Scientists at the University of Wisconsin–Madison have uncovered a possible way to protect key cells in the pancreas that are targeted during the development of Type 1 diabetes.

The researchers found that deleting a single stress-response gene in insulin-producing cells protects mice that are genetically predisposed to Type 1 diabetes from developing the disease. The findings suggest a new path to reduce stress inside those cells and alter how the immune system responds, potentially opening new avenues for early intervention or prevention.

Type 1 diabetes occurs when immune cells destroy pancreatic beta cells, leaving the body unable to produce enough insulin to regulate blood sugar. To date, most treatments have focused on suppressing immune activity.

“Historically, because it’s an autoimmune disease, scientists and clinicians have focused on preventing the immune attack,” says Feyza Engin, a professor in the UW–Madison Department of Biomolecular Chemistry who led the research, which was recently published in Nature Communications. “We looked at it from another angle and asked: Why are beta cells specifically targeted?”

The new research centers on a protein called XBP1. It’s part of a cellular stress response system that helps cells cope with inflammation, environmental toxins and the buildup of misfolded proteins. Earlier work from Engin’s lab showed that deleting a related stress sensor, Ire1α, in beta cells also prevented diabetes in mice. The new study builds on that foundation.

Using a mouse model that spontaneously develops Type 1 diabetes, Engin and her colleagues deleted the Xbp1 gene specifically in beta cells before immune assault. Although the mice initially showed elevated blood glucose, they later returned to normal glucose levels and remained healthy for as long as a year.

“What was really interesting is that early on they show hyperglycemia, but then they recover from it,” Engin says. “They actually go from diabetes back to normal blood glucose levels.”

An analysis revealed that beta cells lacking the Xbp1 gene temporarily lost features that mark them as mature insulin-producing cells. During this phase, immune cells were less likely to recognize and attack them. Over time, the beta cells regained their identity, inflammation decreased and insulin production recovered.

“They’re losing their beta cell identity and look nothing like a typical beta cell,” Engin says. “That’s why immune cells don’t recognize them.”

Importantly, the protective effect occurred without any changes to another stress-related process involving Ire1α, helping to clarify how different components of cells’ stress response influence the disease.

To better understand those differences, the team compared beta cells lacking Xbp1 with those missing Ire1α under identical environmental conditions — an important part of Type 1 diabetes research, where environmental conditions like housing and diet can affect disease rates in mice. Using single-cell sequencing from these mouse models and gene regulatory network analysis performed by UW–Madison collaborator Sushmita Roy’s lab, the team identified both shared stress pathways and ones involving only Xbp1.

“We found unique gene regulatory networks specific to Xbp1 that was never discovered before,” Roy says.

The findings add to evidence that beta cells play an active role in Type 1 diabetes rather than serving as passive targets.

“Our findings further support that beta cells are actually not victims,” Engin says. “They actively participate in their own destruction.”

While the study was conducted in mice, Engin says the work is designed with human disease in mind. People at high risk for Type 1 diabetes can often be identified years before symptoms appear through blood tests.

“If you identify these people who will develop diabetes at that stage, can we interfere?” she said. “Can we inhibit XBP1 and prevent or delay their diabetes?”

The lab is now actively pursuing those questions in further studies, Engin says, both in mice and in lab-grown human pancreatic cells.

This research was supported by the National Institutes of Health (T32 GM007215; DK130919; DK128136; 3-SRA-2023-1315-S-B; 3-SRA-2025-1654-S-B; and R01 GM144708), Greater Milwaukee Foundation and the University of Wisconsin Stem Cell and Regenerative Medicine Center.

Research at the University of Wisconsin–Madison drives innovation, saves lives, creates jobs, supports small businesses, and fuels the industries that keep America competitive and secure. It makes the U.S.—and Wisconsin—stronger. Federal funding for research is a high-return investment that’s worth fighting for.

Learn more about the impact of UW–Madison’s federally funded research and how you can help.

