The study, published Nov. 5 in Science Advances, reported the results of administering arginine, which can be delivered in oral form, prior to standard radiation therapy in 31 patients who had brain metastases. Nearly 78 percent had a complete or partial response in their brain tumors over the follow-up period of up to four years, while only 22 percent of the 32 patients who received a placebo prior to radiotherapy had such a response.

The trial was designed to gauge the effectiveness of arginine as a “radiosensitizer” that enhances the effects of radiation treatment. However, the results, and arginine’s apparent mechanism of action, suggest that the amino acid might be useful more broadly as an anticancer therapy.

“Based on these findings we should continue to investigate arginine in combination with radiotherapy but also in combination with chemotherapy or immunotherapy, and even arginine on its own,” said senior author Dr. Leandro Cerchietti, an associate professor of medicine in the Division of Hematology and Medical Oncology, who participated in designing and implementing the trial at Angel H. Roffo Cancer Institute in Argentina where he was an attending oncologist. The trial was co-led by Dr. Alfredo Navigante at the Roffo Cancer Institute.

Arginine, also called L-arginine, is inexpensive and widely available, generally considered safe, and can get relatively easily from the bloodstream into the brain. The idea of using it to treat cancer arose from observations that tumors often aid their own survival by producing high levels of the related molecule nitric oxide (NO). The latter regulates multiple processes in the body including the flow of blood through blood vessels, and tumors cells often make more NO by upregulating their production of special enzymes called NO synthases, which synthesize NO from arginine.

Reducing NO production is one possible way of exploiting tumors’ dependence on this molecule, but hasn’t worked well, in part because of adverse side effects. The investigators hypothesized that boosting NO production instead — by adding its precursor arginine — might be beneficial, because while tumors can use NO to aid their growth and survival, they must keep its production below certain limits.

“Nitric oxide is a reactive molecule that on its own, or through other reactive molecules derived from it, can stress and damage a cell — so a cell can tolerate only so much of it,” said study lead author Dr. Rossella Marullo, an instructor in medicine in the Division of Hematology and Medical Oncology at Weill Cornell Medicine.

Overloading a high-NO tumor with much more NO prior to radiation treatment could weaken the tumor’s ability to repair radiation-induced DNA damage, she added — and indeed her preclinical experiments in mice confirmed this effect.

In the clinical trial, patients were treated with high-dose arginine or placebo oral suspensions an hour before radiotherapy for their brain metastases — tumors in the brain that represent the spread from primary tumors elsewhere, such as the lungs.

Six months after their courses of radiotherapy, 82 percent of the arginine group had improvement, or at least no worsening, of their neurological symptoms, compared with 20 percent in the placebo group. Most of the arginine-treated patients who died during the study did so because of their cancers’ spread elsewhere in the body.

Moreover, although metastatic cancer usually has a dire prognosis, there were some arginine-treated patients whose tumors in and outside the brain disappeared, suggesting the possibility of cures.

Evidence from this study and prior research also suggests that arginine can not only directly hobble tumor cells but also boost the activity of antitumor immune cells, Dr. Cerchietti said.

The promising results have prompted the team to start and plan further studies of arginine on its own or in combination with other anticancer treatments.

“In principle any tumor that overexpresses NO-producing enzymes would be vulnerable to arginine treatment — and such tumors are very common,” said Dr. Cerchietti, who is also a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. He cautions that further studies are needed and patients should consult their doctor about the use of any supplements outside of a clinical trial. The doses of arginine used in this study are available in formulations that can be only obtained at a medical facility.

Researchers at Indiana University School of Medicine have been investigating how these immune cells in the brain — microglia — relate to a gene mutation recently found in Alzheimer’s disease patients. They published their findings today in Science Advances.

The study, led by Hande Karahan, PhD, postdoctoral fellow in medical and molecular genetics, and Jungsu Kim, PhD, the P. Michael Conneally Professor of Medical and Molecular Genetics, found that deleting the gene — called ABI3 — significantly increased amyloid-beta plaque accumulation in the brain and decreased the amount of microglia around the plaques.

