Friday, January 02, 2026

Researchers want to find out why quick clay is so unstable



Parts of coastal Norway have marine deposits from the last glaciation that can suddenly slide, with catastrophic results. Researchers are working to understand the exact nature of the clay's instability



Norwegian University of Science and Technology

Part of the project group 

image: 

Part of the project group at PoreLab. René Tammen (partly hidden), Erika Eiser, Astrid Silvia de Wijn, Ge Li, Kamila Zabłocka, Klaartje de Weerdt, and Ali Amiri. 

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Credit: Photo: PoreLab, NTNU





Quick clay is actually an old seabed. The clay thus formed under water, but came to the surface when the landscape rose after the last ice age.

However, this clay was not so dangerous, because it was full of salt from the sea. Only when the salt in the clay was washed out of fresh water from rain and groundwater did it turn into quick clay.

But what exactly makes quick clay so unstable?

"We have made very detailed and careful simulations of the friction between clay particles," says researcher and doctor Ge Li at PoreLab and the Department of Mechanical Engineering and Production at the Norwegian University of Science and Technology (NTNU).

A new article from Ge Li and Professor Astrid Silvia de Wijn from the same institutions deals with what happens at the nano level when the clay becomes weaker because fresh water replaces salt water.

Important for many to know more about quick clay

This work is particularly important for us in Norway. In this country, a large number of people live on quick clay, many of these in Eastern Norway and in Trøndelag. But there are also significant amounts of quick clay in Sweden, Finland, Canada, Russia and Alaska, and the research is therefore important for many more people.

"We see that the ions in the salt water settle on the surface in certain places and make it more difficult for the clay particles to slide against each other. In other words, the ions make the surface uneven and stand in the way of slippage," says Ge Li.

Ions are electrically charged atoms or molecules. In this case, the ions from the salt help to keep the clay stable.

Dramatic consequences

Building on quick clay can have dramatic consequences. In 2020, a mudslide in Gjerdrum took 31 housing units with it. Ten people died in the landslide, while ten others were injured. Around 1000 people had to evacuate their homes.

A quick clay avalanche in Levanger in August this year took parts of the E6 and the Nordland Line with it. One person died. Several months later, both the road and the train line are still closed. This has cost society several million every day.

Will find a more gentle alternative

Stabilising quick clay is both expensive and can have significant consequences for the environment.

"When we stabilise quick clay today, we mix and inject lime and cement. But we don't really know how it works. The production of lime and cement also emits a lot of CO₂, which is not good for the environment," says Ge Li.

You might think that it was possible to inject the quick clay with salt instead. In the laboratory, it may look like this, but in practice this will not work.

"However, our hope is that by better understanding how the salt works, it will be easier to find better and more environmentally friendly ways to stabilize quick clay," says Ge L.

The work is part of a large interdisciplinary project called Sustainable Stable Ground funded by the Research Council of Norway. This includes people from civil and environmental engineering, the Department of Structural Engineering, Chemistry, Physics and the Norwegian Geotechnical Institute (NGI).

Reference:

Ge Li, Astrid S. de Wijn, Molecular dynamics simulations of nanoscale friction on illite clay: Effects of solvent salt ions and electric double layer, Journal of Colloid and Interface Science, Volume 703, Part 1, 2026, 139107, ISSN 0021-9797. https://doi.org/10.1016/j.jcis.2025.139107

 

Delayed or absent first dose of measles, mumps, and rubella vaccination


JAMA Network Open



About The Study:

 In this cohort study of children with regular access to care, most received their measles, mumps, and rubella (MMR) vaccine on time, but the proportion not receiving the MMR vaccine by 2 years of age has increased since the COVID-19 pandemic. Children who did not receive their 2- and 4-month vaccines on time were significantly more likely to not receive any MMR vaccine by 2 years, highlighting opportunities for intervention.


Corresponding Author: To contact the corresponding author, Nina B. Masters, PhD, MPH, email ninam@truveta.com.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamanetworkopen.2025.51814)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

Embed this link to provide your readers free access to the full-text article 

 https://jamanetwork.com/journals/jamanetworkopen/fullarticle/10.1001/jamanetworkopen.2025.51814?guestAccessKey=1b34668e-afe8-4888-aa3d-dd05b3b83eff&utm_source=for_the_media&utm_medium=referral&utm_campaign=ftm_links&utm_content=tfl&utm_term=010226

 

Trends in US preterm birth rates by household income and race and ethnicity



JAMA Network Open




About The Study:

 In this population-based cross-sectional study, household income disparities in preterm birth widened over time. Black race moderated the association between income and preterm birth, underscoring the need to examine the role of racism in preterm birth disparities.