Paul Lambert has received international recognition for his many contributions to understanding the role of HPV in cancer, leads three NIH research grants and edits the journal Virology. He says continued funding for research means “more effective therapies and greater understanding of how to fight cancer from every angle.”

Research at the University of Wisconsin–Madison drives innovation, saves lives, creates jobs, supports small businesses, and fuels the industries that keep America competitive and secure. It makes the U.S. — and Wisconsin — stronger. Federal funding for research is a high-return investment that’s worth fighting for. Learn more about the impact of UW–Madison’s federally funded research and how you can help protect it.

Paul Lambert leads the McArdle Laboratory for Cancer Research at University of Wisconsin–Madison where he has developed new anti-cancer therapies for cervical cancer and leads research to prevent and treat cancers caused by viral infections. Lambert, who also serves as chair of the Department of Oncology in the Wisconsin School of Medicine and Public Health, recently sat down for a Q&A about the importance of continued research on tumor viruses, which he says cause about 15% of all human cancers.

What is the focus of the project you’ve been leading, and why is it so important? 

This grant, originally initiated over 46 years ago by Dr. Howard Temin, supports a collaborative program focused on viruses that cause human cancer. It’s one of the few such NIH Program Project grants in the U.S. dedicated to studying tumor viruses, which are responsible for approximately 15% of all human cancers worldwide. These include viruses like HPV (human papillomavirus), Epstein-Barr virus (EBV), hepatitis B and C and Kaposi’s sarcoma-associated herpesvirus (KSHV).

This work has not only deepened our understanding of cancer biology but also directly led to preventive strategies — like vaccines and potential therapies — that save lives.

What viruses are currently the focus of your research?

Today, our research centers on HPV, EBV and KSHV, though over the years we’ve also studied hepatitis B and C viruses and Merkel cell polyomavirus. These viruses cause a range of cancers including cervical, anal, penile, head and neck cancers, liver cancer and lymphomas. Our work seeks to understand how these viruses cause cancer and, just as importantly, how we can prevent or treat those cancers.

What are some major public health impacts of your work so far?

One of the biggest examples is HPV, which alone causes about 5% of all human cancers, and most of these are preventable through vaccination. For example, cervical cancer is one of the leading causes of cancer deaths in women worldwide, yet HPV vaccines can prevent the infections that lead to it. If widely implemented, this could save hundreds of thousands of lives annually. Unfortunately, vaccination rates remain low in many areas, especially in low-resource settings.

We’re also collaborating with the Gates Foundation to develop therapeutic vaccines for use in countries where access to advanced cancer treatments like radiation or chemotherapy is limited. So, the impact of our work stretches from the lab bench to global public health solutions.

How has this research contributed to other areas of cancer science?

Our work on tumor viruses has had profound implications beyond virus-related cancers. For example, studies of HPV’s cancer-causing proteins led to the discovery of key tumor suppressors like p53, which is now known to be the most commonly mutated gene in all human cancers. Our research also uncovered mechanisms of immune evasion used by HPV — mechanisms now known to contribute to resistance to immunotherapy across many types of cancer.

Have your findings led to clinical applications or trials?

Yes. One exciting example is a clinical trial underway at UW–Madison for patients at risk of anal cancer caused by HPV. This work was inspired by basic science from Dr. Nathan Sherer’s lab (focused on HIV) and research from Dr. Evie Carchman, a GI surgeon. They discovered that HIV protease inhibitors, originally used to manage HIV, could also kill HPV-positive cancer cells. Now, these drugs are being repurposed in a trial to help prevent cancer in high-risk patients. It’s a great example of how basic lab research can translate directly into patient care.

What challenges has your research faced recently, particularly around funding?

We recently experienced a seven-week delay in funding renewal, which created significant disruption. We had to pause high-cost genomic studies and animal model work, delaying some projects by months, not just weeks. While funding did eventually come through at expected levels, it highlighted how vulnerable large research programs are to even short-term interruptions. These pauses can stall progress on experiments that take years to complete — especially when working with live models or time-sensitive tissue studies.

