Tuesday, July 22, 2025

  

Heatwaves to increase in frequency, duration under global warming





Portland State University





As the climate becomes warmer on average, it makes intuitive sense that we will see more hot days and we've had predictions of this for some time. However, the duration of heatwaves — how many days in a row exceed a temperature that is unusually hot for a given region — can be very important for impacts on humans, livestock and ecosystems. Predicting how these durations will change under a long-term warming trend is more challenging because day-to-day temperatures are correlated — tomorrow's temperatures have a dependence on today's temperature. This study takes this effect into account, along with the warming seen in current and historical observations and projected for the future by climate models for a wide range of land regions. Not only do the heatwave durations increase, but each additional increment of warming causes a larger increase in the typical length of long heat waves. In other words, if the next decade brings as much large-scale warming as a previous decade, the additional increase in heatwave durations would be even larger than we've experienced so far.


How our body keeps time in the heat




RIKEN
Waveform distortion 

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Theoretical physics uncovers how our biological clock maintains a consistent 24-hour cycle, even as temperatures change

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Credit: RIKEN





Researchers led by Gen Kurosawa at the RIKEN Center for Interdisciplinary Theoretical and Mathematical Sciences (iTHEMS) in Japan have used theoretical physics to discover how our biological clock maintains a consistent 24-hour cycle—even as temperatures change. They found that this stability is achieved through a subtle shift in the “shape” of gene activity rhythms at higher temperatures, a process known as waveform distortion. This process not only helps keep time steady but also influences how well our internal clock synchronizes with the day-night cycle. The study was published in PLOS Computational Biology on July 22.

 

Have you ever wondered how your body knows when it’s time to sleep or wake up? The simple answer is that your body has a biological clock, which runs on a roughly 24-hour cycle. But because most chemical reactions speed up as temperatures rise, how our bodies compensate for changing temperatures throughout the year—or even as we move back and forth between the outdoor summer heat and indoor air-conditioned rooms—has remained largely a mystery.

 

Our biological clock is powered by cyclical patterns of mRNA—the molecules that code for protein production—which result from certain genes being rhythmically turned on and off. Just as the back and forth of a swinging pendulum over time can be described mathematically as a sine wave, smoothly going up and coming down over and over, so can the rhythm of mRNA production and decline.

 

Kurosawa’s research team at RIKEN iTHEMS and a collaborator at YITP, Kyoto University, drew on theoretical physics to analyze the mathematical models that describe this rhythmic rise and fall of mRNA levels. Specifically, they used the renormalization group method, a powerful approach adapted from physics, to extract critical slow-changing dynamics from the system of mRNA rhythms. Their analysis revealed that at higher temperatures mRNA levels should rise more quickly and decline more slowly, but importantly, the duration of one cycle should stay constant. When graphed, this high-temperature rhythm looks like a skewed, asymmetrical waveform.

 

But does this theorized change actually happen? To test this theory in real organisms, the researchers examined experimental data from fruit flies and mice. Sure enough, at higher temperatures, these animals showed the predicted waveform distortions, confirming that the theoretical predictions align with biological reality. The researchers conclude that waveform distortion is the key to temperature compensation in the biological clock, specifically the slowing down of mRNA-level decline during each cycle.

 

The team also found that waveform distortion affects how well the biological clock synchronizes with environmental cues, such as light and darkness. The analysis predicted that when the waveform becomes more distorted, the biological clock is more stable, and environmental cues have little effect on it. This theoretical prediction matches experimental observations in flies and fungi and is significant because irregular light-dark cycles are part of modern-day life for most people.

 

“Our findings show that waveform distortion is a crucial part of how biological clocks remain accurate and synchronized, even when temperatures change,” says Kurosawa. He adds that future research can now focus on identifying the exact molecular mechanisms that slow down the decline in mRNA levels, which leads to the waveform distortion. Scientists also hope to explore how this distortion varies across species—or even between individuals—since age and personal differences may influence how our internal clocks behave.