Corresponding Author: To contact the corresponding author, Erika G. Cordova-Ramos, MD, email gabriela.cordovaramos@bmc.org.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamanetworkopen.2025.50664)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

Embed this link to provide your readers free access to the full-text article 

 https://jamanetwork.com/journals/jamanetworkopen/fullarticle/10.1001/jamanetworkopen.2025.50664?guestAccessKey=1b34668e-afe8-4888-aa3d-dd05b3b83eff&utm_source=for_the_media&utm_medium=referral&utm_campaign=ftm_links&utm_content=tfl&utm_term=010226

 Anthropologists offer new evidence of bipedalism in long-debated fossil discovery


Analysis centers on point of attachment of ligament vital to walking upright




New York University

Crania, ulnae, and femora 

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Crania, ulnae, and femora of (left to right): a chimpanzee, Sahelanthropus, and Australopithecus. 

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Credit: Scott Williams/NYU and Jason Heaton/University of Alabama Birmingham





In recent decades, scientists have debated whether a seven-million-year-old fossil was bipedal—a trait that would make it the oldest human ancestor. A new analysis by a team of anthropologists offers powerful evidence that Sahelanthropus tchadensis—a species discovered in the early 2000s—was indeed bipedal by uncovering a feature found only in bipedal hominins.

Using 3D technology and other methods, the team identified Sahelanthropus’s femoral tubercle, which is the point of attachment for the largest and most powerful ligament in the human body—the iliofemoral ligament—and vital for walking upright. The analysis also confirmed the presence of other traits in Sahelanthropus that are linked to bipedalism. 

“Sahelanthropus tchadensis was essentially a bipedal ape that possessed a chimpanzee-sized brain and likely spent a significant portion of its time in trees, foraging and seeking safety,” says Scott Williams, an associate professor in New York University’s Department of Anthropology who led the research. “Despite its superficial appearance, Sahelanthropus was adapted to using bipedal posture and movement on the ground.”

The study, which included researchers from the University of Washington, Chaffey College, and the University of Chicago, appears in the journal Science Advances. 

Sahelanthropus was discovered in Chad’s Djurab desert by University of Poitiers’ palaeontologists in the early 2000s, with initial analyses focusing on its skull. Two decades later, studies on other parts of that discovery—its forearms, or ulnae, and thigh bone, or femur—were reported. This prompted debate over whether the species was bipedal or not, leaving open the question on its status: Is Sahelanthropus a hominin (a human ancestor)? 

In the Science Advances study, the scientists took a closer look at the ulnae and femur using two primary methods: a multi-fold trait comparison with the same bones of living and fossil species and 3D geometric morphometrics—a standard method for analyzing shapes in greater detail in order to illuminate areas of particular interest. Among the compared fossil species was Australopithecus—an early human ancestor, well-known through the discovery of the “Lucy” skeleton in the early 1970s, who lived an estimated four to two million years ago. 

The analysis revealed three features that point to bipedalism in Sahelanthropus:

  • The presence of a femoral tubercle, which provides attachment for the iliofemoral ligament linking the pelvis to the femur and has so far been identified only in hominins

  • A natural twist, specifically within the range of hominins, in the femur—or femoral antetorsion—that helps legs to point forward, thereby aiding walking 

  • The presence, drawn from the 3D analysis, of gluteal, or butt, muscles similar to those in early hominins that keep hips stable and aid in standing, walking, and running

The latter two traits—femoral antetorsion and gluteal complex—had previously been identified by other scientists; the Science Advances study affirmed their presence. 

The authors also found that Sahelanthropus had a relatively long femur relative to its ulna—additional evidence of bipedalism. The researchers note that apes have long arms and short legs, whereas hominins have relatively long legs. And while Sahelanthropus had much shorter legs than do modern humans, these were distinct from apes and approached Australopithecus in relative femur length, suggesting another adaptation to bipedalism. 

“Our analysis of these fossils offers direct evident that Sahelanthropus tchadensis could walk on two legs, demonstrating that bipedalism evolved early in our lineage and from an ancestor that looked most similar to today’s chimpanzees and bonobos,” concludes Williams. 