What’s the next frontier in your research?

We’re now working on developing novel therapeutics and vaccines for viruses like HPV, especially in settings where conventional treatments are inaccessible. We’re also deepening our understanding of how viruses interact with host cells and how those mechanisms might be exploited for broader cancer therapies. Ultimately, the goal is not just to understand how cancer happens — but to stop it before it starts.

If there’s one takeaway the public should know about your work, what is it?

Many of the cancers we study are preventable. That’s the key message. Whether it’s through vaccination, treatment of viral infections, or better public health outreach, we have the tools — or are developing them — to reduce cancer risk dramatically. Continued investment in this research means more lives saved, more effective therapies and greater understanding of how to fight cancer from every angle.

In an effort to tip the balance toward the upsides of chemotherapy, Glen Kwon, a professor in the University of Wisconsin–Madison School of Pharmacy, is turning to nanoparticles capable of enhancing these drugs’ therapeutic properties.

In new work recently published in the journal ACS Nano, Kwon’s lab developed a stabilized form of a common chemotherapy agent, gemcitabine, and encased it in nanoparticles capable of slowing down their release. In mouse models of human lung cancer, the improved drug inhibited tumor growth more effectively than standard gemcitabine.

“There’s been a lot of hype about nanotechnology,” says Kwon, who has worked in the field for more than 20 years. “It’s an ambitious goal: to target drugs to particular places in our body.”

That goal may be some way off, Kwon says, but particles that ferry drugs into the body — known as nanocarriers — are already proving effective. “What nanocarriers can do is reduce toxicity,” he says.

In work with his graduate student Tony Tam two years ago, Kwon developed an improved system for delivering the chemotherapy drug paclitaxel, commonly sold as Taxol, during treatment. Tam attached a short chain of lactic acid to the drug, which helped it load into nanocarriers made, in part, of lactic acid. The nanocarrier has been used in humans before.

So when turning to gemcitabine, Tam tried the same tactic — add on chains of lactic acid and load it into the nanocarrier.

“But the first trial that we had was not stable at all,” says Tam, now a senior scientist at Merck in San Francisco. To increase the drug’s stability, he turned to 30-year-old work out of Japan.

In the 1980s, researchers at Kyoto University combined chains of lactic acid that were identical except for one key feature — their handedness. Many molecules come in mirror-image forms of themselves, and when the Japanese researchers combined left- and right-handed versions of lactic acid polymers, the resulting crystals, called stereocomplexes, were much more stable.

When Tam produced gemcitabine-linked stereocomplexes of lactic acid and loaded them into the nanocarrier, the drug’s stability spiked. Compared to gemcitabine attached only to the left-handed form of lactic acid, the stereocomplex released gemcitabine 15 times more slowly in an artificial solution. Since gemcitabine breaks down so quickly in the body, it’s usually given at high doses to make sure enough reaches the tumor. If this nanocarrier system slowed release in the body, it could mean gentler doses.

Curiously, the nanoparticles adopted an unexpected shape. While similar nanocarriers envelop drugs in a sphere, images taken at the atomic scale show the gemcitabine stereocomplexes adopting a stretched-out, cylindrical shape. You could stack 10,000 of these cylinders end-on-end within the thickness of a piece of paper.

Atomic-scale images of gemcitabine-loaded nanoparticles reveal an unusual cylindrical shape. Courtesy of Tony Tam

In mice harboring a human-derived non-small-cell lung cancer line, treatment with the stereocomplexed nanocarriers over three weeks kept the tumors from growing. In contrast, the tumors more than doubled in size in the mice treated with standard gemcitabine. The mice were treated at a fairly low dose to assess differences between the forms of gemcitabine.

“Ultimately our goal is to get this into human beings,” says Kwon, adding that many steps, such as scaling up production and preliminary safety studies, will be required.

