These results give hope to stroke patients worldwide who may not be able to access clot-dissolving medications within the approved time window, which in China is within 4.5 hours, said the trial’s principal investigator Min Lou, M.D., Ph.D., a professor at the Second Affiliated Hospital of Zhejiang University’s School of Medicine in China.

In the U.S., alteplase is approved to treat stroke within three hours of symptom onset and is recommended for use up to 4.5 hours for select patients. Other research has indicated it may also work well in some patients 4.5 to 9 hours after stroke onset.

The American Heart Association/American Stroke Association 2019 Guidelines for the Early Management of Patients with Acute Ischemic Stroke note that IV alteplase within 4.5 hours of stroke onset is the standard of care for most ischemic stroke patients in the United States.

Researchers enrolled 372 stroke patients whose symptoms began 4.5 hours to 24 hours earlier. They used widely available CT perfusion imaging (advanced brain scanning) to confirm that these patients still had brain tissue that could recover with treatment. Participants were randomly split into two groups — one group received the clot-busting medication alteplase, while the other received standard stroke care of antiplatelet therapy at the discretion of the investigator, based on the Chinese Guidelines for Diagnosis and Treatment of Acute Ischemic Stroke 2018. Functional recovery was assessed at 90 days.

“We believe these findings mean more people may return to normal or near-normal lives after a stroke, even if they receive treatment later than originally thought beneficial,” Lou said. “This method of treatment could become the new standard, especially in hospitals that use CT perfusion imaging. This technology helps health care professionals see how blood flows in different parts of the brain after an ischemic stroke. This could extend treatment eligibility to millions more patients across the globe.”

The study found:

• 40% of participants treated with alteplase had little to no disability after 90 days, compared to 26% of those who received standard care — a 54% higher chance of functional recovery.
• Less than 3% of participants in either group received rescue mechanical clot removal as an additional treatment.
• Rates of death were the same (10.8%) for both groups.
• The risk of brain bleeding was higher among those who received alteplase than among participants who did not (3.8% vs. 0.5%), but researchers believe this is a manageable risk.

“We also need to look more closely at how safe and effective other clot-dissolving medications, like tenecteplase, are when given after a stroke, especially beyond the usual time frames. It’s also important to learn if our findings apply to other groups of people, especially in areas with different stroke risks and health care resources,” Lou explained.

Study limitations include the that both participants and researcher knew which treatment was being given, which could have introduced bias, and results may not be generalizable to patients outside of China.

Study design, background and details:

• The study enrolled 372 stroke patients in a multicenter, prospective, randomized trial at 26 stroke centers in China.
• The patient’s average age was 72 years, and 43% were women.
• The trial used widely available CT perfusion imaging software to gauge salvageable brain tissue, making the findings more applicable to real-world clinical settings.
• Enrolled patients were assigned to the alteplase group or a standard medical treatment group.
• The primary outcome was a score of 0 or 1 on the modified Rankin scale, which scores disability from 0 (no symptoms) to 6 (death) at 90 days.

The Ray Laboratory, led by Department of Biological Sciences Professor and Associate Chair David Ray, as part of a study on bat genomes published by the scientific journal Nature, helped identify the components of a genome in a specific species of bats that have shown more genetic adaptations in their immune systems than other animals.

The study revealed that a gene common in some bats can reduce the production of the SARS-CoV-2 virus by up to 90%, which could help lead to new medical approaches to combating viral diseases.

“Bats have an amazing ability to resist some of the worst effects of viral infection that make us so vulnerable to certain diseases,” Ray said. “While we get very sick, the bats barely blink an eye when exposed to the same pathogens.”

Ray said his laboratory aided in the annotation of the genome assemblies in the bats. Genome annotation is how scientists characterize all component parts of the genome — the genes, regulatory sequences and non-coding and coding regions. The Texas Tech lab identified the transposable element (TE) regions of the assemblies, where bits of DNA can create new copies of themselves and introduce variations within the genome.

Ray said bats have a unique TE repertoire among mammals, presenting a potentially powerful way to generate new genetic pathways to deal with pathogens like the coronavirus.

“If every individual of a species was genetically identical, they would all have the same risk associated with infection — if one dies, they all die,” Ray said. “TEs are a great way for organisms to generate genetic diversity in the species, allowing some individuals to survive better in the face of environmental pressures like viral diseases.”

This study is part of a larger international project called Bat1K, which is attempting to sequence and assemble the genomes of every living bat species, numbering around 1,500, according to Ray. It was led by the Senckenberg Research Institute and Natural History Museum in Frankfurt, Germany.

Michael Hiller, a professor of comparative genomics at the Goethe University and a member of the Senckenberg Institute is one of the main investigators in the study. He and Ray are both members of the executive board for the Bat1K consortium, and their relationship provided the perfect opportunity for Ray’s lab to collaborate with the international scientific community.

The lab studies genomes and genome evolution with an emphasis on TEs. Their past studies have included genome research on bats and other mammals, crocodiles and various insects. The lab has worked with entities in the past such as the National Science Foundation, the U.S. Department of Agriculture, the state of Texas and the Texas Department of Wildlife and Fisheries.

Researchers in this recent study paid particular attention to the ISG15 gene, which is associated with a severe course of COVID-19 in humans. Bats are known to carry numerous viruses, including those transmissible to humans, but do not show any symptoms of disease when infected.

The ISG15 gene from the bats, the study showed, is able to reduce production of the SARS CoV-2 virus by 80-90%. By contrast, the ISG15 gene from a human genome showed no antiviral effect in this study.

“Thus, the ISG15 gene is likely one of several factors that contribute to viral disease resistance in bats,” Hiller said. “These promising results can be used as a basis for further experimental studies, which are necessary to decipher the unique adaptations of the bats’ immune system.”

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.