UNC researchers publish findings in JAMA Network Open about impact of diagnostic wait time on ovarian cancer survival

Led by a team of UNC researchers, this study explored the relationship between survival and how quickly patients are diagnosed with ovarian cancer.

UNC Gillings School of Global Public Health

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March 27, 2026

The study "Diagnostic Timing and Ovarian Cancer Survival in North Carolina" has been published in the latest issue of JAMA Network Open. Led by a team of UNC-Chapel Hill researchers, this study explored the relationship between survival and how quickly patients are diagnosed with ovarian cancer.

Ovarian cancer is hard to diagnose early. Its symptoms, like bloating and abdominal pain, are vague and similar to other more common conditions. Early diagnosis improves outcomes for many cancers. However, prior research suggests that faster diagnosis does not improve ovarian cancer survival, discouraging investments into better diagnostic tools. One possible explanation that could explain these prior findings is the “wait time paradox”: the sickest patients are easier to diagnose quickly but also have poorer outcomes.

“This could be masking the benefits of early diagnosis and explain why faster diagnosis doesn’t always appear to improve survival,” said Sarah Soppe, MPH, the study’s lead author and doctoral candidate at the UNC Gillings School of Global Public Health. “Taking into account how sick the patient appeared when they first saw the doctor could help address this methodological issue.”

The team looked at the data of over 2,300 North Carolina women with ovarian cancer, such as patient characteristics, year of diagnosis and diagnostic interval—the time from a patient's first symptom-related clinic visit to diagnosis. Using flexible statistical methods, the team found a U-shaped pattern between diagnostic interval and survival: Women diagnosed very quickly and women diagnosed after long delays both had worse survival than those in the middle.

Patients diagnosed most quickly likely had symptoms severe enough that clinicians suspected cancer quickly, with poorer prognosis. Patients diagnosed most slowly also had high rates of advanced disease but may have had less obvious initial symptoms, leading to more medical visits and cancer progression before cancer was suspected. Patients in the middle intervals had the longest average survival times compared to shorter and longer intervals. These patients were diagnosed with fewer signs of advanced disease and were more likely to be younger, white and from higher-income neighborhoods—all factors linked to better access to care.

By considering how sick patients appeared, the study results suggest that earlier diagnosis of ovarian cancer may improve outcomes for some symptomatic patients, shedding light on the relationship between diagnosis time, severity of disease, and patient outcomes.

“The takeaway is that diagnostic delays may actually matter for ovarian cancer,” said Caroline A. Thompson, PhD, the study’s senior author who is an associate professor of epidemiology at the Gillings School and research fellow for the UNC Center for Health Promotion and Disease Prevention (HPDP). “Our hope is that these findings will encourage more research and investment into tools that improve diagnostic timing and outcomes for this aggressive cancer.”

This work was supported by the UNC CDC Health Promotion and Disease Prevention Research Center and Ovarian Cancer Research Alliance [“A Mixed Methods Study of Diagnostic Delay in Ovarian and Uterine Cancer”, HEG-2025-2-1900].

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Caroline Thompson, PhD, MPH, is a research fellow for the UNC Center for Health Promotion and Disease Prevention (HPDP), an associate professor of epidemiology in the UNC Gillings School of Global Public Health, and a member of the UNC Lineberger Comprehensive Cancer Center.

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Journal

JAMA Network Open

DOI

10.1001/jamanetworkopen.2026.2434 

Article Title

Diagnostic Timing and Ovarian Cancer Survival in North Carolina

Article Publication Date

27-Mar-2026

 

Lasting income costs of mental and physical illness

JAMA Health Forum

About The Study: 

This study estimated income losses from the individual perspective in the 10 years following hospital diagnosis of depression, alcohol use disorder, stroke, and breast cancer from 2000 to 2023 in Denmark. The researchers found that (1) income losses following mental disorder diagnoses were larger than those for physical conditions, though all evaluated diseases led to substantive loss; (2) average losses grew in years following diagnosis, particularly among individuals younger than 40 and those in school, suggesting accumulating disadvantage; and (3) even those outside of the workforce at the time of hospital diagnosis experienced sustained future income loss.