With the Wisconsin Alumni Research Foundation, Kwon and Tam submitted a patent based on their modifications to gemcitabine that enhanced its stability and release. And Kwon co-founded Co-D Therapeutics, a preclinical stage company developing nanocarrier-based medicines based on his earlier work with paclitaxel.

“This research relied on really good teamwork in the School of Pharmacy community,” says Tam, noting that members of two other labs in the school contributed to the ACS Nano paper.

“Collaboration is very important.”

This work was supported in part by the National Institutes of Health (grant R01AI01157) and the National Science Foundation (award CHE-9974839).

Biomedical engineering professor Kristyn Masters handles samples in her lab, where she and colleagues identified the early stages of a process that may eventually cause aortic stenosis, a severe narrowing of the aortic valve that reduces blood flow to the body and weakens the heart. (Photo by Stephanie Precourt)

The diminutive size of our aortic valve — just shy of a quarter — belies its essential role in pushing oxygen-rich blood from the heart into the aorta, our body’s largest vessel, and from there to all other organs. Yet for decades, researchers have focused less on damaged valves than on atherosclerosis, the gradual hardening of the blood vessels themselves.

Thanks, in part, to pigs at the University of Wisconsin–Madison’s Arlington Agricultural Research Station, scientists now are catching up on understanding the roots of calcific aortic valve disease (CAVD).

“For a long time, people thought CAVD was just the valvular equivalent of atherosclerosis,” says Kristyn Masters, a professor of biomedical engineering at UW–Madison. “Today, we know that valve cells are quite unique and distinct from the smooth muscle cells in our blood vessels, which explains why some treatments for atherosclerosis, such as statins, don’t work for CAVD, and why the search for drugs has to start from scratch.”

A team led by Masters has jumped a longstanding hurdle in that search with a study published today in the journal Proceedings of the National Academy of Sciences. The researchers teased apart, for the first time, the early cascade of events that may eventually cause stenosis, a severe narrowing of the aortic valve that reduces blood flow to body tissues and weakens the heart.

The only current treatment for stenosis is valve replacement, which typically requires risky and expensive open-heart surgery.

“Our study sheds new light on the differences between atherosclerosis and CAVD, especially in terms of bottleneck events that we can target with drugs,” says Masters, whose work is supported by the National Institutes of Health and the American Heart Association. “With a better understanding of how the disease progresses from early to later stages, we may eventually be able to stop CAVD in its tracks and avoid valve replacement surgery.”

Since the hearts of mice and other small animals are vastly different from the human organ, CAVD research has long been hampered by a lack of good animal models. That’s why the pigs — specifically those bred to have an overdose of fatty molecules in their arteries — were an important starting point for the current study.

Their valves provided a snapshot of early CAVD that is challenging to capture in humans, showing that it typically begins with the accumulation of certain sugar molecules called glycosaminoglycans (GAGs) in valve tissue. But to examine exactly how this tissue responds to increasing levels of GAGs, the researchers needed a greater amount of valve tissue than living pigs could provide.

That prompted them to create a first-of-its-kind platform mimicking hallmarks of early porcine CAVD in a lab dish. Key for this model was the ability to grow valve cells in their native healthy form, an important distinction from many previous studies that had focused on already diseased cells.

When the researchers changed only the amount of GAGs these native valve cells were exposed to, while keeping all other conditions the same, they observed surprising results that challenged previous assumptions.

“We thought the GAGs would play a major role in driving the disease process, but the more we added, the fewer inflammatory factors the cells produced and the happier they were,” says Masters. “When we examined this unexpected finding more closely, we noticed two distinct effects: GAGs directly increased a chemical needed to grow new blood vessels, and also trapped low-density lipoprotein (LDL) molecules.”

Neither of these effects was immediately detrimental for valve cells, but the trapping made it more likely for oxygen to react with LDL molecules, and the accumulation of oxidized LDL appeared to be a bottleneck event for a multi-stage process toward valve cell damage, Masters says.

