Recently, in response to a public records request, the University of Wisconsin–Madison provided records related to research conducted in 2023 to improve the well-being of pet dogs undergoing treatment involving surgeries. The dogs involved in the study were acquired from Ridglan Farms, a facility licensed by the U.S. Department of Agriculture to conduct research and to supply animals for research.

The veterinary medicine research, conducted humanely by experts who care for the well-being of companion animals, explored safer methods for administering anesthesia to dogs that undergo spaying procedures and other lower-body surgeries like liver surgery and emergency procedures for intestinal problems. The research concluded with a study that required six dogs to be humanely euthanized in order to confirm that the anesthesia reached the expected locations in the body. Other dogs involved in the research were adopted.

Veterinarians across the country are now safely using this anesthesia method to keep dogs comfortable and healthy when undergoing many surgical procedures necessary for their care.

For decades, researchers at UW–Madison have performed studies that help advance health and well-being. UW researchers have made significant scientific and biomedical progress, helping to save countless lives.

Studies like this one are performed by scientists whose training and careers are spent trying to improve healthcare. Before their studies can be approved, researchers must demonstrate that they can’t achieve the anticipated scientific outcomes without animals; their studies must be designed to involve the smallest number of animals possible; and researchers must limit to the absolute minimum any discomfort the animals may experience.

Animal studies also require strict ethical and legal oversight at the federal level and from the university. The research to improve surgical care for dogs was conducted only after it was approved by a review committee, which is required by federal law and contains members who are scientists, non-scientists and community members unaffiliated with UW–Madison.

The committee scrutinized the research plans, called protocols, and the research was only permitted to start once the review committee was satisfied that the protocols met the necessary standards for animal care and scientific rigor, which include federal, ethical and university requirements. The anesthesia studies were carefully evaluated to ensure that the knowledge gained would benefit future animals.

UW–Madison facilities that house animals are kept up to standards according to federal law and inspected regularly by veterinarians from the USDA. The animals are cared for by UW–Madison animal care staff and veterinarians trained and certified to help ensure their safety and keep them healthy. At this time, there are no dogs from Ridglan Farms housed at UW–Madison.

The practice of relying on companion animals for research that is intended to improve companion animal health is an evolving one in the field of veterinary medicine. As part of efforts to continuously evaluate our educational, research and clinical practices, UW–Madison will continue to engage in efforts to examine this kind of research going forward.

The University of Wisconsin School of Veterinary Medicine does enroll client-owned animals in clinical trials. The university never conducts research on client-owned animals unless clients explicitly give permission for their pets to be enrolled in clinical research. Just as in human medicine, clinical trials are critical to advancing diagnosis, treatment, and prevention of illness and disease and improving health outcomes. Clients choose to participate in specific clinical studies with the parameters of the study clearly explained.

Infants exposed to the Zika virus during pregnancy may face hidden developmental challenges, even if they appear healthy at birth. A recent study at the University of Wisconsin–Madison highlights the need for better developmental screening during a child’s first year of life.

Zika virus is known to cause severe birth defects — such as brain damage and microcephaly, a much smaller head and brain. However, little is understood about why 30% of babies born without physical symptoms go on to experience developmental problems including vision and hearing loss.

To better understand what happens to newborns affected by Zika infection, UW–Madison occupational therapy professor Karla Ausderau and others studied pregnant rhesus macaque monkeys at the Wisconsin National Primate Research Center. The animals were exposed to Zika virus or a placebo early in pregnancy. The scientists followed the resulting infant monkeys through one year with behavioral tests, vision and hearing assessments, and social observations.

They found that, like human babies, monkeys with prenatal virus exposure, regardless of maternal vaccination status, had increased risk of vision delays, hearing loss and changes in maternal attachment despite having no outward symptoms at birth. The researchers published their findings recently in the journal Nature Communications.

Although the infant monkeys’ eyes appeared structurally normal, researchers found disruptions in how the eyes communicated with the brain, an issue known as cortical visual dysfunction. This type of visual impairment is also seen in children who struggle with vision despite having healthy eyes. Early visual delays appeared in the monkeys as early as 3 months of age; however, those differences resolved by 12 months. The early vision changes did not predict later developmental challenges, however, and researchers say these early disruptions may signal broader effects of prenatal exposure.

