The Academic Minute

What does the fairy tale of the princess and the pea have to teach us about our cells?

Amit Pathak, professor of mechanical engineer and materials science at Washington University in St. Louis, feels the way through the research.

Amit Pathak is a Professor of Mechanical Engineering & Materials Science at Washington University in St. Louis. His research focuses on mechanobiology, exploring how cells sense and respond to mechanical properties of their environment, with applications in cancer metastasis, wound healing, and tissue engineering.

While diseases are traditionally defined by genetic alterations in cells, our bodies undergo mechanical changes as well. In my lab, we study mechanobiology, which asks: how do cells respond to the physical world around them?Over the last two decades, scientists have learned that cells aren’t just passive blobs. They actually sense the stiffness of the surfaces they stick to. This sensing—called mechanotransduction—guides how cells move, grow, and even turn into diseased versions of themselves.In a recent study, we found something surprising. Groups of epithelial cells—the kind that line your organs—can feel through layers of fibrous collagen up to 100 microns deep. It’s a bit like the fairy tale of the princess and the pea. She could feel a tiny pea under a pile of mattresses. In real life, it’s like the difference between sleeping on a mattress on the floor versus one on a bed frame—you feel the support differently. The epithelial cell clusters in our experiments did something similar: they push and pull on their surroundings to “feel” what’s beneath. Depending on the stiffness of their distant layers, which could be soft tissue, a hard tumor, or bone in the body, cells change how they move. This is an emergent property of cell collectives, because single cells can only sense a few microns deep. Based on this work, we suspect there may be specific regulatory proteins that help cells sense distant, disease-like environments—ones we may have overlooked. This kind of long-distance sensing could reveal new targets for cancer therapy.That’s the core mission of my lab: to understand whether and how cells can sense distant environments—ones they’ve encountered before, or ones they’re moving toward. If true, this could mean that mechanical memory shapes how cancer spreads or how healthy cells respond to nearby tumors.

Read More:

[PNAS] - Emergent depth-mechanosensing of epithelial collectives regulates cell clustering and dispersal on layered matrices

Cellular Mechanobiology Laboratory

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On this Student Spotlight: How rich and poor navigated Industrial Manchester may be different from what was previously thought.

Emily Chung, PhD candidate at the University of Cambridge, looks through records to shed more light on the history.

Emily is a PhD Candidate at the University of Cambridge, in the Cambridge Group for the History of Population and Social Structure. She holds a Bachelor’s of Architecture from Cal Poly San Luis Obispo and a master’s in Economic and Social History from Cambridge. Her doctoral research studies residential segregation and urban reform in 19th century Manchester, using census microdata alongside cartographic and qualitative primary sources to reconstruct experiences of life in the industrial city. Her recent paper, published in The Historical Journal, explores questions of proximity and segregation in 1840s Manchester.

Few cities were affected by the Industrial Revolution as quickly and dramatically as Manchester, which went from little more than a village in 1750 to the third largest city in Britain a century later. By the 1840s, the pressures of this growth was reflected in widespread overcrowding, disease, and severe social fragmentation. The image that has survived of industrial Manchester is one where rich and poor rarely, if ever, interacted and it has been assumed that this was the cause of residential segregation, keeping different classes to separate parts of the city. Looking more closely at census data from 1851, however, my research reveals the opposite was true: not only did doctors, engineers, and lawyers live in the same neighbourhoods as the poorest factory labourers, but they even shared the same buildings! Reviewing qualitative primary sources from this period, written by social investigators and observers like Friedrich Engels, Leon Faucher and James Kay-Shuttleworth, I find different explanations for mechanisms of segregation. Here, differences in daily and weekly routines associated with work, consumer practices, and approaches to leisure meant that individuals of very different classes rarely occupied the same spaces, and when they did, it was often at different times. Long industrial workdays, for example, were such that by the time middle-class shopkeepers, teachers, and accountants hit the streets, working-class labourers were long tucked away in factories. Throughout the week, the middle classes and domestics visited markets and grocers for freshly delivered produce, but the poor were forced to wait for their wages to be disbursed on Saturday evenings, by which point only the worst products were left and the wealthier long gone. Even on Sundays, the universal day off, classes self-segregated with the rich attending church and the poor gathering in pubs. Understanding the nuances of segregation remains of key importance today as many cities still struggle with the issue, and the case of Manchester shows that housing is but one of many factors which shape inequality and exclusion in urban space.

Read More:

[Cambridge Core] - Proximity and Segregation in Industrial Manchester

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How can we drive down real estate prices across the country?