“This study can provide further insight into understanding the key functions of microglia contributing to the disease and help identify new therapeutic targets,” Karahan said. Karahan based her research on a human genetics study of more than 85,000 people — fewer than half were Alzheimer’s patients — that identified the mutation in the ABI3 gene. Researchers concluded this mutation increased the risk of late-onset Alzheimer’s.

“However, there was no investigation into the function of ABI3 gene in the brain or about how this gene affects microglia function,” Karahan said, a fact that led to her research. The team deleted the ABI3 gene from an Alzheimer’s disease mouse model and tested the functions of the gene in microglia in cell cultures. In the mouse model, they saw increased levels of plaques and inflammation in the brain and signs of synaptic dysfunction — characteristics associated with learning and memory deficits of the disease.

Additionally, Karahan said the deletion of the gene impaired the movement of microglia. The immune cells cannot move closer to plaques to try to clear up the proteins. Amyloid plaques are commonly found in the brains of patients with Alzheimer’s; amyloid beta proteins clump together and form plaques, which destroy nerve cell connections.

“Our study provides the first in vivo functional evidence that the loss of ABI3 function may increase the risk of developing Alzheimer’s disease by affecting amyloid beta accumulation and neuroinflammation,” Karahan said.

Over the past few years, Karahan has been building upon her Alzheimer’s disease research. In 2019, Karahan received the Sarah Roush Memorial Fellowship in Alzheimer’s Disease Research, established by the Indiana Alzheimer’s Disease Research Center and funded through a generous donation from James and Nancy Carpenter and a matching contribution from Stark Neurosciences Research Institute, where Karahan conducts her research.

Karahan and Kim received three separate grants supporting this research from the National Institute on Aging, the National Institutes of Health (NIH) branch for Alzheimer’s research, resulting in $7.8 million over the next five years.

“One grant will fund the creation of a mouse model that will allow us to delete the ABI3 gene in any cell types in the body, such as brain microglia and peripheral immune cells,” Kim said. “Once we validate this new model, we will make it available to others in the research community to use this model for their own investigations.”

The other grants will fund additional mouse and cell models for the team to further investigate how the ABI3 gene in microglia affects Alzheimer’s disease pathologies as well as fund state-of-the-art techniques, including brain imaging using the Bruker BioSpec 9.4T PET-MRI scanner, located in the Roberts Translational Imaging Facility at Stark Neurosciences Research Institute.

Each of these projects has an end goal of identifying druggable targets for the treatment of the disease, Karahan and Kim said. The team will collaborate with the IU School of Medicine-Purdue TaRget Enablement to Accelerate Therapy Development for Alzheimer’s Disease (TREAT-AD) Center.

These environments include an atom’s nucleus and celestial bodies known as neutron stars, both of which are among the densest objects known to humanity. For comparison, matching the density of a neutron star would require squeezing all the Earth’s mass into a space about the size of Spartan Stadium.

Brown’s theory laid the blueprints for connecting the properties of nuclei to neutron stars, but building that bridge with experiments would be challenging. It would take years and the unique capabilities of the Thomas Jefferson National Accelerator Facility. The facility, also known as Jefferson Lab, is a U.S. Department of Energy Office of Science, or DOE-SC, national laboratory in Virginia. So experimentalists got to work on a decades-long series of studies and Brown largely returned to his other projects.

That is, until 2017. That’s when he said he started thinking about the beautiful precision experiments run by his colleague Kei Minamisono’s group at the National Superconducting Cyclotron Laboratory, or NSCL, and in the near-future at the Facility for Rare Isotope Beams, or FRIB. FRIB is a DOE-SC user facility at MSU that will start scientific user operation in early 2022.

“It’s amazing how new ideas come to you,” said Brown, a professor of physics at FRIB and in MSU’s Department of Physics and Astronomy.

The goal of this new idea was the same as his earlier theory, but it could be tested using what are known as “mirror nuclei” to provide a faster and simpler path to that destination.

In fact, on Oct. 29, the team published a paper in the journal Physical Review Letters based on data from an experiment that took a few days to run. This comes on the heels of new data from the Jefferson Lab experiments that took years to acquire.

“It’s quite incredible,” Brown said. “You can do experiments that take a few years to run and experiments that take a few days and get results that are very similar.”

