How can you get rid of a phobia?

An expert has answers for you about what phobias are and how you can get rid of them.

In the Alfred Hitchcock classic film Vertigo, the protagonist John “Scottie” Ferguson, played by James Stewart, is plagued with acrophobia, or an extreme fear of heights. This condition impairs him to such a degree that he is forced to retire from his job as a police officer, and it creates emotional turmoil central to the movie’s plot.

Phobias.

Many suffer from them. Whether it is a fear of spiders (arachnophobia) or fear of enclosed spaces (claustrophobia) or fear of rats (musophobia), as many as 13% of the US population are affected by them.

Here, Jill Ehrenreich-May, professor in the psychology department at the University of Miami and director of the Child and Adolescent Mood and Anxiety Treatment program, explains more about phobias:

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Team turns DNA into a rewritable hard drive

Researchers are developing a rewritable DNA hard drive.

Around the world, scientists are exploring an unexpected solution to the growing data crisis: storing digital information in synthetic DNA. The idea is simple but powerful—DNA is one of the most compact, durable information systems on Earth.

But one issue has held the field back. Once data is written into DNA, it can’t be changed.

Now, researchers at the University of Missouri are helping solve that problem by transforming DNA from a one-time medium into a rewritable digital hard drive.

“DNA is incredible—it stores life’s blueprint in a tiny, stable package,” Li-Qun “Andrew” Gu, a professor of chemical and biomedical engineering at Mizzou’s College of Engineering, says.

“We wanted to see if we could store and rewrite information at the molecular level faster, simpler, and more efficiently than ever before.”

Why DNA?

Today’s computers store information as a series of zeros and ones. DNA-based data storage goes a step further by turning those bits into sequences of letters—A, C, G, and T—the same building blocks that make up DNA.

To store digital files in DNA, scientists translate the zeros and ones that make up photos, videos, and other data into sequences of those four chemical letters. Machines then build synthetic strands carrying that exact pattern.

DNA’s advantages are striking. It can hold huge amounts of information in tiny volumes—theoretically, all the world’s data could fit into something the size of a shoebox. When kept dry and cool, it remains stable for thousands of years. And storing data this way requires far less energy than running massive data centers.

Until now, however, DNA storage has been permanent. Once the data is encoded, it can’t be updated or reused—a major limitation for anything beyond long-term archiving.

That’s where Gu’s team comes in. They’ve developed a method that allows data stored in DNA to be erased and overwritten repeatedly. This rewritability is essential for any storage system meant for regular, everyday use.

Their method allows DNA to function less like a static archive and more like a modern hard drive—one with extraordinary storage density and longevity.

Retrieving the information requires reading the DNA sequence. The Mizzou team is developing a compact electronic device paired with a molecular-scale detector called a nanopore sensor. As the DNA passes through the sensor, it creates subtle electrical changes that software translates back into zeros and ones and, ultimately, the original data file.

Mizzou’s system is faster, simpler, and more environmentally friendly than existing methods. In the long term, Gu hopes to shrink the device into something about the size of a USB thumb drive.

High-capacity and ultra-secure

DNA stores information in three dimensions rather than on a flat computer chip, giving it unparalleled storage density. And because it exists as a physical molecule rather than a constantly connected electronic system, it offers additional protection against hackers.

“Think of it like a super-secure safe deposit box for your digital life,” Gu says. “DNA storage could protect everything from personal memories and important documents to scientific data and corporate archives—without the added cybersecurity concerns.”

While many research groups are advancing DNA storage, Mizzou’s work moves the field closer to a practical, rewritable system—a key milestone in making DNA a long-term replacement for some of today’s energy-hungry storage technologies.

The study appears in PNAS Nexus.

Source: University of Missouri

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Listen: Why is protein having a moment?

If you’ve walked the aisles of a grocery store, scrolled through social media, watched television, or set foot in a fast-casual restaurant chain in recent months, you know that protein is having its moment.

So, why are brands pushing protein? An International Food Information Council study found that 70% of adults are looking to increase their protein intake. But as it makes its way into more products than ever before, is it too much of a good thing?

Lesley Baradel is a registered dietitian, nutritionist, and lecturer in the College of Sciences at Georgia Tech. In this episode of Generating Buzz, she digs into the protein-packed trend, with implications ranging from health and wellness to marketing and how the rise of GLP-1s factors into the increased focus on the macronutrient:

Georgia Tech · Generating Buzz: A Protein-Packed Industry

Source: Georgia Tech

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Life forms can catch rides to other planets on asteroid debris

Tiny life forms tucked into debris from an asteroid hit could catapult to other planets—including Earth—and survive, a new study finds.

