A weak version of this effect has been observed in modern particle accelerators, but it is completely absent from our daily lives or even normal laboratory environments.

Yuli Lyanda-Geller, professor of physics and astronomy in the College of Science at Purdue University, in collaboration with Aydin Keser and Oleg Sushkov from the University of New South Wales in Australia, discovered that it is possible to produce this effect in a class of novel materials involving bismuth, its solid solutions with antimony and tantalum arsenide.

With this knowledge, the effect can be studied, potentially leading to vastly more sensitive sensors as well as supercapacitors for energy storage that could be turned on and off by a controlled magnetic field.

“Most importantly, one of the deepest quantum mysteries in the universe can be tested and studied in a small laboratory experiment,” Lyanda-Geller said. “With these materials, we can study effects of the universe. We can study what happens in neutron stars from our laboratories.”

Brief summary of methods

Keser, Lyanda-Geller and Sushkov applied quantum field theory nonperturbative methods used to describe high-energy particles and expanded them to analyze the behavior of so-called Dirac materials, which recently became the focus of interest. They used the expansion to obtain results that go both beyond known high-energy results and the general framework of condensed matter and materials physics. They suggested various experimental configurations with applied electric and magnetic fields and analyzed best materials that would allow them to experimentally study this quantum electrodynamic effect in a nonaccelerator setting.

They subsequently discovered that their results better explained some magnetic phenomena that had been observed and studied in earlier experiments.

Funding

U.S. Department of Energy, Office of Basic Energy Sciences; Division of Materials Sciences and Engineering; and the Australian Research Council, Centre of Excellence in Future Low Energy Electronics Technologies

Story Source:

Materials provided by Purdue University. Original written by Brittany Steff. Note: Content may be edited for style and length.

The introduction of non-native species poses challenges to native species, including competition for resources and habitat, exposure to diseases carried by the introduced species and the risk of hybridization, which occurs naturally in wild populations as part of the evolutionary process.

The Oregon State research, just published in the journal Frontiers in Environmental Science, focused on two species: bull trout, a fish native to western North America that is protected under the Endangered Species Act; and brook trout, a native to eastern North America introduced in the West more than 100 years ago for recreational fishing purposes.

Bull trout were once abundant in Oregon, Washington, California, Nevada, Idaho and Montana but today are found in less than half of their historic range, and no longer exist in California. They are threatened by habitat degradation and fragmentation, blockage of migratory corridors, poor water quality, the effects of climate change and fisheries management practices, including the introduction of brook trout.

While some studies have documented hybridization among bull and brook trout, there has not been enough research to allow natural resource managers to quantify hybridization risk, the Oregon State researchers said.

“The goal was to come up with a tool that allows managers to look at the potential long-term impacts when they are planning restoration or conservation projects,” said Michael Manning, the lead author of the paper who worked on the research as an Oregon State graduate student.

The researchers developed a hybridization risk model, which could also be applied to other species that hybridize in freshwaters, such as cutthroat or rainbow trout and coho and chinook salmon.

Guillermo Giannico, a freshwater fish ecologist and a co-author of the paper, compared the model to programs people use when deciding where to live.

“In that case, there is this algorithm that combines information about distance to the nearest supermarket, cost of living, where the schools are,” he said. “This risk model we created is roughly the same. It tells you whether this is a good neighborhood for fish based on the gradient of the stream, the substrate at the bottom of the stream, the temperature of the water, how much the water discharge changes through the year.”

In Oregon, 55% of bull trout habitat is in the northeastern part of the state within the John Day and Powder/Burnt River basins. Additional bull trout habitats are located in the Malheur/Owyhee, Klamath, Deschutes, Willamette Valley and Columbia River drainage basins.

The researchers studied 47 sub-basins, a U.S. Geological Survey term for a subsection of a river drainage area. Sub-basins encompass an average area of about 1,125 square miles. Of the sub-basins they studied, 11 had only bull trout, 16 had only brook trout and 20 had both species.

In Oregon, brook trout are present in 9.8% (120 miles) of bull trout spawning habitat. The model showed that an additional 57 miles of bull trout spawning habitat would be at extreme hybridization risk if brook trout were introduced in those areas.

The model also identified 13% (177 miles) of all bull trout spawning habitat as being in the moderate to extreme hybridization risk category. Of these 177 miles, 90% are in northeastern Oregon.

The researchers note that the model is valuable because of its ability to identify hybridization risks in small sections of streams (to the 100-meter scale) whether brook trout already exist in bull trout spawning habitat or are absent.