To be clear, the experiments in Michigan and Virginia are not competing. Rather, Krishna Kumar, a member and past chair of the Jefferson Lab Users Organization, called the experiments “wonderfully complementary.”

“A detailed comparison of these measurements will allow us to test our assumptions and increase the robustness of connecting the physics of the very small — nuclei — to the physics of the very large — neutron stars,” said Kumar, who is also the Gluckstern Professor of Physics at the University of Massachusetts Amherst. “The progress made in both experiment and theory on this broad topic underscores the importance and uniqueness of the capabilities of Jefferson Lab and NSCL, and the future will bring more such examples as new measurements are carried out at FRIB.”

These projects also underscore the importance of theorists and experimentalists working together, especially when tackling fundamental mysteries of the universe. It was this type of collaboration that kicked off the Jefferson Lab’s experiments 20 years ago, and it’s this type of collaboration that will power future discoveries at FRIB.

A mirror to examine the neutron skin

One of the ironies here is that Brown hasn’t spent a lot of his time working on the two theories central to this story. Brown has published more than 800 scientific papers during his career, and the ones that inspired the experiments at NSCL and Jefferson Lab are distinct from his other work.

“I work on many things and these are very isolated papers,” Brown said. Despite that, Brown shared them quickly. “I wrote both papers in a couple months.”

When Brown completed the draft of his 2017 theory, he immediately shared it with Minamisono.

“I remember I was at a conference when I got the email from Alex,” said Minamisono, a senior physicist at FRIB. “I was so excited when I read that paper.”

The excitement came from Minamisono’s knowledge that his team could lead the experiments to test the paper’s ideas and from the theory’s implications for the cosmos.

“This connects to neutron stars and that is so exciting as an experimentalist,” Minamisono said.

Neutron stars are more massive than our sun, yet they’re only about as big as Manhattan Island. Researchers can make accurate measurements for the mass of neutron stars, but getting exact numbers for their diameters is challenging.

A better understanding of the push and pull of forces inside neutron stars would improve these size estimates, which is where nuclear physics comes in.

A neutron star is born when a very large star becomes a supernova and explodes, leaving behind a core that is still more massive than our sun. The gravity of this massive leftover causes it to collapse on itself. As it collapses, the star also begins converting its matter — the stuff that makes it up — into neutrons. Hence, “neutron star.”

There’s a force between the neutrons, known as the strong interaction, that works against gravity and helps puts the brakes on the collapse. This force is also in action in atomic nuclei, which are made up of neutrons and particles known as protons.

“We know gravity, of course. There’s no issue there,” Brown said. “But we’re not so sure about what the strong interaction is for pure neutrons. There’s no laboratory on the Earth that has pure neutrons, so we make inferences from things we see in nuclei that have both protons and neutrons.”

In atomic nuclei, the neutrons stick out a teensy bit, forming a thin, neutron-only layer that extends beyond the protons. This is called the neutron skin. Measuring the neutron skin enables researchers to learn about the strong force and, by extension, neutron stars.

In the Jefferson Lab experiments, researchers sent electrons hurtling at lead and calcium nuclei. Based on how the electrons scatter or deflect from the nuclei, scientists could calculate upper and lower limits for the size of the neutron skin.

For the NSCL experiments, the team needed to measure how much room the protons take up in a specific nickel nucleus. This is called the charge radius. In particular, the team examined the charge radius for nickel-54, a nickel nuclei or isotope with 26 neutrons. (All nickel isotopes have 28 protons, and those with 26 neutrons are called nickel-54 because the two numbers add up to 54.)

What’s special about nickel-54 is that scientists already know the charge radius of its mirror nucleus, iron-54, an iron nucleus with 26 protons and 28 neutrons.

“One nucleus has 28 protons and 26 neutrons. For the other, it’s flipped,” said Skyy Pineda, a lead author on the new research paper and a graduate student researcher on Minamisono’s team. By subtracting the charge radii, the researchers effectively remove the protons and are left with that thin neutron layer.

“If you take the difference of the charge radii of the two nuclei, the result is the neutron skin,” Pineda said.

