The timing couldn’t be more critical. With more than a quarter of U.S. homes already fully electric, and solar installations set to triple during the next five years, understanding vulnerabilities has become critical for emergency planning and public safety.

“We’re racing toward electrification to combat climate change, but we must also understand the risks involved,” says Stevens professor Philip Odonkor, who led the research project. “So, what happens to these solar and electric homes when the power goes out?”

Summer strength, winter blues

Odonkor, with recent graduates and AI summer fellows Andrew Majowicz M.Eng. ’24 and Chetan Popli M.S. ’24, set out to answer that question.

In a new study published in the Journal of Smart Cities and Society, they explore the future of electrified American homes by leveraging AI and analyzing Department of Energy (DOE) building-stock data.

The team dug deep into the energy patterns of 129,000 single-family homes across eight states. Their goal? Uncover the hidden energy “signatures” that distinguish fully electrified homes — those powered entirely by electricity — from those that use a mix of energy sources.

They didn’t stop there, however. For identified mixed-energy homes, the team also worked to pinpoint exactly which appliances have made the shifts to electric power and which haven’t.

After processing and analyzing the dataset, Odonkor’s team found that homes’ energy signatures were not only distinguishable, but they also granted critical insights into the resilience of individual homes.

Solar-powered homes, for example, demonstrated impressive resilience during summer heat waves. However, they proved remarkably vulnerable during winter storms; in fact, fully electrified homes were nearly three times more vulnerable to winter outages, compared to those drawing power from mixed energy sources.

“Think about Texas in 2021, when millions lost power during a winter storm,” Odonkor explains. “As more homes go fully electric, we need to prepare for these scenarios.” “Solar panels help in summer, but they can’t meet the intense heating demands that occur during winter blackouts.”

New methods to inform planning and response

The study wasn’t only pathbreaking for its findings; it was only notable for the innovative AI-powered methods that were used to conduct the analyses.

Odonkor’s team developed novel machine-learning models capable of identifying an individual home’s energy systems and vulnerabilities with over 95% accuracy, using only its energy-consumption patterns. The new approach enables utilities and emergency responders to pinpoint at-risk households across entire neighborhoods, without the need for invasive surveys or inspections.

“Until now, we actually had to go door-to-door to determine if a home was fully electric,” notes Odonkor. “Now, we can automatically identify the most vulnerable homes while still safeguarding people’s privacy.” “This will shift the way we prepare for and respond to extreme weather, enabling faster, and more targeted action when it’s needed most.”

The study’s potential benefits extend beyond empowering individual homeowners. As cities work to build climate resilience, these new tools could help community emergency-service units prioritize responses during outages. It could also assist urban planners in the long-term development of more resilient housing stock and neighborhoods.

That’s key, because communities nationwide are grappling with a one-two punch of aging power grids subjected to more frequent episodes of severe weather.

As we increasingly transition to electric homes to cope with climate change, the team’s findings serve as a warning that we will need implement strategies that protect vulnerable solar and electric households during winter emergencies.

“The path to sustainable cities isn’t just about going green; it’s about staying resilient,” he emphasizes. “As we shape the future of urban housing, understanding vulnerabilities isn’t just a luxury — it’s essential to keeping communities safe.”

A new review paper, published in Science on February 7, 2025, highlights these changes and their far-reaching implications. The paper, “Disappearing landscapes: The Arctic at +2.7°C global warming,” was led byJulienne Stroeve, senior research scientist at the National Snow and Ice Data Center (NSIDC) and professor at the Centre for Earth Observation Science at the University of Manitoba.

“The Arctic is warming at four times the rate of the rest of the planet,” said Stroeve. “At 2.7 degrees Celsius of global warming, we will see more extreme and cascading impacts in this region than elsewhere, including sea-ice-free Arctic summers, accelerated melting of the Greenland Ice Sheet, widespread permafrost loss, and more extreme air temperatures. These changes will devastate infrastructure, ecosystems, vulnerable communities, and wildlife.”

