Team pinpoints tendon disease trigger

Researchers have discovered a trigger of tendon disease.

Complaints such as pain in the Achilles tendon, tennis elbow, swimmer’s shoulder, and jumper’s knee are familiar to many young sportspeople, as well as to older individuals.

These conditions are all caused by overloading of tendons and are generally very painful.

“Tendons are fundamentally susceptible to overuse,” explains Jess Snedeker, a professor of orthopaedic biomechanics at ETH Zurich and Balgrist University Hospital in Zurich.

“They must withstand powerful loads, with all the forces of our muscles being concentrated to the relatively thin tendons that transmit these forces into movement of our skeleton.”

In medical terms, the aforementioned conditions are known as tendinopathies. They are some of the most frequent conditions seen by orthopedic specialists, but treatment options are extremely limited. Although physiotherapy can help, there are many serious cases for which this treatment does not achieve much. Scientists are therefore keen to research these tendon problems in greater depth with a view to developing effective treatments.

Now, a team of researchers led by Snedeker and by Katrien De Bock, professor of exercise and health at ETH Zurich, has reached a new milestone. In the HIF1 protein, they have identified a central molecular driver of tendon problems of this kind. A part of HIF1 acts as a transcription factor, which controls the activity of genes in cells.

This protein was already known to be present at elevated levels in diseased tendons. However, it was unclear whether the increase was simply a concomitant phenomenon or whether the conditions are actually triggered by the protein. In experiments in mice and with tendon tissue from humans, the team of researchers has now shown the latter to be the case.

In mouse experiments, the researchers either activated the HIF1 protein permanently or switched it off completely. Whereas they observed tendon disease even without overloading in the mice with permanently activated HIF1, no tendon disease occurred in the mice if HIF1 was deactivated in tendons, even in the case of overloading.

Both in the mice and in the experiments with human tendon cells, which the researchers obtained from tendon surgeries at the hospital, they were able to show that elevated HIF1 levels in the tissue leads to a pathogenic remodeling of the tendons: More crosslinks form within the collagen fibers that make up the basic structure of the tendons.

“This makes the tendons more brittle and impairs their mechanical function,” explains Greta Moschini, a doctoral student in De Bock and Snedeker’s groups and lead author of the study. In addition, blood vessels and nerves growth into the tendon tissue. “This could be the explanation for the pain commonly observed in tendinopathy,” says Moschini.

“Our study not only provides new insight into how the disease develops. It also shows that it’s important to treat tendon problems early,” says Snedeker. He is thinking particularly of young athletes, who frequently struggle with tendinopathies. In these cases, it is often still possible to treat the problems.

“However, the damage caused by HIF1 in tendon tissue can accumulate and become irreversible over time. Physiotherapy then no longer helps, and the only treatment at this moment is to surgically remove the diseased tendon.”

The fact that HIF1 has now been identified as a molecular driver raises the question whether it is possible to develop medicines that deactivate HIF1 and therefore can prevent or cure tendon disease. It is not quite that easy, explains ETH Professor De Bock. In many organs of the body, HIF1 is responsible for detecting a lack of oxygen (hypoxia) and activating a physiological adaptation. “Switching HIF1 off throughout the body would likely lead to side effects,” she says.

It may be possible to look for methods that specifically deactivate HIF1 only in the tendon tissue. In De Bock’s view, however, the more promising approach would be to explore the biochemical processes around HIF1 in the cells in greater detail. This could help to identify other molecules that are influenced or controlled by HIF1 and that could be more suitable targets for the treatment of tendinopathy. The researchers will now embark on precisely that search.

The research appears in Science Translational Medicine.

Source: ETH Zurich

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How brain networks work together is key to human intelligence

Researchers have conducted a neuroimaging study to investigate how the brain is organized and how that integrated system gives rise to intelligence.

Modern neuroscience understands the brain as a set of specialized systems. Aspects of brain function such as attention, perception, memory, language, and thought have been mapped onto distinct brain networks, and each has been examined largely in isolation.

While this approach has yielded major advances, it has left unresolved one of the most basic facts about human cognition: its overall unity as an integrated system.

