Researchers discover how our brains react to surprise

University of Sydney

Facebook

XLinkedInWeChatBlueskyMessageWhatsAppEmail

Australian researchers have uncovered what happens behind the scenes in our brain when we’re faced with a predictable situation versus a surprise, giving vital clues in a long-standing mystery in neuroscience.

The researchers found that during surprising events, our brain is wired to direct energy to take in more sensory information from our environment.

This is why we remember unexpected events more vividly and accurately. Our brain then updates its own internal memory.

In comparison, when something is familiar or expected, the brain begins to respond to it before it even happens, which is what saves precious milliseconds. When something predictable appears, the brain makes us respond faster but doesn’t bother encoding it in full detail.

“Our study is a fascinating insight into how the brain uses predictions to help us better perceive and interact with the world,” says senior author Dr Reuben Rideaux from the School of Psychology at the University of Sydney.

“Our brain is constantly under pressure to make decisions, receiving a huge amount of sensory information from our environment. So, it needs to save energy where it can.

“When the brain is faced with a predictable situation, it goes ‘I already know what this is, I don’t need to spend energy processing it carefully.’

“But during unexpected events it’s like a software update or patch. Our brain wants to update our internal memory of the world to make sure we’re prepared for the future, so the energy is dedicated to collect as much information as possible from our environment,” says Dr Rideaux.

The findings, published in The Journal of Neuroscience, resolves a long-standing debate in neuroscience about ‘adaptive efficiency’, how our brain allocates neural energy to meet the pressures of environmental demands.

“The debate had been focused on whether the brain prioritised expected or unexpected information,” said lead author PhD candidate Ziyue Hu, from the School of Psychology.  

“We’ve found the answer is both. The brain has its cake and eats it too.”

“It’s incredible because this process all happens in milliseconds. This advances our understanding of how the brain balances speed and accuracy and how prediction and attention shape how we perceive the world.”

Managing surprises

The best real-world example that demonstrates this is professional sport. For high performance athletes, their experience enables them to predict and respond more quickly.

“Imagine a professional tennis player who knows where her opponent’s next serve is going to land. Their experience makes them move towards that spot before the ball is even struck and to get her racket in position to hit it back cleanly. Her brain had already prepared a motor response for the likely location and didn't bother encoding the precise location of the ball that confirmed what it already predicted,” says Dr Rideaux.

“That prediction buys her precious milliseconds, but if you ask her to recall frame by frame, exactly where the ball bounced inside the service box, her memory will be fuzzy.

“But it’s the rare surprise serve down the middle, which she'll remember with vivid spatial precision.”

The research

To study this phenomenon, 40 participants viewed simple visual flashes appearing around a circle while researchers measured their brain activity using EEG (recording brain waves) and tracked their pupil responses.

The research team recorded the participant’s reaction times and accuracy. But crucially, at times the researchers would manipulate and deliberately change the pattern of the flashes.

Participants responded more quickly and accurately to expected events, but when asked to recall the exact location, their memory was worse than after the unexpected flashes.

One surprising finding was our brain reacts to familiar events in two stages.  

The first is when the brain first predicts what is about to happen and so prepares and primes our body to react quickly.

The second is when the brain recognises that the event is what it expected, and it saves energy by not processing this information from the environment as deeply.

Both expected and unexpected events were represented in the cortex within 100 milliseconds of participants seeing the flash, but the unexpected events were represented more clearly in the brain waves than the expected ones.

For the next stage of the research, Dr Rideaux’s team is interested in understanding how these mechanisms develop over time, and what ecological factors influence those pathways.

The team is also interested in exploring how these mechanisms can be applied in artificial brains (neural networks and artificial intelligence) to improve their efficiency or performance.

