alzheimer disease DOI: https://doi.org/10.1148/radiol.2021200643 Link: https://pubs.rsna.org/doi/10.1148/radiol.2021200643


Provided by WVU today

New Radiology Research Shows Promising Results for Focused Ultrasound Treatment of Alzheimer’s (Medicine)

West Virginia University scientists used MRI scans to show what happens when ultrasound waves target a specific area of Alzheimer’s patient’s brains. They concluded that this treatment may induce an immunological healing response, a potential breakthrough for a disease that accounts for up to 80% of all dementia cases.

Rashi Mehta, a researcher with the WVU School of Medicine and Rockefeller Neuroscience Institute, led the study that appears in the journal Radiology.

“Focused ultrasound is an innovative technique and new way of approaching brain diseases, including Alzheimer’s disease,” said Mehta, an associate professor in the Departments of Radiology, Neuroscience and Neuroradiology. “Novel techniques are needed for Alzheimer’s disease since traditional approaches have not proven effective.”

In 2018, WVU launched a first-of-its-kind clinical trial to explore the use of focused ultrasound to open the blood-brain barrier in early-stage Alzheimer’s patients.

“The blood-brain barrier has long presented a challenge in treating the most pressing neurological disorders,” said Ali Rezai, the executive chair of RNI and principal investigator of the clinical trial. “The ability to noninvasively and reversibly open the blood-brain barrier in deep brain areas, such as the hippocampus, offers a new potential in developing treatments for Alzheimer’s disease.”

The ultrasound targeted the hippocampus in particular because it plays a large role in learning and memory.

Mehta used MRI with contrast-enhancement dye to observe the changes that took place in the brains of three early-stage Alzheimer’s patients—ages 61, 72 and 73—who underwent the ultrasound treatment.

She observed that the dye moved along the course of draining veins following the procedure.

“This imaging pattern was unexpected and enhances our understanding of brain physiology,” she said. “The glymphatic system, which is a fluid-movement and waste-clearance system that’s unique to the brain, has been studied in animals, but there is controversy about whether this system truly exists in humans. The imaging pattern that we discuss in the paper offers evidence not only to support that the system does likely exist in humans but that focused ultrasound may modulate fluid movement patterns and immunological responses along this system.”

Mehta and her colleagues’ analysis of the MRI scans suggests that an immunological healing response may occur around the draining veins following the procedure.

Her research team included Rezai; RNI researchers Jeffrey Carpenter, Marc Haut, Manish Ranjan, Umer Najib, Paul Lockman, Peng Wang and Pierre-Francois D’haese; and Rupal Mehta from the Rush University Alzheimer’s Disease Center.

“This observation may be an important clue in understanding the physiological mechanism by which the focused ultrasound procedure modifies brain amyloid levels and might be used to treat patients with Alzheimer’s disease and other brain disorders,” she said.

Why are amyloid levels important? Unusually high amounts of this protein tend to clump together in the brains of Alzheimer’s patients, forming plaques between nerve cells and sabotaging their function. The ongoing clinical trial aims to assess whether focused ultrasound can reduce amyloid plaques in patients with Alzheimer’s disease.

This project did not involve any medications. The ultrasound itself was enough to elicit a probable immunological response. In the future, however, the treatment may make it easier to medicate the brain with more precision, even in people who don’t have Alzheimer’s disease.

“The blood brain barrier limits our ability to deliver drugs and therapeutic agents directly to the brain,” Mehta said. “Therefore, opening this barrier in patients would allow focal delivery of medications in select brain regions targeted by the procedure.”

The clinical trial—sponsored by INSIGHTEC, the manufacturer of the ultrasound device—continues.

As Mehta and her team enroll more participants, they plan to examine the treatment’s long-term effects. They want to know whether it is safe and effective for slowing—or even reversing—the progression of Alzheimer’s dementia.

So far, the results are promising. The treatment has not harmed any of the participants who have completed it.