In the review paper, the authors used the Sixth Assessment Report of the United Nations Intergovernmental Panel on Climate Change as a starting point. They updated knowledge from the report about three specific areas of the Arctic environment, including sea ice, the Greenland Ice Sheet and permafrost, focusing on existing studies that show consensus about the changes that will take place in the region.

Under 2.7 degrees Celsius of warming, the Arctic region is likely to experience the following effects:

• Virtually every day of the year will have air temperatures exceeding pre-industrial temperature extremes.
• The Arctic Ocean will be free of sea ice for several months each summer.
• The area of the Greenland Ice Sheet that experiences more than a month of surface temperatures above 0 degrees Celsius will quadruple compared with pre-industrial conditions, causing global sea levels to rise faster.
• Surface-level permafrost will decrease by 50 percent of pre-industrial levels.

“Our paper shows that, already today, mankind has the power to wipe out entire landscapes from the surface of our planet,” said Dirk Notz, professor for polar research at the University of Hamburg and co-author of the study. “It’d be amazing if we could become more aware of this power and the responsibility that goes with it, as the future of the Arctic truly lies in our hands.”

Other co-authors on the paper included Jackie Dawson of the University of Ottawa, Edward A.G. Schuur of Northern Arizona University, Dorthe Dahl-Jensen of the University of Manitoba and University of Copenhagen, and Céline Giesse of the University of Hamburg. Funding came from several sources, with the largest piece of Stroeve’s funding from the Canada 150 Research Chairs Program, C150 grant 50296. Data and information from NSIDC’s Sea Ice Today and Ice Sheets Today projects were used in the review.

New research led by the Lippincott-Schwartz Lab shows that a network of subcellular structures similar to those responsible for propagating molecular signals that make muscles contract are also responsible for transmitting signals in the brain that may facilitate learning and memory.

“Einstein said that when he uses his brain, it is like he is using a muscle, and in that respect, there is some parallel here,” says Janelia Senior Group Leader Jennifer Lippincott-Schwartz. “The same machinery is operating in both cases but with different readouts.”

The first clue about the possible connection between brain and muscle cells came when Janelia scientists noticed something strange about the endoplasmic reticulum, or ER — the membranous sheets and folds inside cells that are crucial for many cellular functions.

Lorena Benedetti, a research scientist in the Lippincott-Schwartz Lab, was tracking molecules at high resolution along the surface of the ER in mammalian neurons when she saw that the molecules were tracing a repeating, ladder-like pattern along the entire length of the dendrites — the branch-like extensions on brain cells that receive incoming signals.

Around the same time, Senior Group Leader Stephan Saalfeld alerted Lippincott-Schwartz to high-resolution 3D electron microscopy images of neurons in the fly brain where the ER was also forming regularly spaced, transversal structures.

The ER normally appears like a huge, dynamic net, so as soon as Lippincott-Schwartz saw the structures, she knew her lab needed to figure out what they were for.

“In science, structure is function,” says Lippincott-Schwartz, who also heads Janelia’s 4D Cellular Physiology research area. “This is an unusual, beautiful structure that we are seeing throughout the whole dendrite, so we just had this feeling that it must have some important function.”

The researchers, led by Benedetti, started by looking at the only other area of the body known to have similar, ladder-like ER structures: muscle tissue. In muscle cells, the ER and the plasma membrane — the outer membrane of the cell — meet at periodic contact sites, an arrangement controlled by a molecule called junctophilin.

Using high-resolution imaging, the researchers discovered that dendrites also contain a form of junctophilin that controls contact sites between their ER and plasma membrane. Further, the team found that the same molecular machinery controlling calcium release at muscle cells’ contact sites — where calcium drives muscle contraction — was also present at dendrite contact sites — where calcium regulates neuronal signaling.

