Californians are familiar with landslides that occur around storms, when saturated soil and rock loses its grip and slips from its perch on the substrate. These types of landslides can be triggered by intense rainfall, and incoming storms can be a warning that neighborhoods need to evacuate.

Landslides that happen during the hot, dry summers, though, tend to take people by surprise. In July 2023, for example, a landslide seemed to come out of nowhere to devastate a neighborhood in Rolling Hills Estates, located on the northern side of the Palos Verdes Peninsula in Los Angeles County.

Now, landslide researchers at UCLA and NASA’s Jet Propulsion Laboratory, or JPL, have published a paper in Geophysical Research Letters that shows that the 2023 Rolling Hills Estates event was a slow-moving, progressive landslide that began the winter before, when unusually heavy rainfall infiltrated into the slope and reduced its strength. The researchers used satellite data to measure minute shifts in the surface of the affected area before, during and after the slide and concluded that this method could be used to detect future landslides before they become catastrophic.

“Movement on the Palos Verdes Peninsula’s Portuguese Bend Landslide has been recorded since the late 1950s,” said paper co-author Alexander Handwerger, a research scientist at UCLA’s Joint Institute for Regional Earth System Science & Engineering and JPL. “But there was no discernible movement in this region of the nearby Rolling Hills Estates before 2023. People began reporting movement, as indicated by cracks in houses, in April 2023, which matches our observations. There was initial slow movement that accelerated progressively, culminating in complete collapse several months later.”

The study, led by UCLA postdoctoral researcher Xiang Li, used satellite radar and optical data taken over Los Angeles every few weeks to measure ground motion over time. The satellite radar data for Rolling Hills Estates from 2016 to July 2023 revealed that after very slight movement during the 2019 rainy season, the ground remained stable until heavy winter rainfall, starting in December 2022, kickstarted movement in February. By June, the area had moved 0.04 meters, or about 1.6 inches, and on July 8 — a sunny, dry day preceded by 40 dry days — around 10 meters, or 33 feet, of horizontal motion occurred, destroying 12 homes.

The likely reason for the delay between initial movement in February and complete failure in July is that it took time for increased instability to develop. The researchers hypothesize that as water seeped through the ground, a sliding surface formed, causing the landslide body, including the ground surface, to slide progressively until the entire landslide moved rapidly all at once.

“Formation of the sliding surface will induce some movement, while the collapse will only occur when the sliding surface is fully developed,” Li said. “The progression can happen over hours, months or years.”

The researchers then attempted to determine if the Rolling Hills Estates landslide could have been predicted. By computing the displacement over time, they arrived at a predicted failure date on July 11, three days after the real landslide on July 8. They note that although their results are encouraging, predicting landslides using satellite remote sensing data needs further refinement, and landslides in areas without good historical satellite data might not be possible to predict in this way.

Li said that one of the challenges in forecasting landslides is the time period over which the progression takes place. Accurate forecasting requires continuous historical and ongoing satellite radar or in-situ measurements.

Handwerger is a core member of a project at JPL that is building an analysis-ready surface displacement database from satellite radar data for the entire United States, U.S. territories, Canada within 200 km of the U.S. border, and all mainland countries from the southern U.S. border up to and including Panama. The project, called Observational Products for End-Users from Remote Sensing Analysis, or OPERA, will contain analysis-ready data for near real-time monitoring and, possibly, landslide prediction.

“These motions can be quite subtle before they begin to move fast,” Li said. “Cracks in structures are what people tend to notice first. In fact, local residents in Rolling Hills Estates first reported cracks in their houses starting in April 2023. Signs of active movement require caution and monitoring because they could signal a progressive failure in the future.”

The study, in fruit flies and mice, also identified ways to block this process, which could have implications for treating or preventing the muscle wasting sometimes associated with inflammatory diseases, including bacterial infections, Alzheimer’s disease and long COVID.

The study is published July 12 in the journal Science Immunology.

“We are interested in understanding the very deep muscle fatigue that is associated with some common illnesses,” said senior author Aaron Johnson, PhD, an associate professor of developmental biology. “Our study suggests that when we get sick, messenger proteins from the brain travel through the bloodstream and reduce energy levels in skeletal muscle. This is more than a lack of motivation to move because we don’t feel well. These processes reduce energy levels in skeletal muscle, decreasing the capacity to move and function normally.”

To investigate the effects of brain inflammation on muscle function, the researchers modeled three different types of diseases — an E. coli bacterial infection, a SARS-CoV-2 viral infection and Alzheimer’s. When the brain is exposed to inflammatory proteins characteristic of these diseases, damaging chemicals called reactive oxygen species build up. The reactive oxygen species cause brain cells to produce an immune-related molecule called interleukin-6 (IL-6), which travels throughout the body via the bloodstream. The researchers found that IL-6 in mice — and the corresponding protein in fruit flies — reduced energy production in muscles’ mitochondria, the energy factories of cells.