-ENDS- 

Research link when published: https://doi.org/10.1523/JNEUROSCI.0154-26.2026

---

Journal

JNeurosci

DOI

10.1523/JNEUROSCI.0154-26.2026 

FUNGUY

Ten new species of Inocybe and one new record for China from the Gaoligong Mountains, Southwestern China

SciOpen

Facebook

XLinkedInWeChatBlueskyMessageWhatsAppEmail

 

image: 

(a, b) Basidiomata. (c) Basidiospore. (d) Cheilocystidia. (e) Pleurocystidia. (f) Caulocystidia. (g) Basidia and basidioles. Scales: a, b = 1 cm; c = 1 μm; d, e, g = 10 μm; f = 20 μm.

view more 

Credit: Mycology-An International Journal on Fungal Biology

This study was conducted by the research team of Prof. Zhu-Liang Yang at the Kunming Institute of Botany, Chinese Academy of Sciences. Focusing on the species diversity of Inocybe in the Gaoligong Mountains of southwestern China, the team carried out detailed taxonomic and phylogenetic investigations based on extensive field collections, morphological examinations, and molecular analyses.

 

Inocybe is a large genus in Inocybaceae, Agaricales, Agaricomycetes, Basidiomycota, Fungi. Species of this genus are widely distributed across the world and represent typical ectomycorrhizal fungi that play important ecological roles in the maintenance and functioning of forest ecosystems. In addition, many species of Inocybe contain toxic compounds such as muscarine and psilocybin, which may cause poisoning in humans or animals. Therefore, accurate species identification is important not only for understanding fungal diversity and evolution, but also for poisoning prevention and the sustainable use of fungal resources.

 

Although Inocybe has been studied for nearly two centuries, its diversity in the Gaoligong Mountains has remained insufficiently explored. To address this gap, the research team conducted a systematic study of Inocybe specimens collected from this biodiversity hotspot. Molecular phylogenetic analyses based on combined ITS, LSU, and rpb2 sequence data showed that the studied materials formed ten major lineages in the phylogenetic tree.

 

Based on integrated morphological observations and molecular phylogenetic evidence, the researchers described ten new species from the Gaoligong Mountains: Inocybe hirsuticeps, I. ceratina, I. longistipes, I. gracilipes, I. flocculosipes, I. flavocrocea, I. rufosquamosa, I. aculeata, I. dulongjiangensis, and I. squamulomarginata. In addition, Inocybe albodiscoides was reported as a new record for China. The study also provides a taxonomic key to Chinese species of Inocybe, offering a useful reference for future identification and classification of the genus in China.

 

Through systematic and taxonomic analyses, this work clarifies six major lineages of Inocybe represented in the studied materials and significantly expands current knowledge of the genus in China. The discovery of ten new species and one newly recorded species highlights the Gaoligong Mountains as an important but still underexplored hotspot of fungal diversity. With continued field surveys and taxonomic studies of macrofungi in China, more previously unknown species of Inocybe are expected to be discovered in the future.

 

See the article: 

Ten new species of Inocybe (Inocybaceae, Agaricales) from the Gaoligong Mountains, Southwestern China

 

DOI Link:

https://doi.org/10.1080/21501203.2026.2678690

---

Journal

Mycology: An International Journal on Fungal Biology

DOI

10.1080/21501203.2026.2678690 

Article Title

Ten new species of Inocybe (Inocybaceae, Agaricales) from the Gaoligong Mountains, southwestern China

Article Publication Date

11-Jun-2026

 

A two-pronged vaccine approach to prevent genital herpes

Yale University

Email

Genital herpes is a lifelong infection. While available treatments can manage symptoms, they cannot cure the infection or prevent transmission. Now, Yale School of Medicine researchers have taken a significant step toward a genital herpes vaccine that in preclinical models prevented infection.

In a study published June 19 in Science Immunology, researchers evaluated a two-part vaccination against genital herpes. With the technique, the first part — a typical intramuscular injection like you would receive for a flu shot, for example — is followed by the introduction of nanoparticles to the vagina, where herpes infection occurs in women.

The idea is the initial injection “primes” the immune system while the second localized treatment “pulls” immune activity right to where infection takes place. This study extends the original “prime and pull” approach by developing a new nanoparticle that effectively induces local immunity.

“We’ve found that, in preclinical experiments, this approach is a safe way to recruit the right immune cells in the right place to generate protective immunity,” said senior author Akiko Iwasaki, Sterling Professor of Immunobiology at Yale School of Medicine.