“Neuroscience has been very successful at explaining what particular networks do, but much less successful at explaining how a single, coherent mind emerges from their interaction,” says Aron Barbey, a professor of psychology in the University of Notre Dame’s psychology department.

How cognitive ties form ‘general intelligence’

Psychologists have long known that areas as diverse as attention, perception, memory and language are correlated, forming what they term “general intelligence.” This accounts for how humans function and adapt in a wide range of academic, professional, social, and health contexts. It shapes how efficiently we learn, reason, and perform in response to a multitude of everyday problems and tasks.

For more than a century, this structure has suggested that cognition is unified at a fundamental level. What has been missing is a theory to explain why such unity exists.

“The problem of intelligence is not one of functional localization,” says Barbey, who is also the director of the Notre Dame Human Neuroimaging Center and the Decision Neuroscience Laboratory.

“Contemporary research often asks where general intelligence originates in the brain—focusing primarily on a specific network of regions within the frontal and parietal cortex. But the more fundamental question is how intelligence emerges from the principles that govern global brain function—how distributed networks communicate and collectively process information.”

Barbey and his research team, including Notre Dame graduate student and lead author Ramsey Wilcox, investigated the predictions of the unifying framework, called the Network Neuroscience Theory.

Their study appears in the journal Nature Communications.

The Network Neuroscience Theory

General intelligence is not itself a skill or strategy, the researchers argue. It is a pattern—the tendency for diverse abilities to be positively correlated. The study argues that this pattern reflects differences in how efficiently brain networks are organized and work together.

To test this claim, the cognitive neuroscientists analyzed brain imaging and cognitive data from one of the largest studies conducted to date, examining 831 adults in the Human Connectome Project, along with an independent sample of 145 adults in the INSIGHT Study, which was funded by the Intelligence Advanced Research Projects Activity’s SHARP program. The researchers integrated measures of both brain structure and function to enable a more precise characterization of the human brain.

Rather than identifying intelligence with a particular cognitive function or brain network, the Network Neuroscience Theory characterizes it as a property of how the brain works as a whole. In this view, intelligence reflects how brain networks are coordinated and dynamically reconfigured to solve the diverse problems we encounter in life.

This research represents an important shift, according to Barbey and Wilcox.

“We found evidence for system-wide coordination in the brain that is both robust and adaptable,” Wilcox says. “This coordination does not carry out cognition itself, but determines the range of cognitive operations the system can support.”

“Within this framework, the brain is modeled as a network whose behavior is constrained by global properties such as efficiency, flexibility and integration,” Wilcox says. “These properties are not tied to individual tasks or brain networks, but are characteristics of the system as a whole, shaping every cognitive operation without being reducible to any one of them.”

“Once the question shifts from where intelligence is to how the system is organized,” Wilcox noted, “the empirical targets change.”

Coordinated system of networks

The researchers found evidence to support four predictions of the Network Neuroscience Theory.

First, the theory predicts that intelligence is not localized to a single brain network but arises from processing distributed across multiple networks. Intelligence, therefore, depends on how the brain manages the division of labor across different networks and combines them as needed.

Second, for the brain to manage this distributed processing, it requires integration and effective long-range communications. To synchronize those efforts, Barbey says, there is “a large and complex system of connections that serve as ‘shortcuts’ linking distant brain regions and integrating information across the networks.” These pathways connect structurally distant areas of the brain, enabling efficient communication and supporting coordinated processing across the system.

Third, effective integration requires regulatory control that coordinates interactions among networks by shaping how information flows throughout the brain. These areas serve as regulatory hubs, reaching out to other networks to orchestrate the brain’s ongoing activities. They selectively recruit the appropriate networks for the specific task at hand—whether it be piecing together subtle clues to make sense of a problem, learning a new skill, or deciding whether a situation requires careful deliberation or a rapid, intuitive response.

Finally, Barbey says that general intelligence depends on the brain’s ability to balance local specialization with global integration. In other words, the brain functions best when tightly connected local clusters communicate well, but are still able to link to distant regions of the brain across short communication paths. This makes the most effective problem-solving possible, according to the coauthors.

The research suggests that intelligence is unified not because the brain relies on a single general-purpose processor, but because the same organizational principles shape how all cognitive functions work together.