Because of these clues, the researchers had a hunch that the molecular machinery at the dendritic contact sites must also be important for transmitting calcium signals, which cells use to communicate. They suspected that the contact sites along the dendrites might act like a repeater on a telegraph machine: receiving, amplifying, and propagating signals over long distances. In neurons, this could explain how signals received at specific sites on dendrites are relayed to the cell body hundreds of micrometers away.

“How that information travels over long distances and how the calcium signal gets specifically amplified was not known,” says Benedetti. “We thought that ER could play that role, and that these regularly distributed contact sites are spatially and temporally localized amplifiers: they can receive this calcium signal, locally amplify this calcium signal, and relay this calcium signal over a distance.”

The researchers found that this process is triggered when a neuronal signal causes calcium to enter the dendrite through voltage-gated ion channel proteins, which are positioned at the contact sites. Although this initial calcium signal dissipates quickly, it triggers the release of additional calcium from the ER at the contact site.

This influx of calcium at the contact site attracts and activates a kinase called CaMKII, a protein known to be important in memory. CaMKII alters the plasma membrane’s biochemical properties, changing the strength of the signal that is passed down the plasma membrane.

This process continues from contact site to contact site all along the dendrite to the cell body, where the neuron decides how it will communicate with other neurons.

The new research reveals a novel mechanism for signal transmission in brain cells and helps answer an open question in neuroscience about how intracellular signals travel over long distances in neurons, enabling information received at specific sites on dendrites to be processed in the brain.

It also sheds light on the molecular mechanisms underlying synaptic plasticity — the strengthening or weakening of neuronal connections that enables learning and memory. Figuring out this process at the molecular level could increase understanding of how the brain works normally and in diseases where these processes go awry, like Alzheimer’s.

“We are showing that a structure — a beautiful structure — operating at a level of subcellular organization is having a huge effect on the way the entire neuronal system is operating vis-à-vis calcium signaling,” Lippincott-Schwartz says. “This is a great example of how, in doing science, if you see a beautiful structure, it can take you into a whole new world.”

Mitochondrial defects, however, are associated with the development of diseases such as type 2 diabetes. Patients who suffer from this disorder are unable to produce enough insulin or use the insulin produced by their pancreas to keep their blood sugar at normal levels.

Several studies have shown that insulin-producing pancreatic β-cells of patients with diabetes have abnormal mitochondria and are unable to generate energy. Yet, these studies were unable to explain why the cells behaved this way.

In a study published in Science, researchers at the University of Michigan used mice to show that dysfunctional mitochondria trigger a response that affects the maturation and function of β-cells.

“We wanted to determine which pathways are important for maintaining proper mitochondrial function,” said Emily M. Walker, Ph.D, a research assistant professor of internal medicine and first author of the study.

To do so, the team damaged three components that are essential for mitochondrial function: their DNA, a pathway used to get rid of damaged mitochondria, and one that maintains a healthy pool of mitochondria in the cell.

“In all three cases, the exact same stress response was turned on, which caused β-cells to become immature, stop making enough insulin, and essentially stop being β-cells,” Walker said.

“Our results demonstrate that the mitochondria can send signals to the nucleus and change the fate of the cell.”

The researchers also confirmed their findings in human pancreatic islet cells.

Mitochondrial dysfunction affects several types of cells

Their results prompted the team to expand their search into other cells that are affected during diabetes.

“Diabetes is a multi-system disease — you gain weight, your liver produces too much sugar and your muscles are affected. That’s why we wanted to look at other tissues as well,” said Scott A. Soleimanpour, M.D., director of the Michigan Diabetes Research Center and senior author of the study.

The team repeated their mouse experiments in liver cells and fat-storing cells and saw that the same stress response was turned on. Both cell types were unable to mature and function properly.

“Although we haven’t tested all possible cell types, we believe that our results could be applicable to all the different tissues that are affected by diabetes,” Soleimanpour said.