“Infants exposed to Zika before birth showed altered social-emotional development and changes in cortical visual function during infancy, even when they appeared healthy at birth. And we couldn’t predict those outcomes from the mother’s infection characteristics, which is a problem if we’re trying to identify which babies need closer follow-up,” says Emma Mohr, UW–Madison pediatrics professor and co-author of the new study.

The researchers also found that hearing loss appeared more often in Zika-exposed infants than in unexposed animals, although the difference was not statistically significant.

Social behavior told another important story. Zika-exposed infants spent more time clinging to their mothers than typically expected at this age and gained more weight than the control group due to increased access to nursing. In rhesus macaques, close maternal contact normally decreases as infants grow more independent. Researchers believe this prolonged attachment may reflect difficulties with sensory processing, emotional regulation and assessing threats, skills that are critical for healthy social development.

Zika-exposed infants also showed lower inhibition by approaching new objects and situations more quickly than expected. This behavior may signal early anxiety, delayed emotional learning, or challenges in interpreting sensory information from their environment, which is risky.

The study found that maternal virus levels, placental infection and antibody responses did not predict which infants experienced developmental differences, suggesting that common maternal biomarkers are poor indicators of a child’s long-term risk. Human studies have shown that Zika infection during pregnancy can persist for months and increase the risk of miscarriage and brain abnormalities. However, those severe outcomes were not observed in this animal study — limiting conclusions about how maternal immune responses relate to the most severe cases.

The findings do point to a clear message. Prenatal Zika exposure alone can influence early development, even in the absence of visible birth defects.

“Children with prenatal Zika exposure need long-term neurodevelopmental follow-up, not just a clean bill of health at birth. The subtle differences we’re detecting wouldn’t be picked up on a routine exam, but they’re the kinds of things that can shape learning, behavior and social development as kids grow,” Mohr says.

The study strengthens the case for routine developmental monitoring of all children exposed to Zika during pregnancy, regardless of symptoms at birth, according to the authors. Early detection could allow for timely interventions when delays emerge. They also stress that prevention remains the strongest defense.

“Vaccines and mosquito control are still the best tools we have,” says Mohr. “Once infection occurs, the damage may already be done.”

Support for this research was provided in part by grants from the National Institutes of Health (P01AI132132, R01 AI153130, P01AI132132, P30EY016665 and P50HD105353).

Karen Strier, a Vilas Research Professor and Irven DeVore Professor of Anthropology at the University of Wisconsin–Madison, is among the newly elected members of the American Philosophical Society. Her election is in the area of the biological sciences, recognizing the more than 40 years she’s spent in the field researching the critically endangered northern muriqui monkeys in Brazil.

Strier joins the oldest learned society in the United States, founded in 1743 by Benjamin Franklin for the purpose of “promoting useful knowledge.” The society connects the country’s leading scholars and scientists at semi-annual meetings, provides access to a vast research library and supports ongoing research and discovery. Its election honors extraordinary accomplishments across all academic fields.

When Strier started her work in 1982, she didn’t know that her curiosity about the enigmatic primates would lead her to establish an international collaborative research and conservation project that is still ongoing to this day. Closely studying the same populations of monkeys has allowed Strier and her research team to gain detailed knowledge about how muriquis interact with their environment, socialize and live.

In addition to expanding theoretical perspective about primate behavioral variation, these critical findings are creating a road map for how to help this species survive, which is essential work since there are fewer than 1,000 individuals of this species in the world. She shares her findings with the Brazilian government and nonprofit organizations to help with conservation efforts.

“By establishing forest corridors to connect isolated populations, we can provide the muriquis with the protected routes they need to move freely across the landscape as local conditions change,” Strier wrote in a 2024 essay about the power of persistence in her work. “We have the knowledge we need to save them from extinction; now it is just a question of persistence and a race against time.”

Strier joins other prominent UW–Madison figures who have been elected to the American Philosophical Society, including virologist Howard Temin, who also won a Nobel Prize for his work on retroviruses; Verner Suomi, the father of modern meteorology; cultural historian George Mosse; and biochemist Judith Kimble.

“This recognition was a huge surprise, and I feel very honored to have been elected,” Strier reflects from Brazil, where she is continuing her work. “It is especially meaningful coming at a time when the value of science is being challenged. But right now, the need for scientific understanding to conserve biodiversity has never been greater.”

Researchers at the University of Wisconsin School of Veterinary Medicine have identified a possible way to make longer lasting vaccines for respiratory viruses like influenza and the coronavirus that causes COVID-19.