Across both datasets, individual differences in general intelligence were consistently associated with these system-level properties. No single region or canonical “intelligence network” accounted for the effect.

“General intelligence becomes visible when cognition is coordinated,” Barbey noted, “when many processes must work together under system-level constraints.”

Applications for artificial intelligence

The implications of this study extend beyond intelligence research, he adds. By grounding cognition in large-scale organization, the study offers a principled account of why the mind is unified at all.

This framework helps explain why intelligence develops broadly during childhood, declines with aging, and is particularly sensitive to diffuse brain injury. In each case, it is large-scale coordination—not isolated function—that changes.

The findings also inform ongoing debates about artificial intelligence and how AI models are developed. If general intelligence in humans arises from system-level organization rather than from a dedicated general-purpose mechanism, then achieving general intelligence in artificial systems may require more than the accumulation or scaling of specialized capabilities.

“This research can push us into thinking about how to use design characteristics of the human brain to motivate advances in human-centered, biologically inspired artificial intelligence,” Barbey says.

“Many AI systems can perform specific tasks very well, but they still struggle to apply what they know across different situations.” Barbey says. “Human intelligence is defined by this flexibility—and it reflects the unique organization of the human brain.”

The research was conducted with coauthors Babak Hemmatian and Lav Varshney of Stony Brook University.

Source: University of Notre Dame

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Stuff in cherries may slow agressive breast cancer

Natural compounds found in dark sweet cherries may help slow the growth and spread of one of the most aggressive forms of breast cancer, according to new research.

The study examined the effects of anthocyanins—natural plant pigments that give fruits like dark sweet cherries their deep red color—on triple-negative breast cancer, a disease known for its limited treatment options and high risk of metastasis.

Researchers from the Texas A&M University College of Agriculture and Life Sciences, Texas A&M AgriLife Research, and College of Veterinary Medicine and Biomedical Sciences (VMBS) found that anthocyanin treatment slowed tumor growth, reduced cancer spread to multiple organs, and altered gene activity linked to metastasis and therapy resistance.

“Triple-negative breast cancer is considered ‘the worst’ because it is more aggressive, higher grade, and has a higher mitotic index, meaning the cancer cells divide quickly,” says Giuliana Noratto, AgriLife Research associate research scientist in the College of Agriculture and Life Sciences’ food science and technology department.

“All these characteristics make it more likely to spread to distant organs and recur compared to other breast cancer types.”

Unlike other breast cancer subtypes, triple-negative breast cancer lacks estrogen receptors, progesterone receptors, and expression of the HER2 protein, a growth-promoting protein that helps regulate how cells grow and multiply.

Because of the absence of these molecular targets, the cancer has fewer treatment options and is more likely to metastasize to different organs, particularly to the lungs and brain, according to Noratto.

Tumor growth, metastasis, and gene activity

Rather than focusing only on tumor size, the researchers designed the study to evaluate both tumor growth and metastatic spread, which is the primary cause of cancer-related deaths.

“This is important because cancer lethality is primarily due to metastasis,” Noratto says. “A large primary tumor that does not metastasize may be more manageable, even curable if removed.”

To test whether anthocyanins could influence both tumor growth and spread, mice were divided into four treatment groups: a control group, a group that received anthocyanins before tumor implantation, a group treated with the chemotherapy drug doxorubicin after tumors developed, and a group that received both anthocyanins and chemotherapy.

This design allowed researchers to examine anthocyanins as a preventive strategy and to evaluate whether they could enhance the effectiveness of chemotherapy.

They found that mice receiving anthocyanin-rich dark sweet cherry extracts before tumor implantation showed slower tumor growth without noticeable side effects and that treated mice continued to gain weight throughout the study period.

In comparison, mice treated with chemotherapy alone sometimes lost weight, and tumor growth slowed later in the study. When anthocyanins were combined with chemotherapy, tumor growth slowed earlier and mice maintained their weight.

In addition to these physical changes, researchers examined gene expression in tumors, which refers to which genes are turned “on” or “off” in cancer cells and helps determine which specific cellular processes are affected by dark sweet cherry anthocyanins, according to Noratto.