A two-pronged vaccine for genital herpes immunity

Efforts to develop a genital herpes vaccine have uncovered a key limitation of typical intramuscular injections: They do not establish robust immune cell populations or antibodies against the herpes virus at the vaginal lining where the virus is introduced in women. This limits the extent of immune attack against the herpes virus.

To address this challenge, the Iwasaki lab has explored methods to “pull” an immune response to the vaginal lining. They first tested whether introducing chemokines — proteins that can direct immune cells — to the vagina could establish immunity there. That technique led to only partial protection against herpes as it did not engage necessary immune cells called B cells.

They then evaluated a DNA molecule that stimulates the immune system. While it did reduce the amount of virus at the vagina, it also caused inflammation.

So the researchers wondered if combining the two methods might yield the best of both worlds.

“We had these two really promising strategies in the lab, but each had some shortcoming,” said Sachin Bhagchandani, a postdoc in Iwasaki’s lab and lead author of the study. “So we set out to formulate a particle that could overcome those shortcomings.”

Nanoparticles prevent herpes infection

The result of that work is BEACON (Bioactive Enhanced Adjuvant Chemokine Oligonucleotide Nanoparticles). The researchers made these nanoparticles by linking a piece of immunostimulating DNA to a chemokine.

“Sachin led this work, creating a nanoparticle that was stable and effective, which was no small feat,” said Iwasaki, who is also a professor of dermatology and of epidemiology, as well as an investigator with the Howard Hughes Medical Institute.

For the study, the researchers first primed female mice with an intramuscular vaccination against the herpes virus and then applied BEACON and virus antigen intravaginally. They found that BEACON established strong immune cell and antibody responses against the herpes virus in the vaginal tissue and that it lasted long term, at least six months.

When exposed to the herpes virus, mice given the “prime and pull” treatment were highly resistant to infection: 80% displayed no signs of disease over six months. That’s compared with just 40% of mice that received the intramuscular injection alone.

“That showed us that this approach could be profoundly impactful, establishing local immune responses for a significantly long period of time,” said Bhagchandani.

Further, BEACON enabled the researchers to target the right cells for generating immunity, rather than broadly affecting all cells. This meant they needed less of the DNA molecule than they used in previous experiments, and this smaller amount prevented the development of inflammation.

“This formulation is quite remarkable in that way,” said Iwasaki.

A vaccine for humans

The researchers are now evaluating whether this “prime and pull” method can be used to treat infection as well as prevent it. They’re also thinking about what this might look like for people.

“We’re collaborating with the Appel lab at Stanford to see if we can turn BEACON into translatable formulation, such as a vaginal suppository,” said Bhagchandani. “We’re also exploring a nasal approach wherein the ‘pull’ happens in the nose, which would allow this kind of treatment to work for men as well.”

While further down the road, the researchers aim to test this method in human clinical trials, because ultimately, the goal is to develop a vaccine for humans.

“A lot of the suffering patients go through is not just physical; it’s mental and societal,” said Iwasaki. “But viruses are the same — whether it’s the flu or Epstein-Barr virus or herpes simplex, it’s not the person’s fault that they caught it. And yet there’s a lot of stigma. We hope that this kind of strategy will prevent diseases that affect people in a profound way.”

---

DOI

10.1126/sciimmunol.aea6419 

Article Title

Bioactive enhanced adjuvant chemokine oligonucleotide nanoparticles (BEACONs) for mucosal vaccination against genital herpes

Article Publication Date

19-Jun-2026

 

UMass Amherst-led team discovers new way to make thermally insulative plastics

Plastics with low thermal conductivity could have aerospace and energy-efficient building applications

University of Massachusetts Amherst

LinkedInWeChatBlueskyMessageWhatsAppEmail

 

image: 

An illustration of THDBT (tetrahydroxy deoxybenzoin triazole) filler aggregates at the molecular level. In this “slow chaos” state, there are fewer vibrational pathways available for heat transport, resulting in lower thermal conductivity. Reproduced from Materials Horizons with permission from the Royal Society of Chemistry. 

view more 

Credit: Yanfei Xu, UMass Amherst; Reproduced from Materials Horizons with permission from the Royal Society of Chemistry.