The work demonstrates that a certain hardy bacterium easily withstands extreme pressure comparable to an ejection from Mars after an asteroid hit, as well as the inhospitable conditions it would face during the ensuing interplanetary journey.

The study in PNAS Nexus suggests that microorganisms can survive remarkably more extreme conditions than expected, and raises questions about origins of life. The work also has significant implications for planetary protection and space missions.

“Life might actually survive being ejected from one planet and moving to another,” says senior author K.T. Ramesh, an engineer who studies how materials behave in extreme conditions.

“This is a really big deal that changes the way you think about the question of how life begins and how life began on Earth.”

Impact craters cover the surfaces of most bodies in the solar system. Mars, a planet that could harbor life, is one of the most cratered celestial bodies. We know asteroid strikes can launch material across space—and Martian meteorites have been found on Earth.

However, scientists have long wondered if life forms could also be launched from an asteroid impact. Tucked inside ejected debris, they might land on another planet—a theory called the lithopanspermia hypothesis.

Previous experiments to test the theory have been inconclusive, and targeted organisms widely found on Earth, rather than a life form that would suit the extreme environments of other planets.

To study how a microorganism would realistically handle the stress of a planetary ejection, the team devised a way to replicate the pressure and a singular biological model.

The team chose to test Deinococcus radiodurans, a desert bacterium found in the high deserts of Chile that is notorious for its ability to survive the most inhospitable, space-like conditions—everything from extreme cold and dryness to intense radiation. It has a thick shell and a remarkable ability to self-repair.

“We do not yet know if there is life on Mars, but if there is, it is likely to have similar abilities,” Ramesh says.

The experiment simulated the pressure of an asteroid strike and ejection from Mars by sandwiching the microbe between metal plates and then firing a projectile at it from a gas gun. The projectile hit the plates at speeds up to 300 mph, generating 1 to 3 Gigapascals of pressure.

For perspective, the pressure at the bottom of the Mariana Trench, the deepest part of the Earth’s oceans, is a tenth of a Gigapascal. Even the lowest pressure in this experiment is more than ten times that.

After shooting the microbes, the team determined whether they survived and examined the survivors’ genetic material for clues to how they handled the pressure.

The bacteria proved very hard to kill. They survived nearly every test at 1.4 Gigapascal of pressure and 60% at 2.4 Gigapascals of pressure. The cells showed no signs of damage after the lower pressure hits, but after the higher pressure experiments, the team observed some ruptured membranes and internal damage.

“We expected it to be dead at that first pressure,” says lead author Lily Zhao, a graduate student. “We started shooting it faster and faster. We kept trying to kill it, but it was really hard to kill.”

In the end, what did die was the equipment. The steel configuration holding the plates fell apart before the bacteria did.

When asteroids hit Mars, ejected fragments experience a range of pressures, perhaps close to 5 Gigapascals, though some could see much higher. Here the microbe easily survived almost 3, much higher than previously thought possible.

“We have shown that it is possible for life to survive large-scale impact and ejection,” Zhao says. “What that means is that life can potentially move between planets. Maybe we’re Martians!”

The possibility of life spreading between planetary bodies has significant implications for planetary protection and space missions, the team says.

Space mission protocols evaluate the likelihood of life surviving on the target planet. When missions travel to planets that might sustain life, like Mars, there are tight restrictions and safety measures to prevent contaminating the planet with Earth life. And when a mission brings back materials from a planet, there are very strict measures to control the possible release of that life on Earth. Because this work demonstrates that materials from Mars might reach other bodies, particularly its two nearby moons that aren’t currently restricted, the team says policies might need to be reassessed.

Phobos, in particular, orbits so close to Mars that any ejecta that gets there is probably exposed to much less pressure than what is required to get to Earth, the team says.

“We might need to be very careful about which planets we visit,” Ramesh says.

The team next hopes to explore whether repeat asteroid impacts result in hardier bacterial populations—or whether bacteria adapt to this kind of stress. They’d also like to see if other organisms, including fungi, can survive these conditions.

The work was supported by NASA’s Planetary Protection program.

Source: Johns Hopkins University

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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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