The study found that anthocyanins, whether alone or combined with chemotherapy, reduced the activity of genes associated with cancer spread and therapy resistance, a process in which cancer cells adapt to survive despite treatment.

In addition, anthocyanin treatment also reduced the spread of cancer to the lungs beyond what was observed with no treatment or chemotherapy alone. The treatment also lowered the likelihood of cancer spreading to other organs, including the liver, heart, kidneys, and spleen, although the number and size of tumors varied among individual animals.

What tissue analysis revealed

To better understand how these molecular changes translated into physical changes in the cancer, the research team relied on histology—the study of tissue samples under a microscope—conducted by Lauren Stranahan, a VMBS veterinary pathologist.

Using this approach, Stranahan examined how rapidly cancer cells were dividing—a measure known as mitotic index—as well as how much of each organ was infiltrated by metastatic cancer cells and whether that tissue damage could interfere with organ function.

“Some tumors had a higher mitotic rate, so they were dividing faster,” she says.

Some tumors also showed signs of necrosis, or tissue death, which can occur when rapidly growing tumors outpace their blood supply.

In addition to tumor structure, Stranahan evaluated immune cell infiltration, including T lymphocytes, immune cells that play an important role in recognizing and destroying abnormal cells, including cancer cells.

“When we’re evaluating how aggressive a cancer is, we can also evaluate, ‘is that cancer able to reduce the number of T-cells that are coming after it?'” she says.

Supportive strategies

Their findings also reinforce a growing understanding in cancer research: no single treatment is enough on its own.

“What we’re understanding about cancer now is that no single treatment is going to be effective against a cancer,” Stranahan says. “You’re going to have to employ a number of different treatments.”

Within that broader approach, Noratto says diet-derived compounds may help target cancer-related processes that are not fully addressed by standard therapies, offering researchers additional pathways to explore alongside existing treatments.

While the findings point to promising new directions, additional research would be needed to better understand how anthocyanins influence tumor behavior, including their safety, absorption and potential role alongside existing cancer treatments.

The research appears in the International Journal of Molecular Sciences.

Source: Texas A&M University

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How do plants know when it’s time to bloom?

An expert has answers for you about how plants know when to bloom.

Last December was the warmest on record for Washington state, according to the Washington State Climate Office.

As the mild winter continues, many of the plants in our gardens are starting to show signs of small buds, even though it’s only February.

Takato Imaizumi, a University of Washington professor of biology, studies the genes that plants use to monitor seasonal changes.

Here, Imaizumi talks about how plants know when to bloom and whether this might change in warmer winters:

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A few changes to the home can cut adult asthma attacks

Improving the indoor environment reduces asthma attacks in adults, a new study finds.

For adults with asthma, having fans, air purifiers, or other ventilation and exhaust systems—especially in kitchens and bathrooms—is one of the best ways to reduce the risk of flare-ups at home.

That’s the key finding of a large, statewide survey of how household environments affect adults with asthma in Texas.

“Most studies of this type focus on children, but since most asthma cases in the US are in adults, we looked at them and their indoor environment,” says Alexander Obeng, a doctoral student at the Texas A&M University School of Public Health and the study’s lead author.

He adds that Texas was an ideal setting for the study because of its wide range of climates and housing conditions.

“Air conditioning is a constant across much of the state during warmer months, which reduces natural ventilation and may increase indoor pollutant levels,” he says.

“In addition, many older homes, mobile homes, and multi-unit residences have problems with excess moisture and pests.”

For the study in Atmosphere, the team looked at data on 1,600 adults with asthma collected between 2019 and 2022 to assess the effects between household and environmental determinants of asthma morbidity in Texas. The team analyzed four outcomes—asthma attacks, symptoms, sleep problems, and limitations with daily activities—and how they are linked to a person’s surroundings.

“We found two major triggers for asthma in the home—not having an exhaust fan in the kitchen and bathroom, and smoking—which affirms previous research,” Obeng says.

In addition, the team found that people were more likely to have asthma attacks, frequent symptoms, or trouble sleeping and staying active if they smoke cigarettes or do not use air purifiers. On the other hand, people living in homes that had no problems with mold, mice or rats, and had no furry pets had fewer asthma issues.