 

“In the long term,” Kurosawa notes, “the degree of waveform distortion in clock genes could be a biomarker that helps us better understand sleep disorders, jet lag, and the effects of aging on our internal clocks. It might also reveal universal patterns in how rhythms work—not just in biology, but in many systems that involve repeating cycles.”

 

A simple filter for rare earth elements will ensure a clean domestic supply of these crucial metals



The technique will help make REE recycling financially, logistically and environmentally attractive




University of California - Santa Barbara

REE Dropdown 

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promethium

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Credit: Matt Perko





(Santa Barbara, Calif.) — Rare earth elements sustain the Information Age, and securing a supply of these metals has become a matter of national and economic security. They’re ubiquitous in our smart technologies, high performance materials and industrial catalysts. Yet reclaiming them is complex, dangerous and expensive.

That’s why UC Santa Barbara’s Justin Wilson has partnered with the mineral recovery company REEGen. “We’ve developed a new approach to extract rare earth elements from end-of-life products like electronic waste from phones, batteries and discarded catalytic converters,” said Wilson, a professor in UCSB’s Department of Chemistry & Biochemistry. The new technique, published in Communications Chemistry, combines the strengths of solid-state extraction with precision chemistry. The goal is to make rare earth element recycling financially, logistically and environmentally attractive.

Back to the Periodic Table

The rare earth elements (REEs) encompass scandium, yttrium and the elements from lanthanum through lutetium. They sit deep within the periodic table, in the section that’s often excised and placed underneath.

Although not as rare as their name suggests, the REEs are difficult to obtain in their pure forms. Recovering them from geologic deposits or waste materials is a multi-step process that involves dissolving the feedstock, removing all of the other metals and then isolating each REE individually. “Unfortunately, their chemical similarities make them fiendishly difficult to separate from one another.

Wilson’s lab focuses on compounds called chelators, which bind to metals like a crab claw grabbing a pebble. In 2024, his team synthesized a unique chelator, called G-macropa, that preferentially binds to large metal ions, like the hefty REEs. His team was able to apply this molecule to separate different REEs from another at room temperature without relying on the toxic and caustic compounds currently used for the task. Now Wilson has turned his attention toward the initial step of concentrating rare earth elements from a mixture containing many different metals.

Combining precision chemistry with a simple setup

Scientists at REEGen have engineered microbes to produce organic acids and bio-chelators that the company uses to leach rare earth elements from waste streams. Wilson’s expertise comes in after this initial extraction to separate the REEs from other metals in the bio-leachate, such as alkali metals and alkaline earth metals, as well as iron and aluminum.

Wilson wanted to develop a simple material that could remove the REE ions from the bio-leachate much like a water filter removes metal ions from tap water. He already had the macropa chelator, his team just had to figure out how to modify it to stick to a resin scaffold without losing the molecule’s useful properties.

The concept of using a resin or material to remove metal ions is well known. For instance, Brita filters can remove metal ions from tap water and water softening units in homes can capture calcium and magnesium. The approach by Wilson's lab, however, sought to leverage the unique selectivity of the macropa chelator for very large REEs to develop a resin that could remove these critical elements, while leaving other metal ions relatively untouched.

Once Wilson’s lab successfully attached the macropa to the scaffold, they ran REEGen’s bio-leachate through the device. This process increased the concentration of rare earth elements fourfold —from 5% by number of atoms (or molar percentage) to over 21 mol%. Adding oxalate to remove excess iron further improved this, resulting in a solution with nearly 59 mol% REEs. A simple rinse with hydrochloric acid detaches the ions from the framework, and it’s ready to be used again.

Addressing an unmet need

“The rare earth elements are critical components of many high-tech materials, but their extraction from raw ores is not economically and environmentally friendly,” said lead author Yangyang Gao, a postdoctoral researcher in Wilson’s lab. “We are dedicated to developing clean and green rare earth extraction, enrichment and separation strategies.”

The authors aim to use their technique to produce concentrated solutions of REEs that can then be sent to a company that separates the individual elements. While some firms have begun to extract REEs from e-waste, rare earth recycling is still in its infancy. “Right now nobody is getting the rare earth elements out of these automotive slags,” said co-author Sean Medin, REEGen’s chief technology officer.