This multi-stage process may explain why 25 percent of adults over the age of 65 have CAVD with partially blocked aortic valves, but only one percent go on to develop stenosis due to a valve that can no longer open and close properly. The fact that native valve cells cannot oxidize LDL themselves, while smooth muscle cells in blood vessels can, also highlights a key distinction between CAVD and atherosclerosis.

The study, which included first author Ana Porras, who recently earned a doctorate in biomedical engineering, has important implications for the development of new drugs that may prevent early CAVD from progressing to stenosis by making GAGs less likely to bind LDL.

“The take-home message of our study is that CAVD is a multi-stage process and that healthy valve cells respond differently to LDL than blood vessel cells,” Masters says. “The ability to examine multiple steps in this novel in vitro model for early CAVD opens up several promising avenues for developing drugs that are distinct from those for atherosclerosis.”

The study was funded by the National Institutes of Health (R01HL093281, R21EB019508) and the American Heart Association (15PRE 22170006).

This yellow perch is showing evidence of viral hemorrhagic septicemia virus — for example, hemorrhaging in the eye and bleeding in a pectoral fin.

Photo: Evi Emmenegger/USGS

In May 2007, hundreds of freshwater drum — also known as sheepshead — turned up dead in Lake Winnebago and nearby Little Lake Butte des Morts, both inland lakes near Oshkosh, Wisconsin. The fish were splotched with red and their eyes were swollen and bulging.

The Wisconsin Department of Natural Resources (DNR) launched a quick response and, working with the Wisconsin Veterinary Diagnostic Laboratory (WVDL), quickly learned that a deadly virus was responsible: viral hemorrhagic septicemia virus, or VHSv. First detected in the U.S. among freshwater fish in 2005 — including muskellunge, perch and walleye — VHSv had already caused mass fish die-offs in the Great Lakes and several regional waterways connected to them.

The DNR subsequently encouraged anglers and boaters to adopt practices that have helped slow the spread of VHSv into other inland lakes in Wisconsin, but a new study led by Tony Goldberg, professor of epidemiology and pathobiological sciences at the University of Wisconsin-Madison School of Veterinary Medicine (SVM), shows the virus is still circulating in Lake Winnebago. It also shows that some fish actually survive VHSv infection but could be sources of future infections.

“It’s still possible to transmit the virus to fish in other lakes,” says WVDL Virology Section Head Kathy Toohey-Kurth, a member of the research team and a clinical professor at the SVM. Though large numbers of dead fish are no longer washing up on shore, “it shows the virus is still transmitting and people still have to be careful to follow all the guidelines from the DNR, like not carrying buckets of bait between waters,” she adds.

Drum are a food source for popular game fish like walleye and sauger. VHSv does not infect people, but 28 species of fish are vulnerable to the virus, which causes them to bleed to death. Some of these species, like bass and muskellunge, are iconic fishes that help support Wisconsin’s $2.3 billion-a-year sport fishing industry.

The findings of the current study, and the new diagnostic test upon which it relied, are aiding the DNR in efforts to monitor game fish in waterways throughout the state, in addition to better informing its stocking efforts.

The diagnostic test was developed by Toohey-Kurth — an expert in veterinary diagnostic testing — and Anna Wilson-Rothering, a WVDL scientist and lead author of the study. Wilson-Rothering is a former DNR employee who was involved in early VHSv surveillance efforts and earned her master’s degree from UW-Madison studying the virus. Efforts to develop the test started in 2009, shortly after Goldberg joined the faculty of UW-Madison and became involved in measures to prevent the spread of VHSv.

“I met with the DNR and we discussed some of the problems,” says Goldberg, who is also associate director for research at the Global Health Institute and John D. MacArthur Chair at UW-Madison. “It was very difficult to diagnose. It required you to kill the fish and take its internal organs to isolate the virus. It was also a lengthy process and very labor intensive.”