The work, published March 25 in in the journal Cell Reports, focuses on T cells, a type of immune cell that helps control infections by killing virus-infected cells. Unlike antibodies — the basis of most current vaccines, which can lose effectiveness as viruses mutate — T cells recognize more stable parts of viruses, offering a path to broader protection.

A problem with designing vaccines around T cells, though, is their relatively short lifespan. The new research sheds light on a surprising potential workaround.

“We have discovered essentially a mechanism which we can target — a new clue to generating long-lived T cells,” says M. Suresh, a professor in the Department of Pathobiological Sciences who led the study.

Rethinking how vaccines trigger immunity

Most vaccines are designed to stimulate antibodies that block infection. That approach works well for many infectious diseases, but it can fall short against viruses that evolve quickly.

“So, what do we do? We need a plan B,” says Suresh.

For viruses like SARS-CoV-2 and seasonal influenza, that plan B has meant regularly updating vaccines to target newer virus variants and encouraging the public to get the latest flu and COVID shots each year. But that strategy has its pitfalls.

“With the pandemic we went through, people are just tired of getting vaccinated,” Suresh says. Indeed, vaccination rates have been declining in the United States for years.

The ability to harness T cells could offer a potentially more effective plan B. Rather than preventing infection outright, T cells help limit disease severity and promote early recovery by identifying and destroying infected cells.

“They go and hunt one infected cell at a time and eliminate them,” Suresh says.

Because T cells recognize internal viral proteins that don’t change much over time, they can remain effective even as viruses mutate.

A key challenge, however, is the durability of protection offered by T cells, especially in the lungs, where respiratory infections take hold.

Suresh’s lab studies a specialized group of immune cells known as tissue-resident memory T cells, which remain in the lungs and airways as a first line of defense. These cells can respond quickly to infection.

“But the problem is they don’t stay very long,” Suresh says. “They die off, and we still don’t know why.”

A different early signal, a different immune outcome

In the new study, which was funded by the National Institutes of Health, Suresh and his colleagues looked at what happens in the first hours after vaccination, when the body’s innate immune system is activated.

Different types of pathogens trigger different early inflammatory signals that “program” memory T cells to recognize and go after infected cells. Suresh’s team asked whether changing those signals could reshape how T cells develop.

Using an experimental vaccine approach in mice, the researchers compared two types of early immune signals: one that mimics a viral infection and another that resembles a bacterial response. The difference was striking.

“When we had a virus-like inflammation, the memory T cells dropped off and we quickly lost protection,” Suresh says. “But when we created a bacterial-like inflammation, the mice developed a different kind of memory T cell which actually persisted longer and protected longer.”

Stem-like cells that adapt when needed

The longer-lasting cells had characteristics similar to stem cells, Suresh says, including the ability to persist and regenerate.

Even more surprising, those cells were able to adapt when confronted with a virus. When the researchers exposed vaccinated mice to infection, the T cells shifted into a more typical virus-fighting mode.

“They just flipped,” Suresh says.

That flexibility suggests the T cells could combine durability with the ability to effectively combat a viral infection.

Toward longer-lasting, broader vaccines

The findings offer a potential path toward vaccines that require fewer boosters and provide broader protection across variants.

“The duration of immunity is really, really important,” Suresh says. “Can we vaccinate fewer times, and can shots protect against new strains?”

The research also highlights the importance of delivering immunity where infections occur. For respiratory diseases, that may mean developing vaccines that work in the nose and lungs rather than through injection.

“The best way to immunize against all our respiratory infections is to give through the normal route of infection,” Suresh says.

What comes next

The current study was conducted in mice. The team plans to test the approach in nonhuman primates and in models that better reflect the diversity of human immune systems.

Future work will also explore ways to guide immune cells to the lungs after traditional vaccination — a strategy that could improve protection without requiring new delivery methods.

This research received funding from the National Institutes of Health (U01 AI124299 and R21 AI149793).

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.

A new study by researchers at the University of Wisconsin–Madison provides the first empirical evidence connecting the chromosomal location of genes to natural selection, indicating the arrangement of genes can influence how quickly populations can adapt to rapid environmental change.

Published Friday in the journal Nature Communications, the study analyzed the genomes of three sibling copepod species (Eurytemora affinis species complex) to map how certain mutations — called chromosomal fusions — moved the location of genes as the tiny aquatic crustaceans evolved. The research team was surprised to find that even though these fusions occurred millions of years ago, they have implications for a contemporary species’ ability to adapt.