“We are thankful to the patients who have volunteered for this trial,” Mehta said. “They are brave to undergo this procedure, which if proven effective may benefit patients with Alzheimer’s disease in the future.”

Alzheimer’s disease is the nation’s most common form of dementia, and it’s on the rise. The Alzheimer’s Association reports that 5.8 million Americans age 65 and older had Alzheimer’s dementia in 2020. By 2050, that number could rise to 13.8 million.

The focused ultrasound team at RNI is committed to improving the lives of patients with Alzheimer’s disease by pioneering advances using a truly integrated approach and the latest technologies. 

Research reported in this publication was supported by the National Institute of General Medical Sciences, a division of the National Institutes of Health, under Award Number 5U54GM104942-04. This publication does not necessarily reflect the views of NIGMS or NIH.

Featured image: In 2018, WVU launched a first-of-its-kind clinical trial to explore the use of focused ultrasound to open the blood-brain barrier in early-stage Alzheimer’s patients. Since then, WVU researchers have been investigating the treatment’s effects on the brain. A new study by Rashi Mehta—a researcher with the School of Medicine and Rockefeller Neuroscience Institute—finds that focused ultrasound may induce an immunological healing effect in the brains of Alzheimer’s patients. (WVU Photo/Caylie Silveira)


Reference:

Title: Blood-brain barrier opening with MRI-guided focused ultrasound elicits meningeal venous permeability in humans with early Alzheimer disease DOI: https://doi.org/10.1148/radiol.2021200643 Link: https://pubs.rsna.org/doi/10.1148/radiol.2021200643


Provided by WVU today

Harnessing the Power of Proteins in our Cells to Combat Disease (Biology)

UNLV scientist Gary Kleiger at
the forefront of a potential new
drug modality; research
published in the journal Nature.

Over many decades now, traditional drug discovery methods have steadily improved at keeping diseases at bay and cancer in remission. And for the most part, it’s worked well.

But it hasn’t worked perfectly.

A lab on UNLV’s campus has been a hub of activity in recent years, playing a significant role in a new realm of drug discovery — one that could potentially provide a solution for patients who have run out of options.

“It’s starting to get to the point where we’ve kind of taken traditional drug discovery as far as we can, and we really need something new,” said UNLV biochemist Gary Kleiger.

Traditional drug discovery involves what is called the small molecule approach. To attack a protein that’s causing disease in a cancer cell, for instance, a traditional drug has to – in a very targeted way – find that protein and shut down its activities.

It’d be like filling a baseball player’s glove with a bunch of cement.

“The glove gives a baseball player the ability to do his job and catch a baseball,” Kleiger said. “But if we were to take cement, and fill the pocket of the baseball glove with that cement, it would effectively shut down the ability of that baseball player to function on the team. That’s what traditional drugs do.”

There’s a big but, however. Up until this point, traditional drugs have only had the capability to target proteins that are participating in the disease that also have activities that are amenable to the small molecule approach, or, like the baseball player, actively engaging in the sport on the field.

These proteins make up a seemingly small percentage of the disease-causing proteins in our bodies.

So, as you can imagine, Kleiger said, while this model has helped effectively treat HIV and cancer, and helped treat everyday diseases through the use of antibiotics, it has some major setbacks.

“Cancer cells are clever,” Kleiger said. “They can evolve very, very quickly. So, a drug might be working at first – targeting an enzyme and telling that enzyme, ‘stop doing your activity,’ which can stop the cancer cells from growing. Those cancer cells appear to lie dormant, but all the while there are still little things that happen that eventually enable those cancer cells to bypass that drug.” The upshot is that, to stay ahead of cancer’s capacity to evolve drug resistance, we need to be able to target many additional disease-causing proteins, and thus, limiting the landscape of druggable proteins is a serious disadvantage.