The new test requires just a small blood sample from the fish, which can be caught, sampled and released back to the water. The researchers take the blood back to the lab and look for evidence the fish were once infected with the virus: a specific antibody produced by the fish in response to infection. Like fingerprints on a doorknob at the scene of a crime, antibodies show the virus was once there.

The research team worked with the DNR to collect blood from nearly 600 drum in Lake Winnebago twice a year in 2011 and 2012 — both spring and fall — and used the test to look for VHSv antibodies. The team also collected fish to look for those that may still harbor active virus, finding it in just one: a large, older female. This provided “proof that the virus is still present in the lake,” Goldberg says. “Fish are still being exposed.”

The researchers believe that enough drum have been infected with and survived the virus, their antibodies providing protection from re-infection, that mass fish kills have probably not occurred. This phenomenon is referred to as “herd immunity” and is similar to what happens when a large group of people is vaccinated against a disease like measles. If enough individuals are protected, less of the virus circulates and infects the unprotected.

But once levels of protected individuals fall, either from deaths from other causes, or as large numbers of new, unprotected fish are born, another wave of VHSv-induced deaths could occur. Researchers will continue to monitor for the virus and the study, they say, underscores the importance of collaborative scientific efforts with the DNR and the role these efforts play in addressing the needs of the state.

“This test will continue to be useful to monitor VHSv transmission,”says Toohey-Kurth, “and with further refinements we will be able to better assist our state partners with management of the disease.”

The study, published in the Journal of Clinical Microbiology, was supported by the University of Wisconsin Sea Grant Institute with funding from the National Oceanic and Atmospheric Administration. Co-authors of the study include now-retired fish health specialist Sue Marcquenski and other scientists from the DNR, researchers from the U.S. Geological Survey (USGS), and scientists from the University of Wisconsin-Stevens Point and the University of Iowa.

“There is incredibly important, potentially lifesaving research that goes on in Wisconsin that relies on fetal material received from federally regulated tissue banks,” said Dr. Robert Golden, dean of the UW–Madison School of Medicine and Public Health and the university’s vice chancellor of medical affairs, at a hearing before the State Assembly’s Committee on Criminal Justice and Public Safety. “On our campus, cancers including lymphoma, stomach cancer and other diseases have NIH-supported labs actively working on promising new treatment. All of this will stop if this bill is passed.”

That doesn’t sit well with Mary Jo Gordon, who relies on research with fetal tissues to keep her heart beating.

Gordon and many members of her family have long QT syndrome, a genetic heart disorder that causes heart arrhythmia and cardiac arrests like the one that claimed her sister.

A long list of common drugs from antibiotics to asthma medications can trigger the attacks, so the Federal Drug Administration now requires every new medication to be tested for safety among those with long QT and similar disorders.

“We couldn’t do this without these tissue samples available to the researchers who are doing this work,” Gordon told legislators. “By halting research, you’re putting at risk my beautiful nieces and nephews. I ask that you not put our health and safety at risk, not take away our hope for treatment and a cure.”

With research on various cancers, Parkinson’s disease, arthritis, new vaccines and more threatened by the bill, Dr. Brad Schwartz, biochemist and CEO of the Morgridge Institute for Research, wants legislators to consider the implications of outlawing efforts to help so many.

“It would be an ethical failing if we did not do everything we could to try to help people with these diseases,” Schwartz says.

The bill would also hamstring a vibrant, growing piece of the state’s economy. UW–Madison labs whose work relies in some part on fetal tissue or cell lines employ more than 1,400 people and account for about $76 million in federal research funding in the most recent fiscal year.

“These scientists will leave as soon as they can, taking with them not only their $76 million, but their collaborating fellow scientists,” says Golden, who believes the legislation would also endanger Wisconsin’s only federally supported comprehensive cancer center — where a small, but vital, portion of research employs fetal tissue.

Such a law could also cost the state its future scientific leaders, innovators and entrepreneurs.