Processing automotive waste requires harsh chemicals that introduce logistical, safety and regulatory complications. As a result, it’s only practical at large scale, and simply not economically attractive right now, Medin explained. A filter is well contained, generates less waste and makes the process simple. “And having a cleaner process makes it a lot easier to set these things up onsite,” he added.

The team hopes to make their technique even more selective for REEs and modify the setup to work with a variety of leachates. 

The technique lends itself to sundry applications, including resource extraction, recycling and even environmental remediation. “There could be a certain degree of modularity here,” Wilson said. “If we have different chelators and figure out how to attach them here, we could start to target different metal ions, like mercury, cadmium and lead.” 

Cost is currently the limiting factor. Macropa is a challenging molecule to make, requiring many steps to create. The more complicated the process, the less attractive it is for industrial applications. But Wilson’s lab is working to capture the properties of macropa in other, simpler chelators. They’re also searching for a more optimal resin to further improve efficiency.

Despite their accomplishments, the team is concerned that their progress might suddenly grind to a halt. This work was funded by the National Science Foundation’s Small Business Innovation Research grant, as well as the Department of Energy’s Basic Energy Sciences program. “These funding agencies, which are under considerable threat, are crucial to important areas for national security, like supporting a domestic supply of rare earth elements,” Wilson said.

The federal government has stated that domestic production of REEs is a priority, “However, they’re cutting the agencies that are funding the work to do this,” Medin added. Rolling back regulations may incentivize mining, but that’s not necessarily the most efficient way to source these elements.

“With significant cuts to these federal funding sources, I think we’re going to be hurting as a nation,” Wilson said.

 

Study identifies world-first treatments to prevent a life-threatening virus infection


The study could lead to the first treatments to prevent the spread of this virus that is endemic among many First Nations communities


Walter and Eliza Hall Institute
T-cell 

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HTLV-1 is a virus that infects a type of white blood cell called a T‐lymphocyte, or T-cell (pictured). The new study could lead to the first treatments and potential cure for the virus that impacts around 10 million people each year.

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Credit: National Institute of Allergy and Infectious Diseases.






Around 10 million people globally live with the life-threatening virus HTLV-1. Yet it remains a poorly understood disease that currently has no preventative treatments and no cure.

But a landmark study co-led by Australian researchers could change this, after finding existing HIV drugs can suppress transmission of the HTLV-1 virus in mice.

The study, published in Cell, could lead to the first treatments to prevent the spread of this virus that is endemic among many First Nations communities around the world, including in Central Australia.

The research by WEHI and the Peter Doherty Institute for Infection and Immunity (Doherty Institute) also identifies a new drug target that could lead to the elimination of HTLV-1 positive cells from those with an established infection, and prevent disease progression.

At a glance

  • New research co-led by WEHI and the Doherty Institute could lead to the first preventative treatments for HTLV-1, one of the most complex and neglected viruses in the world.
  • The study found two specific HIV antivirals already on the market can suppress transmission of HTLV-1 in humanised mice and prevent disease, identifying the first prophylactic treatment against HTLV-1.
  • Secondly, when the HIV antivirals were used in combination with a compound that induces cell death, infected cells were killed – flagging a potential future curative strategy for the disease.
  • The unprecedented findings could enable these drugs to enter clinical trials preventing establishment of pathogenic levels of HTLV-1.

Human T-cell leukaemia virus type 1 (HTLV-1) is a virus that infects the same cell type as HIV – T cells, a type of blood immune cell that helps the body fight off infections.

A small proportion of people infected with HTLV-1 after a long duration of infection develop serious diseases, such as adult T-cell leukemia and spinal cord inflammation.  

Co-lead author and WEHI laboratory head Dr Marcel Doerflinger said the promising results of the new study could help find a desperately needed treatment and prevention strategy for one of the most neglected viruses in the world.

“Our study marks the first time any research group has been able to suppress this virus in a living organism,” Dr Doerflinger said.

“As HTLV-1 symptoms can take decades to appear, by the time a person knows they have the infection the immune damage is already in full swing.