To measure the charge radius of nickel-54, the team turned to its Beam Cooler and Laser Spectroscopy facility, abbreviated BECOLA. Using BECOLA, experimentalists overlap a beam of nickel-54 isotopes with a beam of laser light. Based on how the light interacts with the isotope beam, the Spartans can measure the nickel’s charge radius, Pineda said.

Using Brown’s earlier theory, Jefferson Lab scientists needed on the order of a sextillion electrons for a measurement, or a trillion billion particles. Using the new theory, researchers instead need thousands, maybe millions of nuclei. That means that measurements that once required years can be replaced with experiments that take days.

A future of discovery built on a history of teamwork

This new research feels like the passing of a baton in a couple ways. For one, the Jefferson Lab experiments are entering their final phase, while FRIB stands poised to continue the exploration.

FRIB itself represents another leg of the relay. BECOLA started running at NSCL and will continue operating at FRIB.

Each leg builds on the last and on the collective work the runners have put in together.

Again, that formula is nothing new. It’s what enabled a theorist at NSCL to inspire and inform experiments at a world-class lab in Virginia. What stands out about NSCL and FRIB, however, is that the user facilities are connected to a university, letting veterans and the next generation of leaders interact and share ideas that much sooner.

“MSU is unique in having had NSCL and now FRIB. In most cases, labs like these aren’t integrated into a university campus,” said Kristian Koenig, a postdoctoral researcher on Minamisono’s team and a co-lead author on the new paper. “It gives everyone here a great opportunity.”

Joining the MSU team on the Physical Review Letters publication were researchers from Florida State University along with the Technical University of Darmstadt and the GSI Helmholtz Center for Heavy Ion Research in Germany.

This work is supported in part by the National Science Foundation Grant No. PHY-14-30152, PHY-15-65546, PHY-18-11855, PHY-21-10365 and PHY-21-11185, the DOE-SC under Award No. DE-FG02-92ER40750, and German Research Foundation Project ID 279384907 SFB 1245.

NSCL is a national user facility funded by the National Science Foundation, supporting the mission of the Nuclear Physics program in the NSF Physics Division.

Michigan State University (MSU) operates the Facility for Rare Isotope Beams (FRIB) as a user facility for the U.S. Department of Energy Office of Science (DOE-SC), supporting the mission of the DOE-SC Office of Nuclear Physics. FRIB is funded by DOE-SC, MSU, and the State of Michigan, with user facility operation supported by the DOE-SC Office of Nuclear Physics.

Thomas Jefferson National Accelerator Facility (Jefferson Lab) is a U.S. Department of Energy Office of Science (DOE-SC) national laboratory. Jefferson Science Associates, LLC, manages and operates Jefferson Lab for the DOE-SC.

“This research extends our information about glatiramer acetate’s potential use in Alzheimer’s disease,” said M. Kerry O’Banion, M.D., Ph.D., professor of Neuroscience and senior author of the study. “This isn’t a cure, but it could be a step in the right direction for a treatment to slow the symptoms of this debilitating disease.”

Using a mouse model, researchers found changes in microglia — part of the brain’s immune system — and improvements in cognitive behavior when glatiramer acetate was used. These changes were associated with less amyloid plaques and modifications to tau pathology — a protein found in neurodegenerative diseases — in the brain, indicating that molecular hallmarks of Alzheimer’s disease had been impacted. Previous studies have found that glatiramer acetate can alter brain pathology in Alzheimer’s disease mouse models, but the exact mechanisms that are impacted in the brain are still unknown.

“Overall, these findings provide further evidence that therapies that modify the immune system could be effective in the treatment of Alzheimer’s disease,” said Dawling Dionisio-Santos, Ph.D., a first-year resident in Neurology and graduate of the Medical Scientist Training Program and co-first author on the paper. “It adds evidence to support trials that test the use of glatiramer acetate in patients at risk for developing Alzheimer’s.”

Co-authors on this paper include Berke Karaahmet, Elizabeth K. Belcher, Ph.D., Laura D. Owlett, Ph.D., Lee A. Trojanczyk, and John A. Olschowka, Ph.D. The research was funded by the National Institute on Aging.

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Materials provided by University of Rochester Medical Center. Original written by Kelsie Smith Hayduk. Note: Content may be edited for style and length.