“Talented Wisconsin students have the opportunity to learn skills that will be valuable to the economy of the future,” Schwartz says. “Anything we do to make that research impossible to accomplish will drive those talented young people to other parts of the country.”

Learn more about the issue.

Eighteenth-century handwriting may be elegant, but it isn’t always legible.

A team of UW-Madison students has “decoded” a historic ledger and researched items for the Smithsonian’s American Enterprise exhibit, bringing to life a unique record of American life 250 years ago.

“At the start of the semester, I remember one of the students exclaiming, ‘It’s like a code!’” says Ann Smart Martin, a professor of art history who oversaw the project. 

Kept by merchant William Ramsay, the left page of the book (marked “debtor”) recorded the date, customer’s name, what was purchased, and for how much. The right side listed when and how a person paid.

Using an interactive panel — something never before done in a museum — visitors can choose to learn more about each highlighted entry, the person who took part in the transaction and how that object was used in Colonial times. 

Pieces selected for the final display include the following:  

Clockwise from lower left

Paste (glass) buckle, researched by Sona Pastel-Daneshgar
Like handkerchiefs, fancy buckles were purchased by both men and women to adorn shoes and clothing in a variety of ways, though this particular ornate buckle was intended for a man. Ramsay’s ledger showed one “pair knee buckles” sold to a John Douglass. The cut glass stones are set in steel.

Ribbon, researched by Professor Ann Smart Martin
Ribbons were small but important objects with multiple connotations, particularly involving the relationships between men and women. “A black ribbon could be mourning or death, but another purchase could be from a young man to a young woman, bringing life,” says Martin. “Ribbons got this other meaning going on that actually could be kind of sexual, because you’re taking something and putting it around your body.” 

Green earthenware mug, researched by Elizabeth Amherdt
Ramsay owned a ship called the Fairfax, which he unsuccessfully tried to sell in 1751, and the ship had its own account in the ledger. “We think it was used by the crew of the ship because it was charged to the account of the ship,” says Martin.

Pair of shoes, researched by Maddie Hagerman
An August 1753 entry listed eight pairs of “best shoes.” Buyer Vorlinda Wade, a wealthy widow, was sole owner of a large tobacco farm adjoining Mount Vernon. Hagerman and her fellow group members carefully researched shoes from the era to select a pair that most closely represented what a wealthy widow might have considered “best shoes.”

Tiny copy of Lilliputian Magazine; or, the Young Gentleman’s and Lady’s Golden Library, researched by Dani Zwang
“Far too many of the objects in the account are not identified with enough specificity, so we were thrilled that the merchant identified Lilliputian Magazine,” says Martin. “We now know that the earliest and most up-to-date forms of children’s literature in Alexandria was written by the most recent literary talent in the style of the fantastic travel yarns of Gulliver’s Travels.”

Printed handkerchief from India, researched by Shagun Raina
“Some of the textiles had enough detail so that we knew they came from India because of the names attached to it,” says Martin. “Sastracundy was a place in India known to be dyeing these textiles.” By tracing the story of an exported textile from India to the colonies, Martin says Raina’s team has illustrated the global story of how other countries and cultures make their way into the artifactual world.

Silver candle snuffer, researched by Abby Springman
“Although expensive and seldom squandered, candles were an important part of life in an urban place like Alexandria,” says Martin. “Candles required careful, labor-intensive watching and cleaning; the wick needed to be snipped to keep from melting extra wax, smoking or perhaps falling away on fire. The elegant little snippers were developed with a blade, a box to keep the bits and a tray.”

White leather gloves, researched by Anneliese McGavin
According to the display label written by McGavin, customers at Ramsay’s store bought a variety of British-made gloves like the white kid gloves purchased by Captain William McCarthy. Gloves made of elegant glazed lamb, fragile lace, or basic muslin protected the hands of both men and women. Complex codes of dress dictated what designs were appropriate.