There might be a better way, and recent research published in the journal Nature by Kleiger and his collaborator Dr. Brenda Schulman (Max Planck Institute of Biochemistry in Munich, Germany), is helping a consortium of both academic and industry-based researchers who are developing this novel approach.

An ‘unbelievable new playing field’

The new approach uses a family of human enzymes called ubiquitin ligases that exist in human cells. Enzymes are proteins in the cells of the body that speed up chemical reactions occurring at the cellular level and which help your body perform essential functions. There are roughly 20,000 known proteins in the human body, and perhaps some 5-10% are enzymes.

Kleiger first became interested in the ubiquitin protein as a postdoctoral fellow at the California Institute of Technology in the 2000s. At the time, Kleiger heard of a researcher who was working in what was then already appreciated to be an important field but that had yet to fully blossom.

“I didn’t have any idea that the field was going to become this important. I just thought it sounded really cool, and something I wanted to explore,” he said.

Now, nearly 20 years later, Kleiger and colleagues are helping to uncover how ubiquitin ligases work in molecular detail. And this has become especially important, considering that these enzymes are now being employed in a totally novel type of drug discovery modality.

Instead of targeting enzymes that have an active role in the disease – like the baseball player on the field – there might be a way to target practically any protein that has a role in making a person sick. Think of a baseball team manager or the owner, Kleiger said.

“They’re not a part of the team on the field, but they nevertheless can have a huge role to play in making the baseball team work,” he said. “If I want to get rid of that protein, I can’t use the traditional approach.”

That’s where the ubiquitin ligase comes in. In the presence of special new drugs first envisioned by Kleiger’s post-doctoral mentor Dr. Ray Deshaies and his collaborator Dr. Craig Crews, the ubiquitin ligase is now guided to the disease-causing protein to strategically target that protein for degradation, essentially killing it.

“People believe in this new modality, this new therapy so much that every major pharmaceutical company is now at various stages of developing this,” Kleiger said. Indeed, a phase two clinical trial led by the pharmaceutical company Arvinas is already testing the approach in patients for the treatment of prostate cancer. “This would be like the equivalent of you stepping into a batting cage for the old modality, to now being inside of Allegiant Stadium – this is an unbelievable new playing field.”

Why it’s happening now

To do this work effectively, scientists needed to understand the biology of ubiquitin ligases — work that has been going on for less than 30 years, which is a short time in the grand scheme of science and discovery, Kleiger said. And in that time, the technology has gotten sharper and more efficient.

So efficient that for the first time, Kleiger’s collaborators are using new, state-of-the-art cryo electron microscopes to be able to take pictures of what the ubiquitin ligases look like when they’re at work.

“It’s enabling us for the first time to really be able to see how they work, which is going to have huge impacts on the pharmaceutical industry’s ability to make new drug therapies,” Kleiger said. “It’s truly a sea change moment.”

The microscope is able to photograph these enzymes, and in his lab on UNLV’s campus, Kleiger and collaborators use the photographs to hypothesize how the enzymes are working. He then measures the activity of ‘mutated’ enzymes that should now be defective in their activities if their hypothesis is correct.

The work would be similar to a 50,000-year old society being given a picture of a bicycle, and asked to explain how it works.

“They might hypothesize that it’s a bicycle, and that you would use it to ride from point A to point B, or if there was a cart attached, you would use it to transport stuff,” Kleiger said. “You’d then have to test that hypothesis, and that’s what we do at UNLV.”

Kleiger examines the picture, and if it were the bicycle, uncovers that a gear on the bike is very important to its operational ability.

“If you were to bend that gear, now the bike’s not going to work — the chain will just fall off,” Kleiger said. “We can do that at the molecular level with the enzymes.”

His work, in collaboration with colleagues at the Max Planck Institute of Biochemistry and published in the journal Nature, has implications for how diseases will be treated in the future, and could especially be a lifeline for those suffering from diseases beyond cancers such as autoimmune conditions — diseases like rheumatoid arthritis, inflammatory bowel disease, lupus, or multiple sclerosis.