Since the coronavirus pandemic began in early 2020, several more-infectious variants of SARS-CoV-2, the virus that causes COVID-19, have emerged. The original, or wild-type, virus was followed by the alpha variant, which became widespread in the United States in early 2021, and subsequently the delta variant, which is the most prevalent strain circulating today. The variants have acquired mutations that help them infect people and spread more easily. Many of the mutations affect the spike protein, which the virus uses to get into cells. Scientists have been trying to understand how these changes alter the virus’s function.

“Throughout the pandemic, NIDCR researchers have applied their expertise in the oral health sciences to answer key questions about COVID-19,” said NIDCR Director Rena D’Souza, D.D.S., Ph.D. “This study offers fresh insights into the greater infectivity of the alpha and delta variants and provides a framework for the development of future therapies.”

The outer surface of SARS-CoV-2 is decorated with spike proteins, which the virus uses to attach to and enter cells. Before this can happen, though, the spike protein must be activated by a series of cuts, or cleavages, by host proteins, starting with the furin enzyme. In the alpha and delta variants, mutations to the spike protein appear to enhance furin cleavage, which is thought to make the virus more effective at entering cells.

Studies have shown that in some cases protein cleavage can be decreased by the addition of bulky sugar molecules — a process carried out by enzymes called GALNTs — next to the cleavage site. Ten Hagen’s team wondered if this happens to the SARS-CoV-2 spike protein, and, if so, whether it changes the protein’s function.

To find out, the scientists studied the effects of GALNT activity on spike protein in fruit fly and mammalian cells. The experiments showed that one enzyme, GALNT1, adds sugars to wild-type spike protein, and this activity reduces furin cleavage. By contrast, mutations to the spike protein, like those in the alpha and delta variants, decrease GALNT1 activity and increase furin cleavage. This suggested that GALNT1 activity may partially suppress furin cleavage in wild-type virus, and that the alpha and delta mutations overcome this effect, allowing furin cleavage to go unchecked.

Further experiments supported this idea. The researchers expressed either wild-type or mutated spike in cells grown in a dish. They observed the cells’ tendency to fuse with their neighbors, a behavior that may facilitate spread of the virus during infection. The scientists found that cells expressing mutated spike protein fused with neighbors more often than cells with the wild-type spike. Cells with wild-type spike also fused less often in the presence of GALNT1, suggesting that its activity may limit spike protein function.

“Our findings indicate that the alpha and delta mutations overcome the dampening effect of GALNT1 activity, which may enhance the virus’s ability to get into cells,” said Ten Hagen.

To see if this process might also occur in people, the team analyzed RNA expression in cells from healthy volunteers. The researchers found wide expression of GALNT1 in lower and upper respiratory tract cells that are susceptible to SARS-CoV-2 infection, indicating that the enzyme could influence infection in humans. The scientists theorized that individual differences in GALNT1 expression could affect virus spread.

“This study suggests that GALNT1 activity may modulate viral infectivity and provides insight into how mutations in the alpha and delta variants may influence this,” Ten Hagen said. The knowledge could inform future efforts to develop new interventions.

This research was supported by the NIDCR Division of Intramural Research. Support also came from the intramural program of the National Institute of Environmental Health Sciences.

Inflammation is a natural and vital response of our immune system to danger signals and tissue damage. Inflammatory processes help the body to eliminate the triggers, for example bacteria, and to initiate repair mechanisms. Terminating this inflammatory reaction quickly and in a coordinated manner is just as important, however, as otherwise there is a risk of developing chronic inflammatory conditions such as rheumatoid arthritis or Crohn’s disease. One of the important factors for resolving the inflammatory reaction is the elimination of damaged and dead cells, a process that was not very well understood until now. New inflammation can occur if these cells are allowed to accumulate.

How waste from inflammation is disposed of

A research team led by Prof. Gerhard Krönke at the Department of Medicine 3 — Rheumatology and Immunology at Universitätsklinikum Erlangen has now succeeded in gaining a better understanding of the fundamental molecular mechanisms involved. The researchers investigated the function of macrophages at the site where inflammation occurs. These cells are capable of ingesting large quantities of cellular waste and digesting and eliminating the molecular components of this waste in their mitochondria, also referred to as the powerhouse of the cell.