Ramsay’s desk and bookcase
Due to Ramsay’s prominence, his will and many other important papers are available in the Smithsonian archives and became valued parts of the students’ investigation. His tall mahogany desk reveals the elaborate workmanship indicative of his success as a merchant; the weights and measures he used in his trade sit alongside the ledger itself.

Other items researched by UW-Madison students include:

• Combs (Stephanie Goodwin)
• Battledore (Drew Sanders)
• Button (Anna Lee)
• Candlestick (Anneliese McGavin)
• Children’s primer (Anna Lee)
• Copper tea kettle (Drew)
• Doll (Sona Pastel-Daneshgar)
• Fan (Shagun Raina)
• Fiddle strings (Monica Welke)
• Furniture hinge (Abby Springman)
• Glass bottle (Lauren Gottlieb-Miller)
• Knives and forks (Dani Zwang)
• Pewter chamber pot (Monica Welke)
• Pewter plate (Liz Jarvis)
• Pewter salt cellar (Stephanie Goodwin)
• Pewter spoon (Dani Zwang)
• Tea strainer (Elizabeth Amherdt)
• Thimble (Courtney Thrall)
• Whip (Nicole Kauper)
• White salt glaze mug (Nicole Kauper)
• Wig (Courtney Thrall)

Read more about the project. 

On April 11, 2015 the H5N2 virus was detected at a commercial chicken facility in Jefferson County, Wisconsin. By May 5, the virus had struck 9 commercial flocks in four Wisconsin counties, leading to the demise of more than 1.7 million chickens and turkeys. A snowy owl found dead in the wild in Oconto County also tested positive for H5N2. Nationwide, the virus has led to the deaths of more than 32 million birds.

The H5N2 virus has significantly affected the U.S. agricultural economy and will drive rising food costs for consumers. Additionally, while there are no reports of human infections in the current outbreak in the United States, similar viruses have infected more than 800 people in Asia and Europe over the last decade.

The United States Department of Agriculture and the Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) State Veterinarian’s Office are managing the outbreak in Wisconsin. WVDL works with these agencies to provide ongoing testing.

The current H5N2 outbreak first appeared in a backyard poultry flock in Washington State in January 2015. At that time, WVDL, as part of the National Animal Health Laboratory Network, began preparing to test birds in Wisconsin and other states if necessary.

Kathy Kurth-Toohey, virology section head at WVDL, has led diagnostic efforts at the laboratory. The laboratory tests turkeys, chickens, and ducks twice every 14 days in the infected, buffer, and surveillance zones established by DATCP and the USDA.

Researchers at UW-Madison are also leading efforts to study the virus and reduce its harm.

Animal sciences professor Mark Berres is examining the prevalence of the virus among Red Jungle Fowl, the direct ancestors of domestic chickens. Like other wild waterfowl, Red Jungle Fowl can harbor the virus but do not get sick. Berres seeks to understand how chickens lost their resistance to the virus over the course of domestication or through selective breeding.

Yoshihiro Kawaoka, professor of pathobiological sciences in the UW-Madison School of Veterinary Medicine (SVM) is testing the virus found on Wisconsin’s farms to better understand it and the impact it could have on other species. He is also studying how some chickens have survived infection, despite its nearly 100 percent mortality rate.

Given the incidence of similar avian influenza strains in Europe and Asia, with human mortality rates as high as 50 percent, Kawaoka says research to understand the potential for H5N2 to become transmissible from person to person is crucial. However, this work is currently prohibited due to a federal funding pause.

No birds in Wisconsin have tested positive for a strain of H5N2 since May 5 and quarantines in the state have lifted, but DATCP and WVDL warn the outbreak may not be over. Both agencies encourage flock owners to continue using proper biosecurity techniques when working with poultry.

“We are expecting that a combination of weather and wild bird migration season ending will lead to a decline or cessation in positive farms,” says Keith Poulsen, a WVDL diagnostic and case outreach coordinator and an assistant clinical professor at SVM. “But we could see more cases in the fall, when temperatures drop and wild birds migrate again.”