Reversing mitochondrial damage could help cure diabetes

Regardless of the cell type, the researchers found that damage to the mitochondria did not cause cell death.

This observation brought up the possibility that if they could reverse the damage, the cells would function normally.

To do so, they used a drug called ISRIB that blocked the stress response. They found that after four weeks, the β-cells regained their ability to control glucose levels in mice.

“Losing your β-cells is the most direct path to getting type 2 diabetes. Through our study we now have an explanation for what might be happening and how we can intervene and fix the root cause,” Soleimanpour said.

The team is working on further dissecting the cellular pathways that are disrupted and hope that they will be able to replicate their results in cell samples from diabetic patients.

Prior to JoVonn Hill’s finding, only three species of Agroecotettixwere known. Hill, director of MSU’s Mississippi Entomological Museum, said the careful examination of our environment remains critical.

“It is important to keep exploring our biodiversity, especially from a conservation standpoint, before we lose it,” Hill said.

These newly uncovered species, native to the southern U.S. and Mexican deserts, showcase the thriving biodiversity in arid ecosystems. Published in the scientific journal ZooKeys, Hill’s article “Desert Diversification: Revision of Agroecotettix Bruner, 1908 (Orthoptera, Acrididae, Melanoplinae) with Descriptions of Sixteen New Species from the United States and Mexico” provides valuable insights into the region’s evolution and ecology. 

Hill, an assistant professor in MSU’s Mississippi Agricultural and Forestry Experiment Station, said this grasshopper genus likely diversified during the Pleistocene Epoch, also known as the Ice Age. He noted that in the Rocky Mountains, species of this subfamily in alpine grasslands likely became isolated as glaciers receded and their habitats shifted to higher elevations. Hill suspects the desert species his team discovered underwent a similar process of isolation and speciation.

“These grasshoppers we described live in a lowland thorny scrub habitat. Somewhere along the line, they, too, got isolated and speciated, because each one is still associated with a specific mountain range,” he said. “Their sexually selective nature and lack of premating rituals have kept populations stable and tied to specific mountain ranges.”

DNA from collected specimens will be sequenced by collaborators at the University of Michigan and will help confirm these observations. Using a molecular clock, Hill’s team will estimate when the species diverged, revealing how past climate change influenced distributions and how future shifts may affect them.

Understanding the past impacts of climate change can also help us prepare for what we may face in the future, Hill said. Plus, it’s a reminder that there’s still so much to discover, even in our own backyard.”

Funded by the National Science Foundation, this project complements two others. In one, Hill and mentor Daniel Otte, a senior curator at the Academy of Natural Sciences, are coauthoring “The North American Grasshoppers, Volume III.”

“These grasshoppers are a part of the Melanoplinae subfamily, which is the most diverse subfamily of North American grasshoppers, and most of our major grasshopper pest species occur in that genus. There are a lot of new species to be discovered, and we’re trying to get them all described before we produce the book,” he said.

The second project, in partnership with Lacey Knowles at the University of Michigan, examines the factors driving Melanoplinae diversity across North America and Mexico by sampling over 600 species.

“That study aims to determine what produced this diversity, when it occurred and how individual populations may have become isolated over time,” Hill said.

“I loved catching grasshoppers as a kid, and I still get to do it now — discovering new things, uncovering their history and understanding how they’re related,” the MSU researcher said. “Sharing this fascinating piece of American natural heritage makes it all worthwhile.”

Collaborators include Vilas Brown, Brady Dunaway, Ray Fisher, Mallory Grady, Alexandra Hendon, Jennifer Seltzer, Jacqueline Seltzer-Hill, Rowan Seltzer-Hill and Matthew Thorn. Funding partners include the NSF, Texas Ecolab, the National Institute of Food and Agriculture and MAFES.