The scientists were able to demonstrate that the danger signal interleukin 33, which is released from damaged cells, triggers lasting changes to the metabolism of macrophages, so that their waste disposal capacity significantly increases. The sheer quantity of waste produced during the inflammatory reaction places the mitochondria under severe strain, and they produce increased quantities of damaging oxygen radicals as a result. Interleukin 33 regulates the function of the mitochondria by initiating a process known as uncoupling in these cell components and protecting them from overloading. ‘This enables the macrophages to ‘let off steam’ and carry on ingesting waste without interruption despite the heavy strain placed upon them, resolving the inflammation processes as a result,’ explains Maria Faas, lead author of the article recently published in the journal ‘Immunity’.

Protection of mitochondria as a new approach for therapy for inflammation

The findings of the FAU team could pave the way for new approaches for treating chronic inflammatory conditions. ‘It may be possible to accelerate and support the resolution of inflammatory processes in the long term by influencing the cell metabolism of the macrophages and deliberately uncoupling their mitochondria,’ explains Prof. Gerhard Krönke. Interestingly, substances that positively influence the cell metabolism of macrophages have already been discovered. However, they have not yet been approved for use in chronic inflammatory conditions and must undergo further clinical trials. The investigations and experiments were conducted as part of the DFG collaborative research centre CRC 1181 ‘Switching points for resolving inflammation’ and the DFG research group FOR2886 PANDORA (Pathways triggering Autoimmunity and Defining Onset of early Rheumatoid Arthritis). Maria Faas also received a scholarship as part of the DFG research training group 1660 (Key signals of adaptive immune response).

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Materials provided by Friedrich-Alexander-Universität Erlangen-Nürnberg. Note: Content may be edited for style and length.

In a paper published recently in Nature Communications, the authors, including experts from China’s Tsinghua University, the Carnegie Institution for Science and Caltech, said that most of the current electricity demand in advanced, industrialized nations can be met by some combination of wind and solar power. But that positive finding comes with the caveat that extra efforts are going to be necessary to completely satisfy the countries’ requirements.

Most reliable systems, which are dominated by wind power, are capable of meeting electricity requirements in the countries studied 72 to 91 percent of the time, even without energy storage, according to the study. With the addition of 12 hours of energy storage capacity, systems become dominated by solar power and can satisfy demand 83 to 94 percent of hours.

“Wind and solar could meet more than 80 percent of demand in many places without crazy amounts of storage or excess generating capacity, which is the critical point,” said co-author Steve Davis, UCI professor of Earth system science. “But depending on the country, there may be many multi-day periods throughout the year when some demand will need to be met by energy storage and other non-fossil energy sources in a zero-carbon future.”

The team analyzed 39 years’ worth of hourly energy demand data from 42 major countries to evaluate the adequacy of wind and solar power resources to serve their needs. They found that a full conversion to sustainable power resources can be easier for larger, lower-latitude countries, which can rely on solar power availability throughout the year.

The researchers highlighted Germany as an example of a relatively smaller country, in terms of land mass, at higher latitude which will make it more challenging to meet its electricity needs with wind and solar resources.

“Historic data show that countries that are farther from the equator can occasionally experience periods called ‘dark doldrums’ during which there is very limited solar and wind power availability,” said lead author Dan Tong, assistant professor of Earth system science at Tsinghua University. “One recent occurrence of this phenomenon in Germany lasted for two weeks, forcing Germans to resort to dispatchable generation, which in many cases is provided by fossil fuel-burning plants.”

Among the approaches the researchers suggested to alleviate this problem are a building up generating capacity that exceeds annual demand, developing long-term storage capabilities and pooling resources of multiple nations on a continental land mass.

“Europe provides a good example,” said Tong, who began her work on this study as a post-doctoral scholar in UCI’s Department of Earth System Science. “A lot of consistency and reliability could be provided by a system that includes solar resources from Spain, Italy and Greece with bountiful wind available in the Netherlands, Denmark and the Baltic region.”

The researchers found that a wind and solar power system could provide about 85 percent of the total electricity demand of the United States, and that amount could also be increased through capacity overbuilding, addition of batteries and other storage methods, and connecting with other national partners on the North American continent.