John Hatfield, Century Club Professor of Finance at the McCombs School of Business at the University of Texas at Austin, looks into one possible avenue.

John Hatfield’s work in matching theory has facilitated the design of many real-world mechanisms, including FCC spectrum auctions, kidney paired donation, and the redesign of the U.S. Army’s branching mechanisms for assigning cadets. Hatfield also works at the intersection of the theory of industrial organization and the field of law and economics, which has advanced our understanding of anticompetitive practices in real estate agency and other markets.

In October 2023, a Missouri jury found that the National Association of Realtors and large real estate brokerages such as RE/MAX and Keller Williams “knowingly and voluntarily” worked together to keep real estate commissions high, resulting in a billion-dollar verdict. In the United States, real estate commissions comprise 5 to 6 percent of the purchase price of a home; in other countries, such as England, they only comprise one-and-a-half to two percent.In the U.S., real estate commissions for both the buyer’s and the seller’s agents are typically paid by the seller. The seller, upon listing the house for sale, offers a “cooperating commission” to the buyer agent representing the purchaser of the home.Our work shows that this has led to “steering.” Buyer agents steer clients to see homes offering higher commissions for the buyer agent, not necessarily the best homes for the buyer. This induces most sellers to all offer the same commission to buyers’ agents — 3 percent here in Austin. Sellers who offer a lower rate can expect less interest from homebuyers, as evidenced by fewer views on web portals such as Redfin. Their homes can then take 15 to 30 percent longer to sell and are more likely to not sell at all — a substantial risk for many families, who cannot afford to move until their old home is sold.Sellers thus feel compelled to offer high cooperating commissions to buyer agents to ensure that their home is seen by buyers — three quarters or more of sellers do this in the areas we study. And this keeps real estate commissions artificially high, costing a typical home seller thousands of dollars. And it leads to some sellers not moving at all, passing up on better opportunities for themselves and their families.The Department of Justice has suggested that we “decouple” the amount a buyer’s agent is paid from any decision by the seller. Instead, a buyer would negotiate directly with his agent over the agent’s compensation. Under that system, buyer agents would no longer have any reason to steer their clients.Unfortunately, the current settlement does not decouple buyer agent compensation and so far does not seem to be lowering agent commissions. Promoting real competition between agents in this market would drive down the cost of buying and selling a home and benefit consumers across America.

Read More:

[Iowa] - Et Tu, Agent? Commission-Based Steering in Residential Real Estate

SYSTEMATIC NATIONAL EVIDENCE OF STEERING BY REAL ESTATE AGENTS

[Wiley Online Library] - Collusion in Brokered Markets

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How can we transform cervical cancer screening for the better?

Rebecca Richards-Kortum, Malcolm Gillis university professor, professor of bioengineering and co-director of Rice360 Institute for Global Health Technologies, says it could only take an hour.

Rebecca Richards-Kortum is a biomedical engineer guided by the belief that all people deserve access to lifesaving technologies. She is known for improving access to lifesaving health technologies that address cancer, premature birth, sickle cell disease, and malaria. Technologies from her lab have been deployed to over 45 countries, providing a lifesaving impact to millions. Her lab’s current research includes developing systems for improving tumor removal accuracy, slide-free pathology, AI-assisted microendoscopy for early cancer detection, and HPV DNA nucleic acid test for cervical cancer screening.Richards-Kortum is the Rice University Malcolm Gillis University Professor of Bioengineering, Co-Director of the Rice360 Institute for Global Health Technologies, and Co-Chair of NEST360. Richards-Kortum was recognized as a MacArthur Foundation Fellow for her research in developing point-of-care devices for low-resource settings. She is one of five eminent U.S. scientists selected to serve the U.S. Department of State as a U.S. Science Envoy for Health Security. In 2023, Richards-Kortum was awarded the IEEE Medal for Innovations in Healthcare Technology.