Searching for subtypes of immune cells seen only in the most serious, grade 4 brain tumors, called glioblastomas, and using a recently developed technology called spatial genomics, the researchers found that glioblastoma stem cells were co-localized with a type of immunosuppressive cell called myeloid-derived suppressor cell (MDSC), and that these two cells symbiotically feed off of each other to promote tumor growth and aggressiveness. A description of the work was published Jan. 17 in the journal Science. “Tumor stem cells represent only 5% to 10% of the tumor, but they’re the critical cells that are renewing and generating the rest of the tumor and are essentially responsible for the aggressiveness of the tumor,” says senior study author Drew Pardoll, M.D., Ph.D., the Martin D. Abeloff Professor of Cancer Research , co-director of the Mark Foundation Center for Advanced Genomics and Imaging, and director of the Bloomberg~Kimmel Institute for Cancer Immunotherapy. “We found that the myeloid-derived suppressor cells and tumor stem cells literally were in the same place — a region described by pathologists in the 1980s as the pseudopalisading region. There was a very intimate connection.”

To better characterize the cellular components of brain cancer, investigators performed single-cell RNA sequencing on tissue samples from 33 types of brain tumors spanning from low to high grade, finding two populations of MDSCs in IDH-WT glioblastoma. Then, using a technique called spatial transcriptomics to look at patterns of gene expression of over 750,000 immune cells and more than 350,000 tumor and associated cells in these samples, they found MDSCs were co-located with the tumor stem cells.

“Glioblastoma is a highly aggressive brain tumor with remarkable ability to evade the immune system, which has made immune-based therapies largely ineffective to this point,” said first and co-corresponding author, Christina Jackson, M.D., an assistant professor of neurosurgery at the Perelman School of Medicine at the University of Pennsylvania, who was at Johns Hopkins at the time the research was conducted. “Our study revealed a distinct subset of immune cells, known as myeloid-derived suppressor cells that promote glioblastoma growth, providing new insights into how the tumor interacts with the immune system. By identifying these cells and their role, we hope to uncover new therapeutic targets andlay the groundwork for more effective treatments.”

In their studies, investigators discovered that the two types of cells were feeding each other in the brain tumors. Tumor stem cells were producing chemical signals called chemokines that attracted the MDSCs, and making growth factors and activation factors for the MDSCs. In turn, the MDSCs were producing growth factors for the tumor cells.

The researchers were able to further ascertain what specific molecules tumor stem cells were producing to attract and activate MDSCs. Two of the key ones identified by the team were IL (interleukin)-6 and IL-8, which play a role in inflammatory responses, and for which MDSCs have receptors.

“IL-8 is one of the major attractants to bring the MDSCs to the tumor, and IL-6 is one of the major activators of the MDSCs,” Pardoll says.

On the flip side, the team found that MDSCs secreted a growth factor called fibroblast growth factor 11 (FGF11) to feed the stem cells, a molecule never before known to be involved in brain or other cancers.

Along the way, Jackson, Pardoll and colleagues found that tumors with a mutation in the IDH1 gene, which are less aggressive, had almost no MDSCs and far fewer cancer stem cells. This led them to look across all brain cancers at the correlation between MDSC infiltration and survival. Using the National Cancer Institute’s Cancer Genome Atlas (TCGA) database of cancer samples, they indeed found that very tight correlation — the fewer cancer stem cells and fewer MDSCs a person had in their tumors, the better they did.

While additional studies are needed to further understand these cellular interactions, the work is exciting in that it suggests additional potential targets to block in treatment of these aggressive brain tumors, Pardoll says. For example, Jamie Spangler, Ph.D., an associate professor of biomedical engineering at Johns Hopkins, has developed an investigational bispecific antibody that binds to the receptors for IL-6 and IL-8, blocking their signaling.