“Around the world, there are some definite geophysical constraints on our ability to produce net-zero carbon electricity,” said Davis. “It comes down to the difference between the difficult and the impossible. It will be hard to completely eliminate fossil fuels from our power generation mix, but we can achieve that goal when technologies, economics and socio-political will are aligned.”

Dissipationless electric energy transport — also known as superconductivity — is seen as a beacon of hope for the energy industry. Since its discovery more than 100 years ago, scientists around the world have been investigating this well-known quantum phenomenon, which, however, requires the electrons in metals to be cooled to ultra-low temperatures. A team of scientists from the Cluster of Excellence ct.qmat-Complexity and Topology in Quantum Matter at the Universities of Dresden and Würzburg has now made a remarkable discovery: In certain superconducting metals, a compound of four electrons ensures that a completely new state of matter is created. Until now, only electron pairs were known to play a role in superconductivity. The discovery by the research team led by Prof. Hans-Henning Klauss of Technische Universität Dresden is therefore considered a milestone for materials research. The research results have been published in the journal Nature Physics.

Electron family surprises researchers

In quantum physics, superconductivity, discovered as early as in 1911, is probably the best-known phenomenon to date. Its theoretical foundations are understood since the 1950s. It is essential that electrons at ultra-low temperatures no longer move through a metal individually, but as pairs. Electron pairs do not collide with the atomic lattice, so that they can transport their charge without any loss of energy.

When the Dresden researchers led by Henning Klauss experimentally investigated the superconducting metal Ba_1-xK_xFe₂As₂ from the class of iron pnictides, they initially suspected a mistake: “When we discovered that suddenly four electrons instead of two were forming a bond, we first believed it was a measurement error. But the more methods we used to confirm the result, the clearer it became that this had to be a new phenomenon: all data are consistent with the same result. Now we know that the four particle electron family in certain metals creates a completely new state of matter when cooled to ultra-low temperatures. What this will lead to in the future will become clear over the next few years,” comments Dresden physicist Hans-Henning Klauss.

Results tested for more than two years

Already about ten years ago, it was theoretically predicted that there could be an unusual state of matter in certain superconducting metals, in which four instead of two electrons play a role. The international research team of the Cluster of Excellence ct.qmat has now provided the first experimental evidence. It was scrutinized for two years using seven different methods.

“We first discovered the new state of matter in a Swiss particle accelerator. We were then able to confirm our results with six other methods on site in Dresden and at Stockholm University. The great location advantage of Dresden is the short distances: I can bring my sample almost on foot to a Leibniz Institute or Helmholz Center,” emphasizes the project’s lead experimenter, Dr. Vadim Grinenko of TU Dresden. The theoretical interpretation of the measurement results comes from the Swedish physicist Prof. Egor Babaev.

New type of superconductivity possible

The discovery of iron pnictides as a class of materials particularly suitable for superconductivity already triggered a worldwide research boom in physics and materials science starting in 2008. The energy industry has high hopes for the popular quantum phenomenon because up to 15 percent of energy is lost in conventional energy transport due to transport resistance. “If you could actually transport electricity across the country in superconducting metals at room temperature, about ten large power plants would be superfluous right away,” says Klauss. However, basic research — such as Prof. Klauss’ — is concerned with understanding the underlying physics and can at best speculate about future applications.

“One can assume that our results will lead to a whole new line of research, looking for other metals with four connected electrons, for example, or exploring how materials need to be changed to create an electron family,” Klauss explains. “In purely theoretical terms, a whole new type of superconductivity would also be possible with our electron family. The only thing that is certain is that iron pnictides are well suited for technologies such as quantum sensors due to their new aggregate state.”

International participation

In addition to Prof. Hans-Henning Klauss, Dr. Vadim Grinenko of TU Dresden and Prof. Egor Babaev of the Royal Institute of Technology in Stockholm were significantly involved in the current research findings. The experiments were carried out at the Swiss Paul Scherrer Institute in Villigen as well as at the Leibniz Institute for Solid State and Materials Research in Dresden, the high-field magnet laboratory of the Helmholtz Center Dresden-Rossendorf and the AIST Institute in Tsukuba in Japan.