“Flies and mice that had COVID-associated proteins in the brain showed reduced motor function — the flies didn’t climb as well as they should have, and the mice didn’t run as well or as much as control mice,” Johnson said. “We saw similar effects on muscle function when the brain was exposed to bacterial-associated proteins and the Alzheimer’s protein amyloid beta. We also see evidence that this effect can become chronic. Even if an infection is cleared quickly, the reduced muscle performance remains many days longer in our experiments.”

Johnson, along with collaborators at the University of Florida and first author Shuo Yang, PhD — who did this work as a postdoctoral researcher in Johnson’s lab — make the case that the same processes are likely relevant in people. The bacterial brain infection meningitis is known to increase IL-6 levels and can be associated with muscle issues in some patients, for instance. Among COVID-19 patients, inflammatory SARS-CoV-2 proteins have been found in the brain during autopsy, and many long COVID patients report extreme fatigue and muscle weakness even long after the initial infection has cleared. Patients with Alzheimer’s disease also show increased levels of IL-6 in the blood as well as muscle weakness.

The study pinpoints potential targets for preventing or treating muscle weakness related to brain inflammation. The researchers found that IL-6 activates what is called the JAK-STAT pathway in muscle, and this is what causes the reduced energy production of mitochondria. Several therapeutics already approved by the Food and Drug Administration for other diseases can block this pathway. JAK inhibitors as well as several monoclonal antibodies against IL-6 are approved to treat various types of arthritis and manage other inflammatory conditions.

“We’re not sure why the brain produces a protein signal that is so damaging to muscle function across so many different disease categories,” Johnson said. “If we want to speculate about possible reasons this process has stayed with us over the course of human evolution, despite the damage it does, it could be a way for the brain to reallocate resources to itself as it fights off disease. We need more research to better understand this process and its consequences throughout the body.

“In the meantime, we hope our study encourages more clinical research into this pathway and whether existing treatments that block various parts of it can help the many patients who experience this type of debilitating muscle fatigue,” he said.

The ozone layer, a crucial shield protecting life on Earth from harmful ultraviolet (UV) radiation, has been on a path to recovery thanks to the Montreal Protocol. This landmark international treaty, adopted in 1987, successfully led to phasing out the production of numerous substances responsible for ozone depletion. Over the past decades, the ozone layer has shown significant signs of healing, a testament to global cooperation and environmental policy.

However, the stability of this vital atmospheric layer is now facing a new and unexpected challenge. During the 2019/20 Australian wildfires, researchers observed a dramatic increase in stratospheric aerosols — tiny particles that can influence climate, health, and atmospheric chemistry.

Smoke-charged vortex transports aerosol up to 35 kilometers

Utilizing new satellite data and numerical modeling, the research team successfully demonstrated the impact of wildfires through a novel phenomenon: the smoke-charged vortex (SCV).

“The SCV is a powerful, smoke-laden whirlpool that transports wildfire smoke into the middle stratosphere, reaching altitudes of up to 35 kilometers,” explained Prof. Hang Su from the Institute of Atmospheric Physics at the Chinese Academy of Sciences, one of the corresponding authors of the study. “This process led to at least a doubling of the aerosol burden in the southern hemisphere’s middle stratosphere. Once reaching such high altitudes, these aerosols initiated a series of chemical reactions at their surface that impacted ozone concentrations.”

The international team discovered that these wildfire-induced aerosols facilitated heterogeneous chemical reactions in the stratosphere, which paradoxically led to both ozone depletion and ozone increase at different atmospheric layers.

While the lower stratosphere experienced significant ozone depletion, the new study shows that the increase of smoke aerosol particles in the middle stratosphere enhances the heterogeneous uptake and hydrolysis of N₂O₅, which leads to a decrease of reactive nitrogen gases, e.g., NOx, and an increase of ozone. In Southern Mid-Latitudes, the complex interplay managed to buffer approximately 40% (up to 70%) of the ozone depletion observed in the lower stratosphere in the following months of the mega-bushfire events.

So why does this matter?

“Our study uncovers an unexpected and crucial mechanism by which the absorbing aerosols in wildfire smoke, such as black carbon, can induce and sustain enormous smoke-charged vortices spanning thousands of kilometers, fundamentally changing the stratospheric circulation. The vortices can persist for months, carrying aerosols deeply into the stratosphere and affecting the ozone layer in distinct ways at different altitudes. This highlights the need for continued vigilance and research as climate change progresses,” said Prof. Yafang Cheng, another leading author from the Max Planck Institute for Chemistry.