AMHERST, Mass. — University of Massachusetts Amherst researchers have demonstrated a possible new avenue for developing flame-retardant and generally low-conductivity (low heat transfer) plastics that retain the benefits of being strong and flexible by limiting the accessibility of heat-carrying vibrational channels of the material. This new design framework has promising applications, including lightweight thermal insulation materials for spacesuits, thermal protection components for spacecraft and advanced building materials that reduce heating and cooling losses. 

 

Thermal conductivity is a measure of how efficiently heat can move across a material. When heat moves quickly, the material is conductive. If heat moves slowly, the material is a good insulator. Conventionally, materials are made more insulative by the introduction of pockets of air, which are poor conductors. While effective for inorganic materials, this method does not work for plastics because it can weaken the material and complicate manufacturing.  

 

Yanfei Xu, corresponding author of the study and assistant professor in the Riccio College of Engineering at UMass Amherst, and her team investigated a new way to reduce conductivity without introducing porosity. Instead, they looked at the material’s vibration on an atomic level. Heat moves when vibrational energy is passed from one atom to another, much like a bucket brigade passes water down a line. Firefighters (here representing the atoms) move the bucket (representing heat) in coordinated movement, efficiently from point A to point B. 

 

To reduce conductivity, Xu and her team used vibrational engineering so that, instead of strong firefighters efficiently passing big buckets from one person to the next, the polymer behaves like a group of disorganized toddlers—no two children are moving in the same direction and the small hands can only carry small cups instead of big buckets.  

 

As a result, the heat moves along the material very slowly. In their initial trial of this new method (tested using a polymer hybrid of polyurethane and tetrahydroxy deoxybenzoin triazole), the researchers found that this “slow chaos,” as Xu describes the polymer’s behavior, reduced conductivity by 17%. The material also demonstrated flame-retardant behavior. 

 

Xu points out that their reduction in thermal conductivity is small in this initial testing, but she is excited about their discovery of a new mechanism for governing thermal conductivity.  

 

“There is a lot of potential,” she says. “By reducing the density of thermally accessible vibrational channels available for heat transport, thermal conductivity is suppressed. The materials remain dense, mechanically compliant and flame-retardant.”  

 

This research, published in Materials Horizons, was featured on the journal’s front cover. The work was conducted in collaboration with scientists from North Carolina State University, Massachusetts Institute of Technology, Texas A&M University, and Brookhaven, Oak Ridge and Argonne national laboratories. 

 

The research was supported by the U.S. National Science Foundation, the Federal Aviation Administration and UMass Amherst.  

 

---

Journal

Materials Horizons

DOI

10.1039/D6MH00633G 

Method of Research

Experimental study

Subject of Research

Not applicable

Article Title

Suppressing thermal transport in nonporous polymer hybrids by limiting thermally accessible vibrational modes

 

Faster aging in younger generations linked to rise in early-onset cancer

Immune system aging linked to earlier lung cancer; fat tissue aging linked to earlier colorectal cancer

WashU Medicine

Facebook

XLinkedInWeChatBlueskyMessageWhatsAppEmail

Cancer is often considered a disease of aging. Older adults are at higher risk because they have had more time to accumulate cellular damage that can trigger tumor formation. But as cancer rates in younger adults rise, with each successive generation facing higher risks than the one before it, researchers are asking whether cellular damage is accumulating faster in recent generations, accelerating their body’s biological aging.

A new study led by researchers at Washington University School of Medicine in St. Louis provides evidence that younger generations are indeed aging faster biologically than their older counterparts. The causes remain under investigation around the world, including global efforts led by research members of Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, and Cancer Grand Challenges, a global initiative co-founded by the National Cancer Institute and Cancer Research U.K.; but importantly, the new research links this accelerated aging to an increased risk of early-onset cancers in younger generations. In general, early-onset cancers are those diagnosed at age 55 or younger.