This level of detail allows natural resource managers to identify individual reaches of streams that might be candidates for brook trout removal, to model potential hybridization risk if bull trout are reintroduced, or to incorporate scenarios of brook trout introductions or expansion, they said.

Other co-authors of the paper are Ivan Arismendi and J. Andres Olivos, both of the Department of Fisheries, Wildlife, and Conservation Science in Oregon State’s College of Agricultural Sciences.

A new study calculates that exposure to car exhaust from leaded gas during childhood stole a collective 824 million IQ points from more than 170 million Americans alive today, about half the population of the United States.

The findings, from Aaron Reuben, a PhD candidate in clinical psychology at Duke University, and colleagues at Florida State University, suggest that Americans born before 1996 may now be at greater risk for lead-related health problems, such as faster aging of the brain. Leaded gas for cars was banned in the U.S. in 1996, but the researchers say that anyone born before the end of that era, and especially those at the peak of its use in the 1960s and 1970s, had concerningly high lead exposures as children.

The team’s paper appeared the week of March 7 in the journal Proceedings of the National Academy of Sciences.

Lead is neurotoxic and can erode brain cells after it enters the body. As such, there is no safe level of exposure at any point in life, health experts say. Young children are especially vulnerable to lead’s ability to impair brain development and lower cognitive ability. Unfortunately, no matter what age, our brains are ill-equipped for keeping it at bay.

“Lead is able to reach the bloodstream once it’s inhaled as dust, or ingested, or consumed in water,” Reuben said. “In the bloodstream, it’s able to pass into the brain through the blood-brain barrier, which is quite good at keeping a lot of toxicants and pathogens out of the brain, but not all of them.”

One major way lead used to invade bloodstreams was through automotive exhaust.

To answer the complex question of how leaded gas use for more than 70 years may have left a permanent mark on human health, Reuben and his co-authors Michael McFarland and Mathew Hauer, both professors of sociology at Florida State University, opted for a fairly simple strategy.

Using publicly available data on U.S. childhood blood-lead levels, leaded-gas use, and population statistics, they determined the likely lifelong burden of lead exposure carried by every American alive in 2015. From this data, they estimated lead’s assault on our intelligence by calculating IQ points lost from leaded gas exposure as a proxy for its harmful impact on public health.

The researchers were stunned by the results.

“I frankly was shocked,” McFarland said. “And when I look at the numbers, I’m still shocked even though I’m prepared for it.”

As of 2015, more than 170 million Americans (more than half of the U.S. population) had clinically concerning levels of lead in their blood when they were children, likely resulting in lower IQs and putting them at higher risk for other long-term health impairments, such as reduced brain size, greater likelihood of mental illness, and increased cardiovascular disease in adulthood.

Leaded gasoline consumption rose rapidly in the early 1960s and peaked in the 1970s. As a result, Reuben and his colleagues found that essentially everyone born during those two decades are all but guaranteed to have been exposed to pernicious levels of lead from car exhaust.

Even more startling was lead’s toll on intelligence: childhood lead exposure may have blunted America’s cumulative IQ score by an estimated 824 million points — nearly three points per person on average. The researchers calculated that at its worst, people born in the mid-to-late 1960s may have lost up to six IQ points, and children registering the highest levels of lead in their blood, eight times the current minimum level to initiate clinical concern, fared even worse, potentially losing more than seven IQ points on average.

Dropping a few IQ points may seem negligible, but the authors note that these changes are dramatic enough to potentially shift people with below-average cognitive ability (IQ score less than 85) to being classified as having an intellectual disability (IQ score below 70).

Moving forward, McFarland is analyzing the racial disparities of childhood lead exposure, hoping to highlight the health inequities suffered by Black children, who were exposed more often to lead and in greater quantities than white children.

Reuben’s next step will be to examine the long-term consequences of past lead exposure on brain health in old age, based on previous findings that adults with high childhood lead exposure may experience accelerated brain aging.

“Millions of us are walking around with a history of lead exposure,” Reuben said. “It’s not like you got into a car accident and had a rotator cuff tear that heals and then you’re fine. It appears to be an insult carried in the body in different ways that we’re still trying to understand but that can have implications for life.”

The study, published Feb. 8 in Nature Communications, details the precise molecular structure of the multiple sclerosis drug siponimod as it interacts with its target, the human S1P receptor 1 (S1P1), and off-target receptors using a cutting-edge electron microscopy technique called cryo-EM. This knowledge could help scientists develop drugs for the disease that are less likely to miss their targets.