Corresponding Author: To contact the corresponding author, Emily K. Johnson, MSc, email ejohnson@health.sdu.dk.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamahealthforum.2026.0196)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

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Embed this link to provide your readers free access to the full-text article 

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About JAMA Health Forum: JAMA Health Forum is an international, peer-reviewed, online, open access journal that addresses health policy and strategies affecting medicine, health and health care. The journal publishes original research, evidence-based reports and opinion about national and global health policy; innovative approaches to health care delivery; and health care economics, access, quality, safety, equity and reform. Its distribution will be solely digital and all content will be freely available for anyone to read.

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Journal

JAMA Health Forum

 

This could be why COVID and flu are so dangerous to the elderly

UCSF study shows that aging connective tissue in the lungs brings on catastrophic immune dysregulation in older people.  

University of California - San Francisco

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Older adults are much more likely to become seriously ill from flu or COVID because aging lung cells can drive excessive immune responses, according to a new study led by researchers at UC San Francisco.  

The findings enhance the understanding of the inflammation that accompanies aging, explaining how an otherwise minor cough can sometimes send an elderly person to the hospital.  

To understand what goes wrong in old lungs, the scientists engineered the lung’s structural cells, fibroblasts, to turn on an age-related distress signal in young mice. The signal led the lungs to form clusters of inflamed cells, including some marked by the GZMK gene, which was first seen in severe COVID-19. A future therapy might target these cells to counter the damaging spiral of inflammaging. 

“We were surprised to see lung fibroblasts working hand-in-hand with immune cells to drive inflammaging,” said Tien Peng, MD, a professor of Medicine and a member of the Cardiovascular Research Institute and Bakar Aging Research Institute at UCSF. “It suggests new ways to intervene before patients progress to severe inflammation that can require intubation.” 

Peng is senior author of the paper, which appeared in Immunity on March 27. Nancy Allen MD, PhD, a clinical fellow in the Pulmonary and Critical Care Division in the UCSF Department of Medicine, is the first author. 

Fibroblasts maintain the airtight tubes and chambers of the lungs but can trigger inflammation in lung diseases like COPD. Peng’s team wanted to see whether a signal coming from fibroblasts could disrupt otherwise healthy lungs. 

The signal is part of a pathway called NF-kB that is often seen in the diseases of aging. The fibroblasts prompted the lung’s macrophages to rally an immune response. Then, immune cells, including some marked by GZMK, rushed into the lungs from the bloodstream. 

Although the GZMK cells were impotent against disease, they were still capable of damaging the lungs.  

Once they had these immune clusters, the lungs of the young mice experienced severe symptoms from an infection — as if they were old. When the scientists used a genetic trick to eliminate the GZMK cells in these mice, their lungs were able to withstand the infection. 

This suggests the aging lung tissue itself is driving inflammation. 

The team examined lung tissue from older patients hospitalized with COVID-related ARDS (acute respiratory distress syndrome) and found it had clusters of cells that looked like what they had seen in mice. The sicker the patient, the more inflamed clusters they had. Lung tissue from healthy donors had none. 
 
“We saw during COVID that our most vulnerable patients no longer had the infection but still had persistent and devastating lung inflammation,” Peng said. “This circuit of dysfunction between lung and immune cells makes for a promising new therapeutic target.” 

Authors: Other UCSF authors are Christian Ringler; Sang Ho Woo, PhD; Sophie Phipps; Jin Young Lee, PhD; Nabora Reyes, PhD; Ritusree Biswas, PhD; Lucile Neyton, PhD; Andrew Willmore; Sofia Caryotakis; Jessica Roginsky, PhD; Lu Guo; Melia Magnen, PhD; Chaz Langelier, MD, PhD; COMET Consortium; Mark Looney, MD; Averil Ma, MD; Vincent Auyeung, MD, PhD; Carolyn Calfee, MD; and Ari B. Molofsky, MD, PhD; as well as Pedro Ruivo of UC Davis. 