“These are diseases that millions of people around the world suffer from, so that’s one of the reasons why this is such great news,” Kleiger said. “For the first time ever, we’re seeing atomic resolution pictures of the ubiquitin ligase at work, and that’s undoubtedly going to be synergistic with pharmaceutical companies that are creating drugs harnessing the power of the ubiquitin ligase. It really could be a game changer.”

Featured image: Gary Kleiger’s lab on UNLV’s campus has been a hub of activity in recent years, playing a significant role in a new realm of drug discovery — one that could potentially provide a solution for patients who have run out of options. Pictured is a protein complex vital to Kleiger’s recent research published in the journal Nature. © Lonnie Timmons III/UNLV Photo Services


Reference: Horn-Ghetko, D., Krist, D.T., Prabu, J.R. et al. Ubiquitin ligation to F-box protein targets by SCF–RBR E3–E3 super-assembly. Nature 590, 671–676 (2021). https://doi.org/10.1038/s41586-021-03197-9


Provided by University of Nevada Las Vegas

Artificial ‘Brain’ Reveals Why We Can’t Always Believe Our Eyes (Neuroscience)

A computer network closely modelled on part of the human brain is enabling new insights into the way our brains process moving images – and explains some perplexing optical illusions.

It’s very hard to directly measure what’s going on inside the human brain when we perceive motion – even our best medical technology can’t show us the entire system at work. With MotionNet we have complete access.

— Reuben Rideaux

By using decades’ worth of data from human motion perception studies, researchers have trained an artificial neural network to estimate the speed and direction of image sequences.

The new system, called MotionNet, is designed to closely match the motion-processing structures inside a human brain. This has allowed the researchers to explore features of human visual processing that cannot be directly measured in the brain.

Their study, published today in the Journal of Vision, uses the artificial system to describe how space and time information is combined in our brain to produce our perceptions, or misperceptions, of moving images.

The brain can be easily fooled. For instance, if there’s a black spot on the left of a screen, which fades while a black spot appears on the right, we will ‘see’ the spot moving from left to right – this is called ‘phi’ motion. But if the spot that appears on the right is white on a dark background, we ‘see’ the spot moving from right to left, in what is known as ‘reverse-phi’ motion.”

The researchers reproduced reverse-phi motion in the MotionNet system, and found that it made the same mistakes in perception as a human brain – but unlike with a human brain, they could look closely at the artificial system to see why this was happening. They found that neurons are ‘tuned’ to the direction of movement, and in MotionNet, ‘reverse-phi’ was triggering neurons tuned to the direction opposite to the actual movement.

The artificial system also revealed new information about this common illusion: the speed of reverse-phi motion is affected by how far apart the dots are, in the reverse to what would be expected. Dots ‘moving’ at a constant speed appear to move faster if spaced a short distance apart, and more slowly if spaced a longer distance apart.

“We’ve known about reverse-phi motion for a long time, but the new model generated a completely new prediction about how we experience it, which no-one has ever looked at or tested before,” said Dr Reuben Rideaux, a researcher in the University of Cambridge’s Department of Psychology and first author of the study.

Humans are reasonably good at working out the speed and direction of a moving object just by looking at it. It’s how we can catch a ball, estimate depth, or decide if it’s safe to cross the road. We do this by processing the changing patterns of light into a perception of motion – but many aspects of how this happens are still not understood.

“It’s very hard to directly measure what’s going on inside the human brain when we perceive motion – even our best medical technology can’t show us the entire system at work. With MotionNet we have complete access,” said Rideaux.

Thinking things are moving at a different speed than they really are can sometimes have catastrophic consequences. For example, people tend to underestimate how fast they are driving in foggy conditions, because dimmer scenery appears to be moving past more slowly than it really is. The researchers showed in a previous study that neurons in our brain are biased towards slow speeds, so when visibility is low they tend to guess that objects are moving more slowly than they actually are.