Cervical cancer is one of the most preventable diseases in the world, yet it still claims more than 350,000 women’s lives every year. Most of those deaths occur in low- and middle-income countries, where access to regular screening is limited.We wanted to change that. Our team, which includes researchers from Rice University, the University of Texas MD Anderson Cancer Center, and partners in Mozambique, set out to develop a simple, affordable test for human papillomavirus, or HPV, the virus responsible for nearly all cases of cervical cancer.What we created is a one-hour, low-cost HPV test that doesn’t require a specialized laboratory. That means women can be screened and treated during the same clinic visit—something global health experts say could save countless lives.Here’s how it works. The test uses a method called loop-mediated isothermal amplification, or LAMP, to detect HPV DNA. It runs at a single temperature and doesn’t need the complicated DNA extraction step most other tests require. A swab sample is added to the test solution, incubated for about 45 minutes in a portable heater, and then read by fluorescence.Our test detects three of the most dangerous HPV types—16, 18, and 45—which together cause about 75% of all cervical cancers. It costs less than $8 per test and can run on a battery-powered device, making it ideal for clinics without reliable electricity.In clinical trials, the test matched lab results 100% of the time in Houston and 93% in Mozambique.We’re now working to expand the test to cover more HPV types and to make it even easier to use in the field. Our goal is simple: a complete, field-ready kit that helps every woman, everywhere, access fast, accurate screening—and moves us closer to eliminating cervical cancer for good.

Read More:[Rice] - New one-hour, low-cost HPV test could transform cervical cancer screening in Africa and beyond

[Nature] - One-hour extraction-free loop-mediated isothermal amplification HPV DNA assay for point-of-care testing in Maputo, Mozambique

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Economics is everywhere, including art.

Alexandra Nica, director of the undergraduate program and professor of instruction in the department of economics at the Tippie College of Business at the University of Iowa, takes a closer look.

Alexandra Nica is director of the undergraduate program and professor of instruction in the Department of Economics at the University of Iowa Tippie College of Business. She earned her MA and PhD from the University of Iowa and her BA from the University of Transylvania in Romania.

Did Jackson Pollock ever think much about economics? Probably not, but economics students think about Jackson Pollock.

I teach the intermediate macroeconomics class at Tippie and not long ago I noticed that my students struggled to give concise analysis of graphs and data because they were unable to visualize what they looked like. I realized they needed to learn to slow down and look closer at details to help them make more sense of the whole.

I also knew that art was one tool I could use to help them. As a concert pianist myself, I know how art helps with visualization because art rewards those who looks closely at the details. So I brought my students to the university’s renowned Stanley Museum of Art, where docents helped them dive deep into some of the works in our extensive collection.

They closely examined paintings by Joan Miro and Katja Farin. They looked at sculpture from Elizabeth Catlett and pieces from the museum’s extensive collection of African art. They began to see things they didn’t expect and realized that close looking is as effective in finding meaning in one of Pollock’s abstract expressionist masterpieces as in a chart tracking US GDP.

The experience showed the value of creativity in moving past a basic reading and providing concise summaries, especially when looking at graphs. Students learned they can tease out meaning from economic data using an artist’s tools to see that things aren’t always as simple as they seem. As a result, they now write clearer paragraphs with better in-depth analysis than before, even when the graphs are more complicated. This will be important for their careers, when their bosses will expect a concise, three-sentence summary of what a visual says and what it actually means.

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Quitting smoking is good for you, no matter when in life it happens.

Mikaela Bloomberg, senior research fellow in social epidemiology and social statistics at the department of epidemiology and public health at the institute of epidemiology and health care at University College London, explores why.

Mikaela Bloomberg is a Senior Research Fellow in Social Epidemiology and Social Statistics at University College London’s Department of Epidemiology and Public Health. She is part of the English Longitudinal Study of Ageing research team, where her work examines how social and behavioural pathways contribute to inequalities in health and wellbeing in later life. Her research integrates lifecourse perspectives with longitudinal population data to understand how socioeconomic circumstances and behavioural patterns shape cognitive ageing, dementia risk, and other ageing-related outcomes.

The harmful effects of smoking are well known. Smoking damages heart and lung health and is also linked to poorer cognitive outcomes: people who smoke tend to show faster decline in cognitive abilities such as memory and thinking skills and are more likely to develop dementia.However, research suggests that some of smoking’s health harms are reversible—not only for heart and lung health, but also for the brain. For example, people who quit smoking earlier in life have dementia risks and later-life cognitive abilities similar to those who never smoked.What has been less clear is whether quitting later on can still make a difference once cognitive decline has already begun. Age-related cognitive decline typically accelerates from around age 65, so by that stage, many assume their cognitive trajectory is already set. We wanted to know whether quitting could still slow that decline.To find out, we analysed data from over 9000 adults aged 40 and older across 12 countries, tracking their performance on cognitive tests over 18 years. We matched people who quit smoking with continuing smokers based on their age, sex, education level, and cognitive abilities before quitting. We examined cognitive trajectories in the years before and after quitting and compared these with the matched control group. Before quitting, both groups declined at a similar rate. But in the years after, those who quit experienced 20%-50% slower cognitive decline than those who continued to smoke. This was true whether they quit in midlife or later.These findings matter because many long-term smokers believe there’s no point in quitting after decades of smoking. Our results suggest that when it comes to maintaining cognitive health, it is never too late to quit.