“Suppressing the virus at transmission would allow us to stop it before it has the chance to cause irreversible damage to immune function, leading to disease and a premature death.”

In a research effort spanning 10 years, the collaborative team isolated the virus and developed a world-first humanised mouse model for HTLV-1 that enabled them to study how the virus behaves in a living organism with a human-like immune system.

The mice were transplanted with human immune cells that are susceptible to HTLV-1 infections, including with Australia’s genetically novel HTLV-1 strain. International and Australian strains equally caused leukaemia and inflammatory lung disease in these human immune system mice.

The mice were then treated with tenofovir and dolutegravir – two antiviral therapies currently approved to silence HIV and prevent AIDS. The team discovered both drugs could also powerfully suppress HTLV-1.

“What’s most exciting is that these antivirals are already in use for millions of HIV patients, meaning there’s a direct path for the clinical translation of our findings,” Dr Doerflinger said.

“We won’t have to start from scratch because we already know these drugs are safe and effective. And now we’ve shown that their use can very likely be extended to HTLV-1.”

In another remarkable finding, the team discovered that human cells containing HTLV-1 could be selectively killed when mice were treated with HIV drugs in combination with another therapy inhibiting a protein (MCL-1) known to help rogue cells stay alive.

The team is now leveraging precision RNA therapies to develop new ways to target MCL-1 and establish combination treatments that can be clinically tested, which they believe could offer a promising curative strategy for HTLV-1.

Crucial insight

The development of the humanised mouse models central to this study at WEHI was spearheaded by first author Dr James Cooney and Professor Marc Pellegrini, study lead author, WEHI Honourary Fellow and Executive Director at Centenary Institute.

Prof Pellegrini said the mouse models were not only critical in identifying potential therapeutic targets, but also allowed researchers to understand how different strains of the HTLV-1 virus can alter disease symptoms and outcomes. This is particularly important for the unique strain that is present in Australia, HTLV-1c.

“It’s long been hypothesised that differences in viral subtype may influence disease outcomes, but a lack of research into HTLV-1 has made it difficult for us to find the evidence needed to support this claim – until now.

“Our study provides critical insights that enable us to better understand the consequences of the distinct molecular make-up of the virus affecting our First Nations communities. This will further help us to investigate ways to create the tools needed to control the spread of this virus subtype.”

The human HTLV-1 samples needed to develop the mouse models were obtained through the front-line clinical work of Associate Professor Lloyd Einsiedel, a Clinician Scientist at the Doherty Institute and Infectious Diseases Physician, who has provided a clinical service to Central Australia for more than a decade and has dedicated his career to putting HTLV-1 on the map.

Advocacy for a neglected disease

Research by the University of Melbourne’s Professor Damian Purcell, Head of Molecular Virology at the Doherty Institute and co-lead author of the study, isolated the virus from First Nations donors and identified significant genetic differences between the HTLV-1c strains from Central Australia compared to the HTLV-1a strains found internationally.

The new findings show that both HTLV-1 strains cause disease in mice, with HTLV-1c showing more aggressive features. The identified drug therapies were found to be equally effective against both strains.

Prof Purcell and Associate Prof Lloyd Einsiedel worked with the National Aboriginal Community Controlled Health Organisation (NACCHO) HTLV-1 committee and the Australian Department of Health over many years to advocate for guidance on HTLV-1 from the World Health Organization (WHO) that led to them formally classify the virus as a Threatening Pathogen to Humans in 2021.

This resulted in the development of formal WHO policies to reduce transmission internationally and the development of clinical management guidelines for HTLV-1c in Central Australia under NACCHO leadership.

“Despite Australia’s high burden of HTLV-1, the virus and its associated diseases are still not notifiable in most states and true infection rates in the nation remain unknown,” Prof Purcell said.

“People at risk from HTLV-1 deserve biomedical tools like those that provide game-changing therapeutic and prevention options for other blood-borne persistent viral infections, such as HIV.

“There is a real opportunity to prevent the transmission of HTLV-1 and end the diseases caused by these infections. Our research findings are a major leap forward in this.”