Study co-authors were Christopher Cherry, Sadhana Bom, Arbor Dykema, Rulin Wang, Elizabeth Thompson, Ming Zhang, Runzhe Li, Zhicheng Ji, Wenpin Hou, Wentao Zhan, Hao Zhang, John Choi, Ajay Vaghasia, Landon Hansen, Kate Jones, Fausto Rodriguez, Jon Weingart, Calixto-Hope Lucas, Jonathan Powell, Jennifer Elisseeff, Srinivasan Yegnasubramanian, Chetan Bettegowda and Hongkai Ji of Johns Hopkins. Other researchers contributing to the work were from Stanford University School of Medicine in California.

The research was supported by the National Institutes of Health (grants #F32NS108580, #R01HG010889, R01HG009518, RA37CA230400, U07CA230691), the Neurosurgery Research Education Foundation, the Bloomberg~Kimmel Institute for Cancer Immunotherapy, the Mark Foundation for Cancer Research, a Burroughs Wellcome Career Award for Medical Scientists, the Commonwealth Foundation, the Maryland Cigarette Restitution Fund and the NIH Pioneer Award.

Bettegowda is a consultant for Bionaut Labs, Privo Technologies, Haystack Oncology and Depuy-Synthes. He also is a co-founder of OrisDx and Belay Diagnostics. Yegnasubramanian has received grant support through Johns Hopkins from Bristol Myers Squibb and Janssen and grants and personal fees from Cepheid. He is a co-founder of Digital Harmonic and Brahm Astra Therapeutics. Elisseeff is founder of Aegeria Soft Tissue. Powell is an employee of Calico but was not when this research was performed. Pardoll is a consultant for Amgen, Arcturus Therapeutics, ATengen, Bristol Myers Squibb, Compugen, Dragonfly Therapeutics, Immunomic Therapeutics, Normunity, PathAI, RAPT Therapeutics, Regeneron, Takeda Pharmaceuticals and Tizona. He has received grant support through Bristol Myers Squibb, Compugen, Enara Bio and Immunomic Therapeutics, and owns stock in Dracen Pharmaceuticals, Dragonfly Therapeutics, Enara Bio, RAPT Therapeutics and Tizona. Pardoll is on the board of directors of Clasp Therapeutics and Dracen Pharmaceuticals and has patent royalties with Bristol Myers Squibb and Immunomic Therapeutics. These relationships are managed by The Johns Hopkins University in accordance with its conflict-of-interest policies.

In reality, research has shown that human bodily responses and cognitive shifts affect each other in both directions. We feel sorry because we cry, but also cry when feeling sorry. So how then for our primate cousins? To date, their connections have remained largely unexplored.

Now a team of researchers at Kyoto University has led a study on six Japanese macaques living in KyotoU’s Center for the Evolutionary Origins of Human Behavior, in Aichi prefecture. The researchers focused on self-scratching — a bodily response linked to negative emotions like anxiety and fear — and its relationship to pessimistic judgment bias, which is the tendency to expect a negative outcome when faced with ambiguous information.

By presenting the monkeys with a white rewarding button and a black non-rewarding button, together with a gray ambiguous button, the researchers were able to estimate each monkey’s degree of pessimism. They also videoed the monkeys to identify the timing of self-scratching, analyzing the relationship between self-scratching and pessimism.

“Bodily responses associated with negative emotions can predict subsequent cognitive pessimism,” says corresponding author Sakumi Iki, “but not the other way around.”

In other words, the monkeys were more likely to make pessimistic judgments — avoiding the gray button — immediately after self-scratching, yet making a pessimistic judgment did not necessarily lead to self-scratching. This stands in contrast to humans, for whom evidence suggests a pessimistic way of thinking can cause bodily responses. That this influence did not appear in the macaques suggests that their emotional bodily responses may precede cognitive changes.

From an evolutionary standpoint, the coping strategy of first addressing immediate needs through bodily responses and then engaging in cognitive information processing is probably adaptive for dealing with challenges in natural habitats. Thus, this mechanism might have existed long before humans and macaques diverged, pointing to an evolutionarily conserved system.

“In humans, the relationship between mind and body may have evolved in a distinctive way, influenced by our use of language and advanced introspection,” adds Iki.