“The good news is that we can take steps to manage asthma at home by improving airflow, using air purifiers, not smoking indoors, and minimizing dust or pet allergens,” he says.

The data also showed that women, older adults, and Black adults suffer more from asthma complications than other groups, reflecting disparities in income, housing quality, and access to health care that Obeng says may worsen the asthma burden for some.

To help reduce the burden of asthma for these groups, the study recommended three strategies:

• Financial help. Offer vouchers or subsidies to help low-income families afford portable air purifiers, upgrade their homes, and improve household ventilation.
• Support for renters. Require landlords to maintain healthy air standards and fix ventilation issues.
• Better education. Have health care professions teach patients how to remove asthma triggers (like dust or mold) from their homes as part of their regular medical checkups.

“Adults spend as much as 90% of their time indoors, where the air can actually be dirtier than it is outdoors,” Obeng says.

“Adequate environmental changes at home could help adults with asthma manage their condition more effectively.”

Additional researchers from the Texas A&M School of Public Health and the University of Strathclyde in Scotland contributed to the work.

Source: Texas A&M University

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Listen: New treatments are changing lives after spinal cord injuries

When a two-year-old boy suffered a catastrophic injury that severed the connection between his skull and spine, doctors across Europe told his family there was no hope.

His spinal cord was completely severed, and the injury was not considered survivable.

But University of Chicago neurosurgeon Mohamad Bydon saw a possibility.

In this episode of Big Brains, Bydon walks us through the extraordinary, multi-stage surgery at UChicago that not only saved the boy’s life but helped him regain the ability to breathe, talk, and move his fingers and toes.

He examines the future of surgery for spinal cord injury patients—from minimally invasive surgery techniques to robotic surgery and AI to stem cell therapy—is even helping some paralyzed patients regain movement and even walk again after their injuries.

Read the transcript of this episode.

Source: University of Chicago

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Ultraprocessed foods have addictive qualities similar to tobacco

Addictive qualities in ultraprocessed foods are similar to those of tobacco, researchers report.

The researchers from the University of Michigan, Harvard University, and Duke University argue that many ultraprocessed foods—including packaged snacks, sugary beverages, ready-to-eat meals, and many fast foods—aren’t simply junk food or bad nutritional choices. They’re industrially engineered products designed to keep you coming back—using strategies once used to sell cigarettes.

The research, which appears in the current issue of The Milbank Quarterly, draws on addiction science, nutrition research, and the history of tobacco regulation.

It found striking similarities between ultraprocessed foods and tobacco products—both deliberately formulated to amplify reward in the brain, encourage habitual use, and shape public perception in ways that protect profits.

In other words, it may not be by accident that certain snacks feel impossible to put down, says study first author Ashley Gearhardt, University of Michigan professor of clinical psychology and an expert at UM’s Institute for Healthcare Policy and Innovation.

This reframing matters—especially for young adults navigating food environments packed with cheap, hyperpalatable, always-available options, the researchers note. For decades, public health messaging has emphasized personal responsibility: make better choices, try harder, have more self-control.

But the newly published analysis argues it’s time to change the focus. Instead of focusing only on individual decisions, the authors call for a shift toward examining the larger systems that shape what’s on shelves, what’s affordable, and what’s heavily marketed. Just as tobacco regulation eventually moved beyond blaming smokers to holding companies accountable, the researchers suggest food policy may need a similar evolution.

Gearhardt says the takeaway isn’t that eating is the same as smoking. It’s that some of today’s most common foods may be designed in ways that make moderation unusually difficult.

For a generation that grew up surrounded by brightly packaged snacks, drive-thru convenience and 24/7 delivery apps, the question becomes bigger than diet trends or personal discipline.

“It’s about understanding how products are engineered—and who benefits when ‘just one more bite’ turns into a habit,” Gearhardt says.

The researchers hope the findings spark conversation, especially among young adults who are shaping the future of food culture, health policy, and consumer expectations.

Because if certain foods are designed to be hard to resist, the conversation about health might need to move beyond blame—and toward accountability, the researchers say.

Source: University of Michigan

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