Funding: This work was supported by the National Institutes of Health (P30DK063720, R01HL160895, F32HL156452, K08HL169723) and the Bakar Aging Research Institute. 

 

About UCSF: The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. UCSF Health, which serves as UCSF’s primary academic medical center, includes among the nation's top specialty hospitals and other clinical programs, and has affiliations throughout the Bay Area. UCSF School of Medicine also has a regional campus in Fresno. Learn more at ucsf.edu or see our Fact Sheet.
 

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Journal

Immunity

 

Studying bird flu in the air to protect people, agricultural operations in Michigan and beyond

Understanding the virus that causes bird flu in livestock, and how to kill it, could help industrial farms prevent transmission

University of Michigan

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Photos  //  Video

 

Key takeaways:

• A $2M USDA grant will fund research on the infectivity of bird flu in the air.

• Nonthermal plasma has been shown to deactivate airborne virus particles.

• University of Michigan Engineering is collaborating with researchers at the University of Bristol in the U.K.

 

Discovering how the bird flu virus degrades in the air around livestock and how engineering solutions can effect that degradation quickly and efficiently are core aims of a new University of Michigan Engineering-led project funded by the U.S. Department of Agriculture. This work could help prevent or mitigate future outbreaks.

 

Detection of bird flu infection within flocks and herds leads to the mass culling of animals, which disrupts food supply chains. The ongoing outbreak of HPAI H5N1 that began in 2022 in the U.S. has led to the loss of 175 million birds and, as of late 2024, has cost the industry roughly $1.4 billion.

 

The $2 million grant from the USDA's Animal and Plant Health Inspection Service aims to answer two fundamental questions about bird flu:

• How quickly does the virus that causes bird flu lose its infectivity in the air, specifically air found in enclosed livestock environments?

• What technologies can effectively reduce bird flu's infectivity in those environments?

 

Herek Clack, U-M associate professor of civil and environmental engineering, will lead the project, conducting tests on how nonthermal plasmas can render aerosols containing the virus that causes bird flu incapable of infecting humans and livestock. His team's approach essentially exposes air to strong electric fields, temporarily creating free electrical charges that damage viruses and render them harmless.

 

"Both the USDA and the agricultural industry want a playbook—science-based guidelines—for how to operate under the threat of bird flu," Clack said. "We're after a better understanding of how the airborne virus behaves in enclosed livestock operations and what technologies can best protect animals and workers."

 

How nonthermal plasma inactivates viruses

 

Previously, Clack and his team developed a plasma reactor capable of reducing the number of infectious viruses in the air by 99.9%. Building on that work, they will test how nonthermal plasma inactivates viruses in air that contains traces of pollutants, such as ammonia, that are common around livestock. 

 

Clack and his team have previously shown that such air pollutants can, at very low concentrations, inhibit the effectiveness of nonthermal plasmas for inactivating viral aerosols. Under this new grant, they will expand the range of air pollutants tested and explore enhancements to the nonthermal plasma that could counteract those pollutants' effects. Of particular interest is how air pollutants and plasma treatment separately influence the air's pH, a chemical measure related to acidity. 

 

"A key question we're looking at is, 'What will happen with pH levels—how do they impact the infectivity of the viruses?'" Clack said. "The air pollutants tend to raise the pH in the air, but nonthermal plasma reduces pH."

 

If part of the plasma's effectiveness depends on lowering the pH of the air, it may not be as effective if the air's pH starts higher.

 

Measuring normal bird flu virus infectivity loss in air

 

Allen Haddrell, a research fellow at the University of Bristol in the U.K., will employ a relatively new technology of his own design to answer the question of how long the virus that causes bird flu retains its infectivity in the air. The traditional method for measuring how quickly airborne viruses decay involves filling a cylindrical drum with virus-laden air, then slowly rotating the drum to keep the virus particles in the air. But setup for this method is slow.