Read More:

[The Lancet] - Cognitive decline before and after mid-to-late-life smoking cessation: a longitudinal analysis of prospective cohort studies from 12 countries

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Juvenile birds may lean on siblings more than parents to learn to solve a puzzle.

Sonja Wild, postdoctoral researcher at the University of California, Davis, explores why.

Sonja Wild is a postdoctoral researcher at the University of California Davis. Her research aims to uncover the mechanisms underlying behavioral plasticity in free-ranging social animals. She is particularly interested in underlying cognitive processes — such as social learning phenomena and individual decision-making processes — and the fitness outcomes of behavioral variation at the individual level. Her research across different animal species from dolphins over songbirds to ground squirrels has sparked far-reaching interest beyond the scientific community.

Learning from others is one of the most efficient ways to obtain new skills or information. In animals — including us humans — this process called ‘social learning’ is especially important for young individuals who have to learn essential survival skills right after birth. In many species, parents play a key role in this process. Offspring copy what their parents do, a form of ‘cultural inheritance’ that leads to behaviors being passed down within families through generations. But what happens in species where parents do not stick around for very long?That’s what we set out to explore in the great tit, a small songbird whose young reach independence from their parents after just a few weeks. We presented juvenile birds with foraging puzzles that could be opened by sliding a door either to the left or to the right. Through automated tracking, we recorded if and when each bird learned to solve the puzzle. Young birds whose parents knew how to solve the task were much more likely to learn it themselves, which points to cultural inheritance. But having a closer look at the learning pathways, a different story emerged. The first juvenile to learn in each family often learned not from its parents, but mostly from unrelated adults. And once one sibling learned to solve, all other siblings tended to copy the already knowledgeable sibling rather than their parents. Our study provides a contrast to the strict trans-generational cultures where transmission mainly occurs from parents to offspring and gives insights into the more variable learning pathways via siblings and non-parental adults in species with limited parental care and multiple offspring.

[PLOS Biology] - Siblings and nonparental adults provide alternative pathways to cultural inheritance in juvenile great tits

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Do men and women experience asthma differently?

Shannon Kay, assistant professor at the Yale School of Medicine, determines how to make care more personalized.

Shannon Kay was born in Long Island and raised in New York City. She received her B.S. and M.S. in Chemical Engineering from Manhattan College, and completed medical school at Stony Brook University School of Medicine. She then completed internship, residency, and Chief residency in Internal Medicine at the University of Michigan in Ann Arbor before coming to Yale as a Pulmonary and Critical Care fellow in 2019.

Asthma is the most prevalent respiratory disease in the world, and it is caused by inflammation in the lungs related to an individual’s genetics and their environment. There are clear differences in the way asthma affects males and females across the lifespan. For example, asthma is more common and more likely to be triggered by allergies in young boys compared to girls. After puberty, asthma becomes more prevalent in females, who are more likely to experience asthma throughout adulthood. Females report changes in their asthma symptoms corresponding with their menstrual cycle, pregnancy, menopause, and taking medications like hormonal contraceptives or hormone replacement therapy. This suggests a hormonal influence on lung inflammation. Importantly, females are more likely to have severe asthma that is less responsive to our current therapies.In this study, we set out to explore the way asthma affects males and females differently by looking at gene expression levels in blood and respiratory samples. Gene expression is a measurement of which genes from our DNA are being used to make proteins, which gives us a clue about the biology happening in our bodies. We combined studies from across the world to maximize our analysis. Ultimately, we found differences in the expression of 61 genes between males and females with asthma. The expression level of these genes in blood samples correlated with important features including patient-reported symptoms, lung function measurements, and markers of inflammation. Our findings suggest that these changes in gene expression may contribute to sex differences in asthma.We hope to build on this work by studying hormonal effects in the lungs, evaluating differences in response to newer asthma medications called biologics, and exploring the intersection between asthma and other conditions like obesity. Ultimately, we hope to contribute to more personalized medical care for all patients with asthma.

Read More:

[ATS Journals] - Sex-biased Gene Expression Underlies Immune Dysfunction in Asthma

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Hepatitis C infection can be dangerous for mothers and babies, so how do we treat it?