“We’ve made a significant step forward in simulating the SCV as a new effective pathway for wildfires to modify stratospheric dynamics and chemistry, especially the ozone layer. I love this study because it once again demonstrates how closely different parts of the Earth system are connected. Smoke from a forest fire can significantly change the wind and circulation tens of kilometers above the ground, which allows the smoke to modify the ozone layer, influencing life on our planet,” said Dr. Chaoqun Ma, the first author of the study and postdoc researcher in Cheng’s team at the MPIC.

The ozone layer’s role in filtering UV radiation is crucial for protecting all life forms on Earth. The Montreal Protocol’s success in reducing ozone-depleting substances was a monumental achievement. Still, the new findings highlight that natural events, exacerbated by climate change, pose additional risks to this fragile atmospheric layer. With the increasing frequency and intensity of wildfires driven by global warming, the formation of SCVs and their impact on the stratosphere could become more common, posing a threat to the ozone layer.

The human brain is remarkably adept at adjusting what we hear based on contexts, like our current environment or priorities, but it’s still unknown how exactly the brain helps us detect, filter and react to sounds.

Now, biologists at the University of Maryland are a step closer to solving that mystery. Using an animal model, the researchers found that the orbitofrontal cortex (OFC), a brain region associated with decision-making but not typically linked to hearing, plays a central role in helping the auditory cortex (a primary hearing center of the brain) adapt to changing contexts or situations. The team’s findings were published in the journal Current Biology on July 11, 2024.

“Our hearing doesn’t just depend on the sounds around us. It also relies heavily on what we’re doing and what’s important to us at that moment,” explained UMD Biology Assistant Professor Melissa Caras, the paper’s senior author. “Understanding the neural mechanisms responsible for these adjustments can also lead to a better understanding of and potential treatments for neurodevelopmental disorders like autism, dyslexia or schizophrenia — conditions where sensory regulation goes awry.”

To closely examine the brain circuitry involved in the hearing process, the researchers turned to gerbils, small mammals whose basic hearing system is similar to that of humans. The animals were exposed to sound patterns in two different contexts. In one context, the animals listened to sounds passively without needing to do anything. In the other, the animals had to perform a specific action in response to the sounds they heard. By recording and manipulating the brain activity of the animals, the team discovered that the OFC helped the animals switch between passive and active listening.

“In short, the OFC sends signals to the auditory cortex when it’s time to pay closer attention to sounds,” Caras said. “It’s not certain whether the signals are sent directly or indirectly via an intermediary brain region, but we do know that activity in the OFC is essential to how the gerbils behaved in our experiments.”

When the OFC was silenced, the animals’ auditory cortex did not switch between passive and active listening, impairing their ability to pay attention to and react to a behaviorally relevant sound.

“In terms of a more human-oriented analogy, it would be as if I told you to suddenly pay attention to your refrigerator humming in the background,” Caras explained. “If your OFC was silenced and unable to send a signal to your auditory cortex, you might have difficulty doing so because the ability to rapidly alter your sound perception would be impaired.”

While this study was conducted in animals, Caras says the findings may have notable implications for human health and well-being. The ability to quickly shift attention to important sounds is essential for many day-to-day activities including communicating with others and navigating busy or dangerous environments.

“We’re just beginning to understand how the brain fine tunes hearing sensitivity in response to sudden shifts in behavioral contexts. We plan to explore exactly how the OFC communicates with the auditory cortex and see whether it’s possible to strengthen the connection and improve hearing ability,” Caras said. “This work is paving the way for researchers and health care professionals to develop better strategies for improving hearing in both healthy individuals and those with sensory impairments.”

This research was supported by the National Institutes of Health (Award Nos. R00DC016046 and R01DC020742).

Now, however, in a study published recently in the Journal of Clinical Immunology, researchers from Tokyo Medical and Dental University (TMDU) and Kagoshima University have identified a previously undocumented manifestation among patients with 18q del syndrome: late-onset combined immunodeficiency (LOCID), affecting both B and T cells. This novel finding underscores the critical importance of routinely assessing the functionality of both B and T cells in individuals with 18q del syndrome.

Elaborating further on this novel finding, Professor Kanegane says, “In this study, we came across two patients with chromosome 18q del syndrome presenting with LOCID, which, to the best of our knowledge, has not yet been reported in patients with the syndrome.”

Patient 1 was a 29-year-old man diagnosed with 18q del syndrome. Despite initially having few infections, he developed Pneumocystis pneumonia (PCP). Array-based comparative genomic hybridization (CGH) analysis showed a deletion in the 18q21.32-q22.3 chromosome region.

Patient 2 was a 48-year-old woman who had not been previously diagnosed with 18q del syndrome. However, she was diagnosed with granulomatous lymphadenitis, and a biopsy of her lymph nodes revealed a loss of 18q21.33-qter.