 

"What they miss with that approach is roughly the first 20 minutes of the infectivity decay," Haddrell said. "Consequently, they can get wildly different results. Different research groups can look at the same virus and come to different conclusions."

 

Haddrell will use a technique developed at the Bristol Aerosol Research Centre.

 

"We levitate virus-containing droplets into an electrodynamic field," he said. "We expose the population of viruses containing aerosols to different environmental conditions, where we change things like relative humidity or gas composition. 

 

"After a set period, we deposit the aerosol and measure how much the viral infectivity has changed. We use this approach to measure how different environments affect airborne viral decay. And we use this information to figure out the fundamental drivers of decay."

 

A better grasp of the decay dynamics associated with the virus that causes bird flu and a proven means of inactivating the virus in ventilation air would give the agricultural industry tools to better deal with the virus's next appearance. But it will also lay the groundwork for an industry response to the next human pandemic.

 

"During COVID, workers in these enclosed livestock or processing operations were 50 to 70 times more at risk for contracting the virus, according to a GAO report from 2023," Clack said. "It told us those close working conditions were the source of greater risk."

 

Understanding the decay rate of airborne viruses like those that cause bird flu will help us devise more effective protection for workers and animals from future infectious respiratory diseases.

 

Study explains Antarctic sea ice growth and sudden decline

Although climate models predicted Antarctic sea ice would steadily dwindle, its extent grew for decades until 2016. A new study finds the ice finally receded when wind-driven upwelling unleashed warmer, deeper water.

Stanford University

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A new Stanford University study has helped solve a mystery about dramatic swings in sea ice extent around Antarctica. 

Despite rising global and regional temperatures, Antarctic sea ice expanded from the 1970s through 2015. Then, in 2016, sea ice extent declined abruptly to record lows and has not recovered.

Based on data gathered by floating, robotic probes, the new study links this unprecedented sea ice loss to the rapid release of accumulated ocean heat. That heat had built up prior to 2015 as increased precipitation formed a less salty, lower-density lid on the ocean’s surface, effectively trapping warmer, deeper water. An increase in stormy weather around Antarctica in recent decades, likely tied to climate change, led to more upwelling, eventually bringing on the low-ice era. 

“We’ve traced the recent extremes in sea ice extent to the combination of enhanced precipitation and upwelling due to winds,” said Earle Wilson, an assistant professor of Earth system science in the Stanford Doerr School of Sustainability and lead author of the study published March 23 in Proceedings of the National Academy of Sciences. “We identified these two competing effects, both of which were increasing in concert with each other, but by different amounts over the years. For a while, precipitation was winning until upwelling took over.”

The findings significantly add to the complex picture of conditions at the bottom of the world, where the Southern Ocean drives global ocean circulation and absorbs much of the heat trapped by emissions from human activity. The results also dovetail with other recent research by Wilson’s group attributing the perplexing decades-long cooling trend in the Southern Ocean to underestimated rainfall and meltwater. 

“The Southern Ocean is a central cog in the global climate system, and sea ice mediates much of what happens there,” said Wilson. “To establish confidence in our regional climate projections, including for processes such as Antarctic ice sheet melting and sea level rise, we need to understand the mechanisms that drive Antarctic sea ice variability.”

Valuable under-ice data

For the study, Wilson and his coauthors took advantage of a rich, yet seldom-accessed dataset for Antarctic sea ice research. 

Over the past quarter-century, collection of subsurface data has advanced greatly thanks to the deployment of thousands of autonomous floats that comprise the global Argo array. While the floats operate mostly in open water outside the Antarctic sea ice zone, some floats also travel below the seasonal ice, cruising along, taking readings, and resurfacing come summertime to transmit their gathered data. The Stanford researchers compiled and analyzed 20 years of this overlooked under-ice data. 

“It was very exciting to be able to use a combination of data and idealized modeling to explain both the observed expansion and retreat phases of sea ice,” said study coauthor Lexi Arlen, a PhD student in Earth system science in the Polar Ocean Dynamics Group led by Wilson.