Revealing more about the reverse-phi illusion is just one example of the way that MotionNet is providing new insights into how we perceive motion. With confidence that the artificial system is solving visual problems in a very similar way to human brains, the researchers hope to fill in many gaps in current understanding of how this part of our brain works.

Predictions from MotionNet will need to be validated in biological experiments, but the researchers say that knowing which part of the brain to focus on will save a lot of time.

Rideaux and his study co-author Dr Andrew Welchman are part of Cambridge’s Adaptive Brain Lab, where a team of researchers is examining the brain mechanisms underlying our ability to perceive the structure of the world around us. 

This research was supported by the Leverhulme Trust and the Isaac Newton Trust.


Reference: Rideaux, R. & Welchman, A.E.: ‘Exploring and explaining properties of motion processing in biological brains using a neural network.’ Journal of Vision, Feb 2021. DOI: 10.1167/jov.21.2.11


Provided by University of Cambridge

Comet Makes a Pit Stop Near Jupiter’s Asteroids (Planetary Science)

After traveling several billion miles toward the Sun, a wayward young comet-like object orbiting among the giant planets has found a temporary parking place along the way. The object has settled near a family of captured ancient asteroids, called Trojans, that are orbiting the Sun alongside Jupiter. This is the first time a comet-like object has been spotted near the Trojan population.

The unexpected visitor belongs to a class of icy bodies found in space between Jupiter and Neptune. Called “Centaurs,” they become active for the first time when heated as they approach the Sun, and dynamically transition into becoming more comet-like.

Visible-light snapshots by NASA’s Hubble Space Telescope reveal that the vagabond object shows signs of comet activity, such as a tail, outgassing in the form of jets, and an enshrouding coma of dust and gas. Earlier observations by NASA’s Spitzer Space Telescope gave clues to the composition of the comet-like object and the gasses driving its activity.

“Only Hubble could detect active comet-like features this far away at such high detail, and the images clearly show these features, such as a roughly 400,000-mile-long broad tail and high-resolution features near the nucleus due to a coma and jets,” said lead Hubble researcher Bryce Bolin of Caltech in Pasadena, California.

Describing the Centaur’s capture as a rare event, Bolin added, “The visitor had to have come into the orbit of Jupiter at just the right trajectory to have this kind of configuration that gives it the appearance of sharing its orbit with the planet. We’re investigating how it was captured by Jupiter and landed among the Trojans. But we think it could be related to the fact that it had a somewhat close encounter with Jupiter.”

The team’s paper appears in the February 11, 2021 issue of The Astronomical Journal.

The research team’s computer simulations show that the icy object, called P/2019 LD2 (LD2), probably swung close to Jupiter about two years ago. The planet then gravitationally punted the wayward visitor to the Trojan asteroid group’s co-orbital location, leading Jupiter by about 437 million miles.

Video: After traveling several billion miles toward the Sun, a wayward young comet-like object orbiting among the giant planets has found a temporary parking place along the way. The object has settled near a family of captured ancient asteroids, called Trojans, that are orbiting the Sun alongside Jupiter. This is the first time a comet-like object has been spotted near the Trojan population. Credits: NASA

Bucket Brigade

The nomadic object was discovered in early June 2019 by the University of Hawaii’s Asteroid Terrestrial-impact Last Alert System (ATLAS) telescopes located on the extinct volcanoes, one on Mauna Kea and one on Haleakala. Japanese amateur astronomer Seiichi Yoshida tipped off the Hubble team to possible comet activity. The astronomers then scanned archival data from the Zwicky Transient Facility, a wide-field survey conducted at Palomar Observatory in California, and realized that the object was clearly active in images from April 2019.