The research team is currently in talks with the companies behind the HIV antivirals used in this study, to see if HTLV-1 patients can be included in their ongoing clinical trials. If successful, this would pave the way for these drugs to become the first approved pre-exposure prophylaxis against HTLV-1 acquisition.

These findings are supported by The Australian Centre for HIV and Hepatitis Virology Research, The Phyllis Connor Memorial Trust, Drakensberg Trust and the National Health and Medical Research Council (NHMRC).

The study, “Combination antiretroviral therapy and MCL-1 inhibition mitigate HTLV-1 infection in vivo”, is published in Cell (DOI:10.1016/j.cell.2025.06.023).

New AI study clarifies the origins of Papua New Guineans



Estonian Research Council
Mayukh-Mondal.jpeg 

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Study author Mayukh Mondal in Tartu.

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Credit: University of Tartu Institute of Genomics





Papua New Guineans are living proof of how isolation, ancient mixing, and survival in remote islands can preserve a unique piece of our shared human story.

A team of European researchers has shed new light on the genetic origins of Papua New Guineans. The team uses advanced Artificial Intelligence (AI) tools to demonstrate that Papua New Guineans are closely related to other Asian populations. They share a common ancestry from the same ‘Out of Africa’ event that also gave rise to other non-African groups.

Papua New Guineans look strikingly different from other Asian groups and share some features with Sub-Saharan African populations, which fueled theories that they might have descended separately from other non-African populations.

According to lead author Dr. Mayukh Mondal, the unique physical features of Papua New Guineans probably come from natural selection: “Perhaps adaptations to tropical climates that make them look more like Sub-Saharan African groups, even though their genetics clearly link them to other Asian populations. More studies are needed to uncover how evolution shaped this remarkable population.” 

The genetic origin remains unresolved

Scientists generally agree that modern humans left Africa about 50,000 to 70,000 years ago, spreading into Europe, Asia, and beyond. Early archaeological studies have suggested that the ancestors of Papua New Guineans came from a separate, earlier migration (also known as the ‘First Out of Africa’ hypothesis), taking a coastal route through India and Southeast Asia. Archaeological evidence confirms that some of the Papuan New Guineans' genetic ancestry could have come from this ‘First out of Africa’ event. This is because the earliest human site in Oceania dates back to around 50,000 - 60,000 years ago, older than Europe’s oldest sites.

In recent decades, advances in DNA sequencing have tested this ‘First out of Africa’ hypothesis. However, studies of maternal (mitochondrial) and paternal (Y-chromosome) DNA have found no clear evidence that the main ancestry of Papua New Guineans came from an earlier migration. Instead, analyses suggest that their lineages connect to other non-African populations. Still, we cannot rule out a trace number of ancient migrations from the ‘First out of Africa’ population.

Interestingly, the Papua New Guinean genome carries a significant percentage of Denisovan DNA — a ghostly relative of Neanderthals. This unique inheritance likely came from mixing with Denisovans in Southeast Asia or Oceania — another element that confirms the complexity of Papua New Guinean ancestry.

Despite these researches, the genetic origin of Papuan New Guineans remains unresolved. Did Papua New Guineans split off before Europeans and Asians? Or have similar populations contributed to their genome? Did they carry ancestry from the enigmatic ‘First out of Africa’ population? Or are they part of the same family tree as other Asians living in proximity?

Unique demographic history

In this study, scientists used high-quality genomic data and AI-powered models to compare different demographic scenarios for the origin of the Papuan New Guineans' genetic diversity. Their results suggest that Papua New Guineans are a sister group to other Asian populations. Contribution from a ‘First Out of Africa’ migration might not be needed to explain their origins.

The researchers found that the ancestors of Papuan New Guineans went through a dramatic population bottleneck — most likely their numbers dropped sharply after reaching Papua New Guinea and stayed low for thousands of years. Unlike other non-African groups, they did not experience the farming-driven population boom that reshaped Europe and Asia. This unique demographic history left genetic signatures that, if misunderstood, could look like evidence of a contribution from an unknown population.