“It has been enlightening to finally have enough broadly distributed under-ice data to discern year-to-year ocean trends around Antarctica,” said Wilson. “Our paper is one of the first to fully leverage these data to explain Antarctic sea ice trends over the past two decades.”

Partitioned waters

A key insight from the research team’s data analysis is that upwelling of warm water surprisingly started several years before the sea ice reversal of the mid-2010s. “These data told us another process must have delayed the release of subsurface warm water and thus sea ice decline, which led us to examine salinity and freshwater trends,” said Wilson.

Increases in precipitation, including snow and rainfall, over the Southern Ocean are known to make surface waters less salty and less dense than deeper waters, stratifying the water column into separate salinity and density regimes. In recent years, this stratification became stronger, making it harder for the waters to mix vertically and even out their temperatures. 

The deeper layer in the Southern Ocean runs about two to three degrees warmer than the colder surface water, which is exposed to the frigid atmosphere and registers right around freezing. The trapping of that relatively warmer water allowed sea ice to expand, even against background climatic warming, until prevailing winds caused enough upwelling to force sea ice retreat.  

Complicating this explanation, however, is that the Argo floats did not detect the same set of conditions on the Pacific-facing side west of the Antarctic Peninsula, wrapping around to the Ross Sea, as were detected on the Atlantic side. Yet sea ice expanded and contracted on the Pacific side as well. 

“We saw opposite trends in the Pacific sector, with the ocean interior getting cooler rather than warmer after the sea ice declined,” said Wilson. “This remains an unanswered part of the puzzle.”

The researchers plan to study and model other mechanisms that could be having a stronger impact on the Pacific side, which also likely play roles throughout the region. Examples include changes in sea ice drift and increases in turbulent ocean mixing due to more frequent storms. 

“The ocean has a long memory and can drive multiyear changes in ways weather can't,” said Wilson. “We plan to continue monitoring the ocean data and work toward developing a theory that will help us anticipate changes in Antarctic sea ice extent in decades to come.”  

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Acknowledgements:

Co-author Ethan C. Campbell is affiliated with University of Washington. This research was supported by the National Science Foundation and the Washington Research Foundation. The Argo float data analysis was supported through a Big Ideas for Oceans grant from the Oceans Department and the Woods Institute for the Environment in the Stanford Doerr School of Sustainability.

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Journal

Proceedings of the National Academy of Sciences

DOI

10.1073/pnas.253083212 

Article Title

Recent extremes in Antarctic sea ice extent modulated by ocean heat ventilation

Article Publication Date

23-Mar-2026

 

Temperature dynamics, not just extremes, impact heat tolerance in mussels

University of Washington

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image: 

Mussels from Washington state waters. This common coastal species often consumed by humans can also be used to study the impacts of environmental variability.

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Credit: Andrew Dale

Intertidal mussels, forming bumpy layers on shoreline rocks, withstand significant temperature swings as the tide ebbs and flows. These creatures live in one of the most thermally variable environments on Earth, but a new study shows that the rate, timing and duration of heating and cooling impact their metabolic rate, a proxy for overall health. At the UW’s Friday Harbor Laboratories, researchers exposed mussels to temperature regimens with equal highs and lows but different patterns of change. Even when the average temperature for a set period was the same, the mussels’ response was distinct. These results, published March 19 in Proceedings of the Royal Society B, show that predicting how marine organisms respond to climate change means considering how temperature changes over time, not just how warm it gets.

For more information, contact lead author Michael Nishizaki, assistant professor of biology at the College of the Holy Cross and a mentor for the UW Friday Harbor Laboratories REU program, at mnishizaki@holycross.edu.

The other UW co-author is Sara (Grace) Leuchtenberger. A full list of co-authors and funding is available in the paper.

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Journal

Proceedings of the Royal Society B Biological Sciences

DOI

10.1098/rstb.2025.0261 

Article Title

Thermal variability: how realistic temperature fluctuations alter physiological performance in intertidal mussels