They followed up with observations from the Apache Point Observatory in New Mexico, which also hinted at the activity. The team observed the comet using Spitzer just days before the observatory’s retirement in January 2020, and identified gas and dust around the comet nucleus. These observations convinced the team to use Hubble to take a closer look. Aided by Hubble’s sharp vision, the researchers identified the tail, coma structure and the size of the dust particles and their ejection velocity. These images helped them confirm that the features are due to relatively new comet-like activity.

Although LD2’s location is surprising, Bolin wonders whether this pit stop could be a common pull-off for some sunward-bound comets. “This could be part of the pathway from our solar system through the Jupiter Trojans to the inner solar system,” he said.

The unexpected guest probably will not stay among the asteroids for very long. Computer simulations show that it will have another close encounter with Jupiter in about another two years. The hefty planet will boot the comet from the system, and it will continue its journey to the inner solar system.

“The cool thing is that you’re actually catching Jupiter flinging this object around and changing its orbital behavior and bringing it into the inner system,” said team member Carey Lisse of the Johns Hopkins University Applied Physics Laboratory (APL) in Laurel, Maryland. “Jupiter controls what’s going on with comets once they get into the inner system by altering their orbits.”

The icy interloper is most likely one of the latest members of the so-called “bucket brigade” of comets to get kicked out of its frigid home in the Kuiper belt and into the giant planet region through interactions with another Kuiper belt object. Located beyond Neptune’s orbit, the Kuiper belt is a haven of icy, leftover debris from our planets’ construction 4.6 billion years ago, containing millions of objects, and occasionally these objects have near misses or collisions that drastically alter their orbits from the Kuiper belt inward into the giant planet region.

The bucket brigade of icy relics endure a bumpy ride during their journey sunward. They bounce gravitationally from one outer planet to the next in a game of celestial pinball before reaching the inner solar system, warming up as they come closer to the Sun. The researchers say the objects spend as much or even more time around the giant planets, gravitationally pulling on them—about 5 million years—than they do crossing into the inner system where we live.

“Inner system, ‘short-period’ comets break up about once a century,” Lisse explained. “So, in order to maintain the number of local comets we see today, we think the bucket brigade has to deliver a new short-period comet about once every 100 years.”

An Early Bloomer

Seeing outgassing activity on a comet 465 million miles away from the Sun (where the intensity of sunlight is 1/25th as strong as on Earth) surprised the researchers. “We were intrigued to see that the comet had just started to become active for the first time so far away from the Sun at distances where water ice is barely starting to sublimate,” said Bolin.

Water remains frozen on a comet until it reaches about 200 million miles from the Sun, where heat from sunlight converts water ice to gas that escapes from the nucleus in the form of jets. So the activity signals that the tail might not be made of water. In fact, observations by Spitzer indicated the presence of carbon monoxide and carbon dioxide gas, which could be driving the creation of the tail and jets seen on the Jupiter-orbiting comet. These volatiles do not need much sunlight to heat their frozen form and convert them to gas.

Once the comet gets kicked out of Jupiter’s orbit and continues its journey, it may meet up with the giant planet again. “Short-period comets like LD2 meet their fate by being thrown into the Sun and totally disintegrating, hitting a planet, or venturing too close to Jupiter once again and getting thrown out of the solar system, which is the usual fate,” Lisse said. “Simulations show that in about 500,000 years, there’s a 90% probability that this object will be ejected from the solar system and become an interstellar comet.”

The Hubble Space Telescope is a project of international cooperation between NASA and ESA (European Space Agency). NASA’s Goddard Space Flight Center in Greenbelt, Maryland, manages the telescope. The Space Telescope Science Institute (STScI) in Baltimore, Maryland, conducts Hubble science operations. STScI is operated for NASA by the Association of Universities for Research in Astronomy, in Washington, D.C. NASA’s Jet Propulsion Laboratory, a division of Caltech in Pasadena, California, managed the Spitzer mission for NASA’s Science Mission Directorate in Washington, D.C. Science operations were conducted at the Spitzer Science Center at IPAC at Caltech. Spitzer’s entire science catalogue is available via the Spitzer data archive, housed at the Infrared Science Archive at IPAC. Spacecraft operations were based at Lockheed Martin Space in Littleton, Colorado.