“This discovery will help us improve drugs for multiple sclerosis and reduce their side effects,” said the study’s co-senior author Dr. Xin-Yun Huang, professor of physiology and biophysics at Weill Cornell Medicine.

In patients with multiple sclerosis, immune cells called lymphocytes attack and destroy the protective sheath around nerve cells, causing progressive neurologic symptoms. Scientists developed immune-suppressing drugs that block the release of these lymphocytes from the lymph nodes by binding to S1P1 receptors. But the first-generation version of these drugs could also bind to related receptors including S1P3, which caused unwanted side effects including an abnormal heart rhythm. To address this problem, scientists created next-generation medications like siponimod that bind more selectively to S1P1 and another receptor called S1P5. But this didn’t eliminate all unwanted side effects.

The new study, co-led by Dr. Shian Liu, a research associate at Weill Cornell Medicine, and Navid Paknejad, a graduate student at Memorial Sloan Kettering, reveals how siponimod binds to these two receptors and the features of the molecule that prevent it from binding to unwanted targets like S1P2, S1P3 and S1P4. Scientists can use this information to modify the drug to help it attach more tightly to its target (S1P1) and less likely to bind with unintended target (S1P5), reducing the risk of side effects.

“This new structural information will help us develop the next generation of multiple sclerosis drugs,” Dr. Huang said.

The study also helps explain how naturally occurring lipids can regulate the immune system, the nervous system and lung function. The team found that nearly identical lipids called sphingosine 1-phosphate and lysophosphatidic acid assumed very different shapes when bound to their target receptors.

“Lipids are highly plastic molecules, and the structures reveal how the receptors leverage subtle differences in the lipids structures to discriminate between them,” said co-senior author Dr. Richard Hite, a structural biologist at Memorial Sloan Kettering and an assistant professor in the biochemistry and structural biology and the physiology, biophysics and systems biology programs at the Weill Cornell Graduate School of Medical Sciences.

“This explains how lipids can play very different roles in the body even though their chemical structures are very similar,” Dr. Huang said.

The finding highlights the importance of carefully designing lipid-based drugs to prevent them from missing their targets. “We need to make lipid-based drugs that are very specific to reduce the risk of side effects,” he said.

These new insights may help scientists develop improved treatments for other autoimmune diseases like inflammatory bowel disease, psoriasis and systemic lupus. They might also help scientists create lipid-based therapies for conditions that affect the brain or lungs. For example, Dr. Huang noted that there are currently lipid-based drugs in clinical trials to reduce lung stiffening in patients with COVID-19.

Story Source:

Materials provided by Weill Cornell Medicine. Note: Content may be edited for style and length.

In a new study published in Conservation Science and Practice, New England Aquarium scientists reviewed marine mammal sightings to gain a better understanding of habitat use along the U.S. East Coast. The research team used North Atlantic Right Whale Consortium data from aerial and boat surveys conducted by 49 organizations between 1979 and 2020 to calculate marine mammal species diversity in the North Atlantic Ocean between Florida and Nova Scotia, Canada. The data set contained 189,175 sightings of more than 1 million animals from 30 unique species or species groupings.

High species diversity occurred more frequently in the northern part of the Atlantic Coast, particularly around the Monument, on the edge of the continental shelf, and across the Gulf of Maine and Georges Bank, they found. “It was very exciting to see these results,” said Brooke C. Hodge, the study’s lead author and Associate Scientist in the Spatial Ecology, Mapping, and Assessment (EcoMap) Program for the Anderson Cabot Center for Ocean Life at the New England Aquarium.. “Our research shows us that the Monument is diverse compared to the East Coast. It is clearly well-sited and protects a unique and diverse marine mammal community.”

Last October, the Biden-Harris Administration reinstated the Monument’s federal protection status, which had been removed by the previous administration. The nearly 5,000-square mile underwater sanctuary is located 130 miles southeast of Cape Cod and is home to vibrant deep-sea ecosystems that include coral reefs, fish, and endangered whales. In 2016, Aquarium scientists provided strong scientific evidence that helped the Monument’s initial designation under President Obama. In 2021, Aquarium scientists explored the consequences of removing protections from the Monument and demonstrated that opening the Monument to fishing increased the risk of entanglement, bycatch, and habitat destruction for species from the sea surface to sea floor.

In this study, scientists found that species diversity was highest in the northern and mid-Atlantic regions with steep continental shelf edges. Canyons and areas with high salinity and low temperatures also had a high diversity of marine mammals. “Well designed and effectively managed marine protected areas can lead to conservation success,” Hodge said. In the study, the authors wrote: “Our analyses contribute to efforts to designate MPAs (marine protected areas) to conserve habitat that is important for protecting species by identifying drivers of biodiversity and potential sites for protecting 30 percent of the plant by 2030.” The Biden-Harris Administration aims to protect 30 percent of federal U.S. lands and waters by 2030.