The paper’s other authors were Xue Wang and Jordan Guerra, both NYU doctoral students, Isabella Araiza, an NYU graduate student at the time of the study and now a doctoral candidate at the University of Washington, Marc Meyer, an anthropology professor at Chaffey College, and Jeffery Spear, an NYU graduate student at the time of the study and now a researcher at the University of Chicago.

This research was supported by a grant from the National Science Foundation (BCS-2041700).

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Why Some Bacteria Survive Antibiotics and How to Stop Them - New study reveals that bacteria can survive antibiotic treatment through two fundamentally different “shutdown modes”





The Hebrew University of Jerusalem

Disrupted Bacteria 

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Disrupted Bacteria

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Credit: Balaban Lab




New study reveals that bacteria can survive antibiotic treatment through two fundamentally different “shutdown modes,” not just the classic idea of dormancy. The researchers show that some cells enter a regulated, protective growth arrest, a controlled dormant state that shields them from antibiotics, while others survive in a disrupted, dysregulated growth arrest, a malfunctioning state marked by vulnerabilities, especially impaired cell membrane stability. This distinction is important because antibiotic persistence is a major cause of treatment failure and relapsing infections even when bacteria are not genetically resistant, and it has remained scientifically confusing for years, with studies reporting conflicting results. By demonstrating that persistence can come from two distinct biological states, the work helps explain those contradictions and provides a practical path forward: different persister types may require different treatment strategies, making it possible to design more effective therapies that prevent infections from coming back.

 

Antibiotics are supposed to wipe out harmful bacteria. Yet in many stubborn infections, a small number of bacterial cells manage to survive, only to re-emerge later and cause relapse. This phenomenon, known as antibiotic persistence, is a major driver of treatment failure and one reason infections can be so difficult to fully cure.

For years, persistence has largely been blamed on bacteria that shut down and lie dormant, essentially going into a kind of sleep that protects them from antibiotics designed to target active growth. But new research led by PhD student Adi Rotem under the guidance Prof. Nathalie Balaban from Hebrew University reveals that this explanation tells only part of the story.

The study shows that high survival under antibiotics can originate from two fundamentally different growth-arrest states, and they are not just variations of the same “sleeping” behavior. One is a controlled, regulated shutdown, the classic dormancy model. The other is something entirely different: a disrupted, dysregulated arrest, where bacteria survive not by protective calm but by entering a malfunctioning state with distinct vulnerabilities.

“We found that bacteria can survive antibiotics by following two very different paths,” said Prof. Balaban. “Recognizing the difference helps resolve years of conflicting results and points to more effective treatment strategies.”

Two “Survival Modes” and Why They Matter

The researchers identified two archetypes of growth arrest that can both lead to persistence, but for very different reasons:

1) Regulated Growth Arrest: A Protected Dormant State

In this mode, bacteria intentionally slow down and enter a stable, defended condition. These cells are harder to kill because many antibiotics rely on bacterial growth to be effective.

2) Disrupted Growth Arrest: Survival Through Breakdown

In the second mode, bacteria enter a dysregulated and disrupted state. This is not a planned shutdown, but a loss of normal cellular control. These bacteria show a broad impairment in membrane homeostasis, a core function needed to maintain the integrity of the cell.

That weakness could become a key treatment target.

A Framework That Could Transform Antibiotic Strategies

Antibiotic persistence plays a role in recurring infections across a wide range of settings, from chronic urinary tract infections to infections tied to medical implants. Yet despite intense research, scientists have struggled to agree on a single mechanism explaining why persister cells survive. Different experiments have produced conflicting results about what persisters look like and how they behave.

This study offers an explanation: researchers may have been observing different types of growth-arrested bacteria without recognizing they were distinct.

By separating persistence into two different physiological states, the findings suggest a future where treatments could be tailored, targeting dormant persisters one way, and disrupted persisters another.

How the Researchers Saw What Others Missed

The team combined mathematical modeling with several high-resolution experimental tools, including:

  • Transcriptomics, to measure how bacterial gene expression shifts under stress
  • Microcalorimetry, to track metabolic changes through tiny heat signals
  • Microfluidics, allowing scientists to observe single bacterial cells under controlled conditions

Together, these approaches revealed clear biological signatures distinguishing regulated growth arrest from disrupted growth arrest, along with the specific vulnerabilities of the disrupted state.

Cartoon Bacteria

Credit

Balaban Lab