The larger the gap between biological age — that is, how old our bodies appear to be — and chronological age — which is how many years we have actually lived — the higher the cancer risk, according to the researchers. They found that people in more recent birth cohorts had larger age gaps than those in older birth cohorts, which may help explain the rise in early-onset cancer in recent generations.

Their study also identified links between faster aging in particular organ systems and increased risks for certain cancers. For instance, an immune system that appears older than its actual age was associated with early-onset lung cancer. Similarly, fat tissue that appears older than its chronological age was associated with early-onset colorectal cancer.

The study, published June 22 in the journal Nature Medicine, suggests that measures of accelerated aging could help identify individuals at higher risk of early-onset cancer and guide new strategies for cancer prevention and early detection.

“Our ultimate goal is to decode how modern environments become biologically embedded to drive cancer risk, transforming prevention from broad recommendations to personalized interventions,” said Yin Cao, ScD, a molecular epidemiologist and an associate professor of surgery and of medicine at WashU Medicine. “This brings us closer to identifying risk earlier and developing prevention strategies that are tailored to an individual’s biology.”

Exploring biological aging

Cao’s team has been at the forefront of identifying individual factors that influence cancer risk across the life course, such as obesity, metabolic dysregulation, alcohol consumption, sedentary behavior, poor diet quality and cesarean delivery. Although these discoveries have revealed important clues to the origins of cancer at younger ages, the contribution of any single factor is modest.

With that in mind, Cao, also a research member of Siteman, and her colleagues have sought ways to capture the influence of multiple risk factors operating together to spur cancer development. With support from Cancer Grand Challenges, Cao, as co-lead of Team PROSPECT, has been able to go after this problem.

For the current study, Cao’s team analyzed data from more than 154,000 young adults in the UK Biobank, a large biomedical dataset containing biological, health and lifestyle data, and from more than 10,000 individuals in the U.S. participating in the National Institutes of Health’s (NIH) All of Us Research Program, an effort to build a comprehensive health dataset on more than 1 million people living in the U.S.

To estimate the level of biological aging — or age gap — the researchers, including first author Ruiyi Tian, a doctoral student in the Cao lab, examined aging at two levels: across the body as a whole, known as systemic aging, and within individual organs, known as organ-specific aging. For systemic aging, the researchers used established measures, including clinical biomarker-based measures such as PhenoAge and the Klemera-Doubal Method, as well as a metabolomic age score, which provides a measure of individual metabolism.

PhenoAge, for example, measures nine blood biochemistry markers such as albumin, made by the liver, and creatinine, a waste product removed by the kidneys. For organ-specific aging, the researchers used blood proteomic data, which measure levels of multiple proteins linked to specific organ systems, to estimate biological aging in individual organs.

The researchers calculated the average age gap for each birth cohort and used standard deviation to describe how much each group differed from the study average. Standard deviation is a measure of how spread out data points are around the average.

The researchers found that individuals in the UK born between 1965 and 1974 had systemic aging that was 23% of one standard deviation higher compared with those born between 1950 and 1954, after accounting for chronological age. In other words, people in the younger birth cohort showed a modest shift toward older biological profiles than people in the older birth cohort when at the same chronological age.

The researchers observed a similar pattern in the U.S cohort. Participants born between 1990 and 1999 had systemic aging that was 92% of one standard deviation higher compared with those born between 1965 and 1969.

This increased systemic aging in the younger group was associated with an 8% increased risk of early-onset solid cancers, especially lung, gastrointestinal and uterine cancers. When participants were divided into three groups based on their level of systemic aging, those with the most advanced systemic aging had a 15% increased risk of early-onset solid cancer compared with those with the least advanced systemic aging. According to the analysis, the increased risk persisted even after controlling for inherited genetic risks of cancer and genetic susceptibility to accelerated aging.

By zooming into organ-specific aging, the researchers found that advanced immune system aging was associated with increased risk of early-onset lung cancer, and advanced adipose (fat) tissue aging was associated with increased risk of early-onset colorectal cancer.