Until the last 80 years, these copepods largely lived in coastal estuarine ecosystems. Recently, these crustaceans have invaded freshwater ecosystems like the Great Lakes through the transport and dumping of ship ballast water. Carol Eunmi Lee, a professor of integrative biology at UW–Madison, has been studying copepod genetics for over 20 years to understand how they can adapt and thrive in new environments.

The short lifespan and relatively small genome of copepods make them the perfect model organism to investigate these questions. Even still, it took postdoctoral researcher Zhenyong Du nearly three years to sequence the genomes and map how the chromosomal fusions relocated genes to uncover patterns of natural selection. The work also revealed that each sibling species has an entirely different number of chromosomes.

“We were absolutely shocked,” says Lee.

These three sibling species, or clades, of copepods share a common ancestor and can breed with one another, something that is rare for organisms with different chromosome numbers, explains Du, who co-authored the paper with Lee. The clade from Europe has 15 chromosomes, while the Gulf clade has seven. Meanwhile, the Atlantic clade, which now also lives in the Great Lakes, has just four chromosomes.

Du and Lee immediately set out to understand why these sibling species have packaged their genes so differently from one another.

“We looked at the evolutionary history of the chromosomes, and we found that fusions are bringing multiple chromosomes together,” says Du.

Chromosomal fusions — the joining of different chromosomes into one — are a type of mutation that can happen all the time. This process can bring genes from different chromosomes together on the same chromosome, physically linking them as a potential unit of inheritance during natural selection.

Du and Lee started to wonder if the fusions that resulted in different chromosome numbers were beneficial for survival and thus were favored by natural selection in the past.

“During the evolutionary history of these copepods, salinity is the major variable of their living conditions,” Du explains.

One of the main mechanisms that copepods use to adapt to changes in salinity are proteins called ion transporters. Du and Lee found that these ancient chromosomal fusions caused genes that code for key ion transporters to be grouped together.

They observed that these fusions also caused the groupings of genes to move away from the recombination-prone arms of the chromosome and closer to its center, where recombination would not rip apart combinations of beneficial gene variants.

Genes are often subject to recombination, a process that occurs in the exchange of DNA during procreation and allows for new combinations of genetic material in offspring. Recombination is beneficial in creating genetic diversity that can help a species survive. And sometimes the fusions are so beneficial that they become permanent in the evolutionary process.

Scientists have hypothesized for years that genomic architecture evolution, particularly chromosomal fusions, might play an important role in evolutionary adaptation. This is the first study to produce empirical evidence of that particular link. The UW researchers’ study shows as copepods evolved, natural selection seemed to favor fusions that moved these ion-transporter genes toward the center of the chromosomes.

Importantly, the findings also suggest that fusion sites that were created millions of years ago are still hot spots for natural selection in invasive populations in the Great Lakes today.

While this study focuses on copepods, Du and Lee expect there will be implications for how scientists consider genetic architecture evolution and mechanisms of adaptation in other invasive species. There are also important implications for predicting which populations will be able to survive and adapt to future climate change.

“Genome architecture likely has profound impacts on how populations respond to natural selection. It’ll affect the mechanism of natural selection in a population, and determine how quickly it can evolve and respond,” says Lee.

This project was funded by National Science Foundation grants IOS-2412790, OCE-1658517, and DEB-2055356, and French National Research Agency ANR-19-MPGA-0004.

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.

Shawn Wiederhoeft is a pretty regular guy in his 30s. The Madison native works as a video game developer and maintains an active lifestyle. He’s healthy — in the best shape of his life — and regularly spends time with friends and family in southern Wisconsin.

But it wasn’t always a given that Wiederhoeft would be able to participate in life so fully. In fact, “Uncle Shawn,” as he’s known to family, is healthy today thanks in large part to a new kidney he received in 2020 from his sister, Meagan Hahn, of Wauwatosa.

The transplanted kidney has given Wiederhoeft a new lease on life, and because he and his sister chose to participate in a cutting-edge clinical trial at the University of Wisconsin School of Medicine and Public Health, he’s also able to live without the need for anti-rejection medications.

With no daily medications and only occasional medical checkups, Wiederhoeft says he sometimes almost forgets he’s the recipient of a kidney transplant.

“I have to consciously remind myself that there’s a third kidney in here,” he says. “I feel healthier than I’ve ever been.”