Featured image: Astronomers found a roaming comet taking a rest stop before possibly continuing its journey. The wayward object made a temporary stop near giant Jupiter. The icy visitor has plenty of company. It has settled near the family of captured asteroids known as Trojans that are co-orbiting the Sun alongside Jupiter. This is the first time a comet-like object has been spotted near the Trojan asteroid population. Hubble Space Telescope observations reveal the vagabond is showing signs of transitioning from a frigid asteroid-like body to an active comet, sprouting a long tail, outgassing jets of material, and enshrouding itself in a coma of dust and gas. Credits: NASA, ESA, and B. Bolin (Caltech)


Reference: Bryce Bolin et al., “Initial Characterization of Active Transitioning Centaur, P/2019 LD2 (ATLAS), Using Hubble, Spitzer, ZTF, Keck, Apache Point Observatory, and GROWTH Visible and Infrared Imaging and Spectroscopy”, Astronomical Journal, 161(3), 2021. https://iopscience.iop.org/article/10.3847/1538-3881/abd94b


Provided by NASA

Researchers Map Metabolic Signaling Machinery For Producing Memory T Cells (Medicine)

Discovery of a metabolic pathways that inhibit memory T cell production has potential for enhancing the immune system’s ability to fight infections and cancers.

Immunologists at St. Jude Children’s Research Hospital have mapped the previously unknown biological machinery by which the immune system generates T cells that kill bacteria, viruses and tumor cells.

The findings have multiple implications for how the adaptive immune system responds to infections to generate such memory T cells. The experiments revealed mechanisms that inhibit development of the long-lived memory T cells that continually renew to protect the body over time. Blocking these inhibitory mechanisms with pharmacological or genetic approaches could boost protective immunity against infection and cancers.

The researchers also discovered a subtype of memory T cells that they named terminal effector prime cells. Mapping the pathway that controls these cells raises the possibility of manipulating this pathway to enhance the ability of the immune system to kill microbes and cancer cells.

Mapping the control pathway also provided the insight that diet may have a greater influence on immune function than previously thought.

Led by Hongbo Chi, Ph.D., of the Department of Immunology, the research appears today in the journal Cell. The first authors are Hongling Huang, Ph.D., and Peipei Zhou, Ph.D., of Immunology.

CRISPR-assisted mapping of the metabolic machinery

When the body encounters an infection, the immune system begins to generate effector T cells to attack the invading bacteria or viruses. There are two types of these T cells. One type is the memory precursor cells, which can develop into memory T cells that persist long-term to protect the body. These are the T cells that vaccinations generate. The second type are short-lived terminal effector T cells, which have immediate cytotoxic activity.

In this study, researchers sought to map the metabolic machinery that controls how the immune system decides to produce memory T cells. Chi and his colleagues focused on the little-known mechanisms that inhibit the generation of this type of T cell.

The scientists used a gene-manipulating technology called CRISPR to sift through more than 3,000 metabolism-controlling genes in mouse cells. The goal was to discover genes that regulated the “fate” of effector T cells and memory T cells.

Nutrients play an unexpected role in T cell fate

The research revealed a previously unknown role that nutrients, such as amino acids and certain sugars, play in regulating T cell fate. To the investigators’ surprise, the analysis identified nutrient-related pathways that suppressed memory T cell production.

“The preconceived notion about nutrients’ role in immune cell function was that the cells rely on nutrients as an energy source and for building blocks,” Huang said. “But our study provides another view—that nutrients are involved in inhibitory pathways, and that deprivation of certain nutrients or metabolites might be good for adaptive immunity.

“It seems to suggest that what you eat and drink may have a greater influence on immune function than previously appreciated,” Huang said. “This will be an important pathway for future research.”