“But it might be observable in monkeys if different bodily reactions or cognitive processes are examined.”

Future research involving a wider range of primates and other animals could shed more light on the evolutionary origins of human emotions, and deepen our understanding of the connection between the mind and the body.

However, satellite measurements of the flow speed of ice streams show that such simulations are inaccurate and have shortcomings to correctly reflect reality. This leads to considerable uncertainties in estimates of how much mass the ice streams are losing and how quickly and how high sea levels will rise.

Ice streams both judder and flow

Now, a team of researchers led by ETH professor Andreas Fichtner has made an unexpected discovery: deep within the ice streams, there are countless weak quakes taking place that trigger one another and propagate over distances of hundreds of metres. This discovery helps to explain the discrepancy between current simulations of ice streams and satellite measurements, and the new findings should also impact the way ice streams are simulated in the future.

“The assumption that ice streams only flow like viscous honey is no longer tenable. They also move with a constant stick-slip motion,” says Fichtner. The ETH professor is confident that this finding will be integrated into simulations of ice streams, making estimates of changes in sea level more accurate.

Riddles relating to ice cores resolved

Moreover, the ice quakes explain the origin of numerous fault planes between ice crystals in ice cores obtained from great depths. These fault planes are the result of tectonic shifts and have been known to scientists for decades, although no explanation had been found for them until now.

“The fact that we’ve now discovered these ice quakes is a key step towards gaining a better understanding of the deformation of ice streams on small scales,” explains Olaf Eisen, Professor at the Alfred Wegener Institute and one of the study’s co-authors.

The study by this international research team led by ETH Zurich has just been published in the journal Science and also involved researchers from the Alfred Wegener Institute, Helmholtz Centre for Polar and Marine Research (AWI), the University of Strasbourg, the Niels Bohr Institute (NBI), the Swiss Federal Institute WSL and other universities.

Fire and ice are related

The fact that these ice quakes cannot be observed at the surface and have therefore remained undiscovered until now is due to a layer of volcanic particles located 900 metres below the surface of the ice. This layer stops the quakes from propagating to the surface. Analysis of the ice core showed that these volcanic particles originate from a massive eruption of Mount Mazama in what is now Oregon (USA) some 7,700 years ago. “We were astonished by this previously unknown relationship between the dynamics of an ice stream and volcanic eruptions,” Fichtner recalls.

The ETH professor also noticed that the ice quakes start from impurities in the ice. These impurities are also leftovers from volcanoes: tiny traces of sulphates that entered the atmosphere in volcanic eruptions and flew halfway around the world before being deposited on the Greenland ice sheet in snowfall. These sulphates reduce the stability of the ice and favour the formation of microfissures.

A 2,700-metre borehole in the ice

The researchers discovered the ice quakes using a fibre-optic cable that was inserted into a 2,700-metre-deep borehole and recorded seismic data from inside a massive ice stream for the first time. This borehole was drilled into the ice by researchers from the East Greenland Ice-core Project (EastGRIP), led by the Niels Bohr Institute and strongly supported by the Alfred Wegener Institute, resulting in the extraction of a 2,700-metre-long ice core. Once drilling work was complete, the researchers took the opportunity to lower a fibre-optic cable 1,500 metres into the borehole and record signals from inside the ice stream continuously for 14 hours.

The research station and borehole are located on the North East Greenland Ice Stream (NEGIS), around 400 kilometres from the coast. The NEGIS is the biggest ice stream of the Greenland ice sheet, whose retreat is a large contributor to current rising sea levels. In the area of the research station, the ice is moving towards the sea at a speed of around 50 metres per year.

As ice quakes occur frequently over a wide area in the researchers’ measurements, ETH researcher Fichtner believes it is also plausible that they occur in ice streams everywhere, all the time. To verify this, however, it will be necessary to take seismic measurements of this kind in other boreholes — and there are already plans to do just that.