“If we can identify younger people with the highest cancer risk when they are still healthy, we can focus on prevention and early-detection strategies for the individuals who will benefit most from early interventions,” Cao said.

This research is part of Team PROSPECT, a Cancer Grand Challenges team co-led by Cao. Cancer Grand Challenges is a global research funding initiative co-founded by Cancer Research UK and the National Cancer Institute (NCI) that brings together world-leading researchers to take on cancer’s toughest challenges.

“Right now, we don’t have a definitive answer to what’s driving the rise of early-onset cancers around the world, but studies like this are helping us piece together the bigger picture, showing that cancer may be influenced not just by changes inside individual cells, but by wider changes happening across the body as a whole,” said David Scott, PhD, director of Cancer Grand Challenges.  “Research on this scale is possible through Cancer Grand Challenges, which brings together scientists from different fields around the world to tackle these complex questions together.”

Cao and her colleagues are leading efforts to transform the understanding of why cancers are increasingly striking younger generations. Their next frontier is to decipher how environmental, lifestyle and societal changes leave lasting biological imprints, including accelerated aging and other markers of heightened susceptibility. By illuminating the pathways through which risk accumulates across the life course, they seek to uncover the origins of early-onset cancers and redefine opportunities for prevention. In parallel, their work will enable more precise approaches to identify those at greatest risk and intervene earlier, shifting the paradigm from reacting to disease to preventing it before it begins.

--

Tian R, Zong Y, Ren D, Tica S, Hong D, Odulyale O, Buenrostro J, Govindan R, Cao Y. Biological aging and generational shifts in early-onset cancer risk. Nature Medicine. June 22, 2026. DOI: 10.1038/s41591-026-04448-w.

This work was part of the PROSPECT team supported by the Cancer Grand Challenges initiative funded by Cancer Research UK, grant numbers CGCATF-2023/100043 and CGCATF-2023/100037; the National Cancer Institute of the NIH, grant numbers OT2CA297577 and OT2CA297576; the French National Cancer Institute; and the Bowelbabe Fund for Cancer Research UK. The project was also supported by grants from NIH/National Cancer Institute, grant number R37CA246175; the NIH/National Institute of Diabetes and Digestive and Kidney Diseases, grant number P30DK052574; the Alvin J. Siteman Cancer Center through the Foundation for Barnes-Jewish Hospital. Further support was provided by a pre-doctoral fellowship in the Cancer Biology pathway supported by NIH Molecular Oncology Training Grant T32CA113275 to Washington University School of Medicine in St. Louis; the Pediatric Gastroenterology Research Training Program grant T32DK077653 to Washington University School of Medicine in St. Louis; the Washington University School of Medicine in St. Louis Institute of Clinical and Translational Sciences, grant number UL1TR002345; and the Foundation for Barnes-Jewish Hospital. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

About WashU Medicine

WashU Medicine is a global leader in academic medicine, including biomedical research, patient care and educational programs with 3,100 faculty. Its National Institutes of Health (NIH) research funding portfolio is the second largest among U.S. medical schools and has grown 78% since 2016. Together with institutional investment, WashU Medicine commits over $1.6 billion annually to basic and clinical research innovation and training. Its faculty practice is consistently among the top five in the country, with more than 2,550 faculty physicians practicing at 200 locations. WashU Medicine physicians exclusively staff Barnes-Jewish and St. Louis Children’s hospitals — the academic hospitals of BJC HealthCare — and Siteman Cancer Center, a partnership between BJC HealthCare and WashU Medicine and the only National Cancer Institute-designated comprehensive cancer center in Missouri and southern Illinois. WashU Medicine physicians also treat patients at BJC’s community hospitals in our region. With a storied history in MD/PhD training, WashU Medicine recently dedicated $100 million to scholarships and curriculum renewal for its medical students, and is home to top-notch training programs in every medical subspecialty as well as physical therapy, occupational therapy, and audiology and communications sciences.

---

Journal

Nature Medicine

DOI

10.1038/s41591-026-04448-w 

Article Title

Biological aging and generational shifts in early-onset cancer risk

Article Publication Date

22-Jun-2026