Wiederhoeft’s remarkable journey from serious illness to a medication-free recovery is just one of a growing number of living kidney transplant success stories that an international team of physicians and researchers reported in the July issue of the American Journal of Transplantation.

Led by UW–Madison surgery professor Dr. Dixon Kaufman, who directs the UW Health Transplant Center, the team shared results of a Phase 3 clinical trial that evaluated the effectiveness and safety of a living kidney transplant tolerance protocol that also includes the transplantation of certain stem cells from the kidney donor to the transplant recipient.

These stem cells are injected into the recipient several days after transplantation and take up residence in bone marrow, where they divide and multiply into immune cells that share the genes of the donated organ. The goal is to keep the recipient’s immune system from attacking the new organ, which it would otherwise recognize as a threat.

“This procedure doesn’t replace the immune system, but it complements it with around 5 to 10% of the immune system being from the donor,” says Kaufman.

In doing so, the new method removes the need for costly anti-rejection medications that severely suppress the recipient’s immune system, carrying a whole host of lifelong side effects.

The prospect of participating in a clinical trial that carried such a possibility was surreal for some of the study’s initial participants, including Wiederhoeft and Hahn.

“It felt straight out of a science fiction novel,” says Wiederhoeft.

The feeling of entering uncharted territory was even more pronounced for the trial’s first participants, sisters Barb Okey and Brenda Quale, both of Platteville.

“To say I was nervous — that’s an understatement,” says Okey, who received one of Quale’s kidneys followed by an infusion of her stem cells in 2018. Within months of the procedure, as hoped, tests showed that Quale’s cells had begun multiplying and circulating in Okey’s blood, and Okey was eventually weaned off her anti-rejection medications. Today, the only medication Okey takes is to help control her blood pressure.

“It’s amazing,” Okey says. “To have an opportunity to continue life with a new kidney and without taking medications is pretty fabulous.”

Okey and Wiederhoeft are among the small group of kidney recipients who can forgo anti-rejection medications thanks to UW–Madison’s clinical trial, but there are plans to expand eligibility for the procedure.

The initial phase required donors and recipients to be siblings and a “perfect,” or identical, match, meaning they have compatible blood types and other physiological compatibilities. Kaufman says that the initial trial’s success means that eligibility could soon be extended to living donor transplants of non-identical matches and eventually to recipients of organs from deceased donors.

Kaufman described the trial’s positive results as “immensely gratifying” and a testament to the value of long-term investments in research.

Indeed, before the procedure could be attempted in human patients, researchers at the Wisconsin National Primate Research Center and elsewhere spent years testing its safety and effectiveness in non-human primates. In 2023, the team led by Kaufman reported promising results from its latest primate studies that could pave the way for expanding the procedure to non-identical transplant pairs.

The studies that enabled this clinical trial received substantial support over the years from the National Institutes of Health (NIH). Kaufman credits UW–Madison’s proven track record of executing complex biomedical research for the sustained federal investment.

“The clinical and research environments at UW are outstanding” he says. “I’ve been to other programs, trained at other programs, and been faculty at other programs, and the unique things that make the ability to do complicated clinical trials like this successful at the University of Wisconsin are the strong collaborative culture and fantastic resources. We’ve got a history and a tradition of advancing the field in innovative ways for the benefit of many. We want to keep reaching higher and keep making those advances.”

While the recognition and support from NIH and other funding agencies have underpinned the trial’s success, Kaufman says it’s the patients and donors who are willing to participate in new and potentially risky trials who are ultimately responsible for helping to advance the field.

“Getting [the patients] back on the road to living a happy and fulfilling life is really what this is all about,” he says.

For Hahn, who felt compelled and grateful to participate in the trial as Wiederhoeft’s donor, the results have been immeasurably positive.

“To be able to have Uncle Shawn there for all the family events, and for it to be the most normal version of him — the most healthy version of him — I have to remind myself that this all happened and that this isn’t normal for so many people. But for us, it’s quite a blessing.” ■

Dixon Kaufman, MD, PhD, is the Ray D. Owen endowed professor in the UW–Madison Department of Surgery.

The research that supported this clinical trial occurred over 12 years, first in non-human primates before human trials, with more than $20 million in funding provided by the National Institutes of Health over that period (U01AI102456, MSN150727, T32AI25231, U54). NIH also supports the Wisconsin National Primate Research Center (P51OD011106). The Phase 3 clinical trial described here was sponsored by Medeor Therapeutics (MDR-101) in association with Stanford University.