“Identifying MPAs in our study area is critical because U.S. East Coast waters face intensive human use from fishing, shipping, planned wind energy development, and features that support marine mammal foraging are subject to specific threats,” researchers wrote in the study. “The Gulf of Maine is one of the most rapidly warming marine ecosystems in the world, and evidence of changes in productivity have already been observed. Designating MPAs and establishing effective management measures to meet the goal of protecting areas of particular importance to biodiversity are needed to protect marine mammals and the ecosystems on which they depend.” However, the authors acknowledge that further research is needed to more fully characterize marine mammal species diversity in these areas and to assess the biodiversity of the full wildlife community and the habitat, such as seabirds, deep-self invertebrates, deep-sea corals, sponges, and fish.

The study’s coauthors include several New England Aquarium scientists: Daniel E. Pendleton, Research Scientist; Laura C. Ganley, Postdoctoral Associate Research Scientist; Orfhlaith “Orla” O’Brien, Associate Scientist; Scott D. Kraus, Emeritus Scientist; and Jessica V. Redfern, Senior Scientist and Chair of the Spatial Ecology, Mapping, and Assessment Program. Ester Quintana-Rizzo of Simmons University also contributed to the research.

Story Source:

Materials provided by New England Aquarium. Note: Content may be edited for style and length.

“Each of these diseases has a unique protein tangle, or fibril, associated with it,” said Anthony Fitzpatrick, PhD, principal investigator at Columbia’s Zuckerman Institute. “These proteins associated with diseases have their own shapes and behaviors,” added Dr. Fitzpatrick, also an assistant professor of biochemistry and molecular biophysics at Columbia University Irving Medical Center and a member of Columbia’s Taub Institute for Research on Alzheimer’s Disease and the Aging Brain.

Published today in Cell, the research by Dr. Fitzpatrick and an international team of 22 collaborators reveals a new fibril in diseased brains, one formed by a protein normally busy cleaning cells.

“We have a surprising and provocative result that we hope could have some bearing on managing neurodegenerative diseases,” said undergraduate Andrew Chang, a co-first author on the paper in the Fitzpatrick lab. Drug researchers have long pursued the tangle-forming proteins as targets for new medicines, but this pursuit so far has largely delivered disappointing results.

Fibril-associated diseases, some common and some rare, collectively affect millions of people around the world. Their incidence is slated to increase as the population grows and people live longer. Untangling what is going on in these neurodegenerative diseases has a personal facet for Dr. Fitzpatrick: He lost an uncle to one of them, progressive supranuclear palsy (PSP).

“We have found that a protein called TMEM106B can form fibrils, and this behavior was not known before,” said Xinyu Xiang, formerly a member of the Fitzpatrick lab at the Zuckerman Institute and now a graduate student at Stanford University’s Department of Structural Biology. “This protein is a core component of lysosomes and endosomes, which are organelles that clean up the junk that builds up in our cells as we get older.”

Normally, TMEM106B molecules span the membranes of those waste-management organelles. In a feat of laboratory sleuthing, Fitzpatrick’s team discovered that TMEM106B molecules can split into two fragments. Fragments inside the organelles can then self-assemble into what the researchers suspect could be cell-hobbling fibrils.

To make this discovery, the researchers first extracted proteins from brain tissue donated by 11 patients who had died from three neurodegenerative diseases associated with misfolded proteins: PSP, dementia with Lewy bodies (DLB) and frontotemporal lobar degeneration (FTLD). FTLD is the most prevalent form of dementia for those under 60 years of age.

“It’s so motivating to remember that the only way we can do this research is because of people who generously donated their brains,” said Marija Simjanoska, a co-first author and one of the three undergraduates working on the project.

Co-corresponding author Ian Mackenzie, MD, of the University of British Columbia, and co-authors Dennis Dickson, MD, and Leonard Pertrocelli, PhD, of the Mayo Clinic in Florida, helped procure this precious research resource. Joining Drs. Fitzpatrick and Mackenzie as co-corresponding authors on the paper is Michael Stowell, PhD, of the University of Colorado, Boulder. Filling out the 23-member team are researchers from several other institutions, including three in Belgium.