Madeline McCrary, assistant professor of medicine at Washington University in St. Louis, determines one option.

Leah Madeline McCrary is an Assistant Professor in the Division of Infectious Diseases at WashU Medicine. She specializes in infectious complications of substance use, including Hepatitis C and Serratia endocarditis, and works to expand access to treatment for people who use drugs, pregnant individuals, and rural populations. She is currently collaborating to integrate infectious disease care into perinatal substance use programs to improve Hepatitis C treatment during and after pregnancy.

Hepatitis C is a viral infection that can damage the liver and, if untreated, lead to cirrhosis, cancer, or even death. Many people are first diagnosed during pregnancy. The stakes are high—not only for mothers, but also for babies: the virus can be passed from mother to child, with a transmission rate of about 1 in 10.

Unfortunately, treatment often never begins. Insurance may end, follow-up gets missed, or the demands of the postpartum period make clinic visits difficult. As a result, some women return for a second or third pregnancy still infected, despite the availability of a highly effective cure.

But curing hepatitis C protects more than just one person. It prevents long-term complications, reduces household transmission, and lowers the risk of passing the virus to future children.

To address this gap, we partnered across maternal–fetal medicine and infectious diseases to pilot a new approach. Instead of referring mothers to outpatient clinics, we offered hepatitis C treatment at the bedside before hospital discharge. We also used streamlined referrals and telehealth, building on earlier work.

We reviewed records from 149 women diagnosed with hepatitis C during pregnancy. Those who began treatment in the hospital were about twice as likely to complete therapy and be cured, compared to those referred to outpatient care. More than half in the outpatient group never even attended their first appointment.

Treating hepatitis C before discharge helps reduce loss to follow-up, increases cure rates, and protects long-term health. And the impact goes beyond the individual—by curing the infection, we protect families and future pregnancies.

This success was possible through collaboration across specialties. With new guidelines supporting treatment during pregnancy, the goal ahead is clear: cure should be the norm, not the exception.

Read More:

[WashU Medicine] - Innovative approach helps new mothers get hepatitis C treatment

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On this Student Spotlight: Can you become addicted to ultra-processed foods?

Lucy Loch, doctoral candidate in the department of psychology at the University of Michigan, examines whether this is the case.

Lucy Loch is a doctoral candidate in the Department of Psychology at the University of Michigan, where she is mentored by Dr. Ashley Gearhardt and Dr. Julie Lumeng. Her research focuses on the life course development of addictive-like eating, examining how early experiences and exposure to ultra-processed foods influence appetite, self-regulation, and risk for later life health outcomes. Supported by the National Science Foundation Graduate Research Fellowship, Lucy bridges developmental and addiction science to uncover why certain foods and life experiences may make some individuals more susceptible to overeating. Her work has appeared in journals including Addiction, Current Obesity Reports, and Physiology & Behavior.

Ultra-processed foods are industrially made products that often contain high levels of refined carbohydrates, added fats, and other ingredients designed to make them especially tasty and rewarding. Over the past few decades, these foods have become a major part of the American diet. Research shows that some people experience addictive-like responses to ultra-processed foods, including intense cravings and difficulty controlling their intake.This study examined how common ultra-processed food addiction, is among older adults in the United States, and how it relates to health and social well-being. Data was analyzed from more than two thousand adults between the ages of fifty and eighty who participated in a nationally representative survey. Participants completed a validated questionnaire that applies the diagnostic criteria for substance use disorders such as, cravings, loss of control, and continued use despite negative effects, to food ultra-processed food consumption. Older adults in this study also reported on their physical health, mental health, and feelings of social isolation.The findings showed that about one in eight older adults met the criteria for ultra-processed food addiction. Rates were higher among women than men, and highest among women aged fifty to sixty-four, where roughly one in five met the diagnostic criteria for ultra-processed food addiction. Additionally, ultra-processed food addiction was strongly linked to poorer health outcomes. Those who described themselves as overweight, or in worse physical or mental health, were significantly more likely to meet criteria for UPFA. People who reported feeling socially isolated were also at increased risk.These results suggest that ultra-processed food addiction is an overlooked issue among older adults, especially women who were in a developmentally vulnerable period when these foods became widespread in the American food supply in the 1970s and 1980s. This study highlights important connections between addictive eating behaviors, physical and mental health, and social well-being, offering new insights for understanding nutrition and aging.

Read More:

[Wiley] - Ultra-processed food addiction in a nationally representative sample of older adults in the USA

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