Both patients exhibited hypogammaglobulinemia, characterized by abnormally low levels of immunoglobulins (IgG, IgA, IgM, and IgE). Patient 1’s serum immunoglobulin levels were significantly below normal ranges. He reported IgG of 188 mg/dL (normal: 870-1,700 mg/dL), IgA of 105 mg/dL (normal: 110-410 mg/dL), IgM of 26 mg/dL (normal: 33-190 mg/dL), and IgE of <5 IU/mL (normal: 232 IU/mL). His CD4⁺ T cells had a decreased percentage of naïve T cells, accounting for only 3.58% of the total CD3⁺CD4⁺ cell population. Moreover, his T-cell receptor excision circles (TREC) levels and Ig κ-deleting recombination excision circle (KREC) levels were extremely low at 25.27 copies/105 cells (normal: > 565 copies/105 cells) and 93.36 copies/105 cells (normal: ≥ 456 copies/105 cells) respectively, indicating poor T-cell production.

Similar conditions were noted for patient 2, who reported IgG of 8 mg/dL, IgA of 9 mg/dL, IgM of 131 mg/dL, and IgE of 0.3 IU/mL. Her CD4⁺ T cells and naïve CD4⁺ T cells were depleted, with naïve T cells accounting for only 6% of the CD3⁺CD4⁺ cell population. Her TREC levels were 0 copies/10⁵ cells, and her KREC levels were 11.4 copies/10⁵ cells.

Importantly, CD4⁺ and CD8⁺ T cells failed to divide in response to phytohemagglutinin (PHA) stimulation, indicating severe functional impairment of T cells in both the patients.

Based on their immune profiles and clinical history, both of them were diagnosed with LOCID, a condition where both humoral (antibody-mediated) and cell-mediated immune responses were impaired, making them highly susceptible to infections.

This novel finding is significant, as Dr. Tomomasa, the co-authored of this study, states, “While cases involving deletion of the same region as those of the two patients presented in this study have been reported earlier, patients with 18q del syndrome developing LOCID have never been reported. We speculate that these patients simply have not yet developed LOCID or that they might not have been adequately assessed for it.”

On the basis of these results, the researchers recommend annual testing for both cellular and humoral immunity in patients with 18q del syndrome. This proactive approach can allow for the early detection of combined immune deficiencies, facilitating timely interventions and personalized treatment strategies. Ultimately, such regular monitoring can significantly improve clinical outcomes and enhance the quality of life for individuals diagnosed with 18q del syndrome.

These are the questions that a team of mechanical engineers and computer scientists at the University of California San Diego sought to answer in a study presented recently at the ICRA 2024 conference in Japan.

“To our knowledge, this is the first study investigating robots that infer human perception of risk for intelligent decision-making in everyday settings,” said Aamodh Suresh, first author of the study, who earned his Ph.D. in the research group of Professor Sonia Martinez Diaz in the UC San Diego Department of Mechanical and Aerospace Engineering. He is now a postdoctoral researcher for the U.S. Army Research Lab.

“We wanted to create a framework that would help us understand how risk-averse humans are-or not-when interacting with robots,” said Angelique Taylor, second author of the study, who earned her Ph.D. in the Department of Computer Science and Engineering at UC San Diego in the research group of Professor Laurel Riek. Taylor is now on faculty at Cornell Tech in New York.

The team turned to models from behavioral economics. But they wanted to know which ones to use. The study took place during the pandemic, so the researchers had to design an online experiment to get their answer.

Subjects-largely STEM undergraduate and graduate students-played a game, in which they acted as Instacart shoppers. They had a choice between three different paths to reach the milk aisle in a grocery store. Each path could take anywhere from five to 20 minutes. Some paths would take them near people with COVID, including one with a severe case. The paths also had different risk levels for getting coughed on by someone with COVID. The shortest path put subjects in contact with the most sick people. But the shoppers were rewarded for reaching their goal quickly.

The researchers were surprised to see that people consistently underestimated in their survey answers indicating their willingness to take risks of being in close proximity to shoppers infected with COVID-19. “If there is a reward in it, people don’t mind taking risks,” said Suresh.

As a result, to program robots to interact with humans, researchers decided to rely on prospect theory, a behavioral economics model developed by Daniel Kahneman, who won the Nobel Prize in economics for his work in 2002. The theory holds that people weigh losses and gains compared to a point of reference. In this framework, people feel losses more than they feel gains. So for example, people will choose to get $450 rather than betting on something that has a 50% chance of winning them $1100. So subjects in the study focused on getting the reward for completing the task quickly, which was certain, instead of weighing the potential risk of contracting COVID.

Researchers also asked people how they would like robots to communicate their intentions. The responses included speech, gestures, and touch screens.

Next, researchers hope to conduct an in-person study with a more diverse group of subjects.