With a world-class cryogenic electron microscope (cryo-EM), the team took snapshots of individual protein molecules at many different angles. From these, the researchers constructed three-dimensional models of the protein in atomic detail. Those models, in turn, helped the researchers identify TMEM106B by making educated guesses about the exact sequence of the protein’s amino-acid building blocks. Much in the way letters string into words with specific meanings, different amino-acid molecules build into proteins, each with its own shape and function.

The researchers fully expected that one of the long-known fibril-forming proteins, such as the tau protein in Alzheimer’s disease, would end up matching with the models from the cryo-EM data. Instead, the matching exercise, which involved searching in a massive database of protein sequences, delivered a head-turning result.

The researchers found that the mysterious protein matched a 135-amino-acid fragment of TMEM106B. That was an exciting revelation because this same protein was identified more than a decade ago in a broad hunt for genes potentially associated with FTLD.

So far, the data in hand shows only that TMEM106B fibrils are present in diseased brain tissue, not that the fibrils cause the diseases. Still, Dr. Fitzpatrick points out, the prevalence of TMEM106B fibrils in tissue from different brain diseases, combined with the protein’s normal place in lysosomes and endosomes, points toward a possible disease-causing role.

In their Cell paper, the researchers speculate that the formation of TMEM106B fibrils disrupts lysosome function, which, in turn, promotes the formation of fibrils made of the other known fibril-forming proteins. These malfunctions could kill brain cells, leading to dementia, movement problems, speech pathologies and other symptoms of Alzheimer’s, PSP, FTLD and other brain diseases with telltale protein tangles.

“We now have a promising new lead,” said Dr. Fitzpatrick. “It could point towards a common thread linking a range of neurodegenerative diseases and could open the way to new interventions.”

This work was supported by the National Institutes of Health (NIH)/National Institute of Neurological Disorder and Stroke (UO1NS110438, U54NS110435); the Association for Frontotemporal Degeneration; Canadian Institutes of Health Research (74580); and MCDB Neurodegenerative Disease Fund.

Black holes are some of the most mystifying objects in our universe, largely due to the fact that their inner-workings are hidden behind a completely obscuring veil — the black hole’s event horizon.

In 1974, Stephen Hawking added more mystique to the character of black holes by showing that, once quantum effects are considered, a black hole isn’t really black at all but, instead, emits radiation, as if it was a hot body, gradually losing mass in the so-called “Hawking evaporation process.” Further, Hawking’s calculations showed that the emitted radiation is quantum mechanically entangled with the bowels of the black hole itself. This entanglement is the quantum signature of the Hawking effect. This astounding result is difficult, if not impossible, to be tested on astrophysical black holes, since the faint Hawking radiation gets overshined by other sources of radiation in the cosmos.

On the other hand, in the 1980’s, a seminal article by William Unruh established that the spontaneous production of entangled Hawking particles occurs in any system that can support an effective event horizon. Such systems generally fall under the umbrella of “analog gravity systems” and opened a window for testing Hawking’s ideas in the laboratory.

Serious experimental investigations into analog gravity systems — made of Bose-Einstein condensates, non-linear optical fibers, or even flowing water — have been underway for more than a decade. Stimulated and spontaneously-generated Hawking radiation has recently been observed in several platforms, but measuring entanglement has proved elusive due to its faint and fragile character.

“We show that, by illuminating the horizon, or horizons, with appropriately chosen quantum states, one can amplify the production of entanglement in Hawking’s process in a tunable manner,” said Associate Professor Ivan Agullo. “As an example, we apply these ideas to the concrete case of a pair of analog white-black holes sharing an interior and produced within a non-linear optical material.”

“Many of the quantum information tools used in this research were from my graduate research with Professor Jonathan P. Dowling,” said 2021 PhD alumnus Anthony Brady, postdoctoral researcher at the University of Arizona. “Jon was a charismatic character, and he brought his charisma and unconventionality into his science, as well as his advising. He encouraged me to work on eccentric ideas, like analog black holes, and see if I could meld techniques from various fields of physics — like quantum information and analog gravity — in order to produce something novel, or ‘cute,’ as he liked to say.”

“The Hawking process is one of the richest physical phenomena connecting seemingly unrelated fields of physics from the quantum theory to thermodynamics and relativity,” said Dimitrios Kranas, LSU graduate student. “Analog black holes came to add an extra flavor to the effect providing us, at the same time, with the exciting possibility of testing it in the laboratory. Our detailed numerical analysis allows us to probe new features of the Hawking process, helping us understand better the similarities and differences between astrophysical and analog black holes.”

Story Source:

Materials provided by Louisiana State University. Note: Content may be edited for style and length.