New T cell subtype identified

The studies also revealed a new subtype of effector T cell, which they named terminal effector prime cells. Blocking development of these cells may be key to enhancing T cell-mediated immunity. The researchers’ work identified a pathway that controls the transition of developing T cells from an intermediate stage to mature terminal effector prime cells.

The researchers found they could manipulate this pathway to keep terminal effector prime cells at this intermediate stage that would induce them to proliferate to produce more memory T cells. “These findings highlight the possibility of targeting this pathway to boost protective immunity against both infections and tumors,” Chi said.

“We are extremely excited by these findings,” Chi said. “By identifying this nutrient signaling axis, our studies provide new biological insights and therapeutic targets for enhancing memory T cell responses and protective immunity against pathogens and tumors.”

The other authors are Jun Wei, Lingyun Long, Hao Shi, Yogesh Dhungana, Nicole Chapman, Guotong Fu, Jordy Saravia, Jana Raynor, Shaofeng Liu, Gustavo Palacios, Yong-Dong Wang, Chenxi Qian and Jiyang Yu, of St. Jude.

The research was supported by the National Institutes of Health (AI105887, AI131703, AI140761, CA176624, CA221290) and ALSAC, the St. Jude fundraising and awareness organization.

Featured image: From left: Hongbo Chi, Ph.D., Hongling Huang, Ph.D., and PeiPei Zhou, Ph.D., all of St. Jude Immunology, have mapped the previously unknown biological machinery by which the immune system generates T cells that kill bacteria, viruses and tumor cells.   © St. Jude Children’s Research Hospital


This science news is confirmed by us from St. Jude Children’s Research Hospital


Provided by St. Jude Children’s Research Hospital

Tiny Crustaceans’ Claws Capable of Fastest Repeatable Movements Ever Seen in Marine Animals (Biology)

New research shows that amphipod claws make snapping movements at 100 kilometres per hour and can accelerate nearly as fast as a bullet.

A group of crustaceans called amphipods can accelerate as fast as a bullet—literally, according to a new study by biologists at the University of Alberta and Duke University.

This study shows that a tiny and unusual species is responsible for making the fastest repeatable movements yet known for any animal in water.

“The high speeds of these repeatable movements reach nearly 30 metres per second or more than 100 kilometres per hour,” explained Richard Palmer, professor emeritus in the Department of Biological Sciences and co-author on the study.

“They have the highest accelerations of any animal in water, reaching more than 0.5 million metres per second squared, which is close to the acceleration of a bullet.”

Video: A high-speed video camera captures footage of an amphipod’s claw snapping at 300,000 frames per second. (Video: Sheila Patek, Duke University)

Amphipods are a type of crustacean related to marine beach hoppers and freshwater scuds. Male amphipods use their large claws to make ultra-fast, repeatable snapping motions. The snaps make a popping sound and create rapid water jets that may be used to defend their territory.

“Each new discovery of extreme movements in a novel group of organisms raises fascinating questions about how such extreme adaptations are achieved in terms of biomechanics and functional behaviour, and how they evolved from more common, slower-moving relatives,” said Palmer.

Though faster movements have been seen in other creatures, these movements only happen once and cannot be repeated. As Palmer noted, the mechanism that allows amphipods to create such high-speed movements repeatedly could inspire human engineering efforts.

“This may suggest novel engineering solutions to design and build small structures that can move extremely fast over and over.”

This research was led by Sarah Longo and Sheila Patek at Duke University, in collaboration with Palmer in the U of A’s Faculty of Science. Funding was provided by the Natural Sciences and Engineering Research Council of Canada.

The study, “Tiny snaps of an amphipod push the boundary of ultrafast, repeatable movement,” was published in Current Biology.

Featured image: Amphipods can snap their outsized claws at 100 kilometres an hour. As it snaps shut, the pincer accelerates nearly as fast as a bullet, according to new research. (Photo: Arthur Anker)


Provided by University of Alberta