Genomic research led by the University of California, Davis, reveals clues about montane red foxes’ distant past that may prove critical to their future survival. The study, published in the journal Molecular Biology and Evolution, examines the potential for genetic rescue to help restore populations of these mountain-dwelling red foxes. The research is especially relevant for the estimated 30 or fewer native red foxes living in the Lassen Peak region of California.

The study found that inbreeding is impacting the Lassen red fox population. Thousands of years ago — long before unregulated trapping and poison knocked back their populations in the 1890s and early 1900s — red foxes were not only abundant in these mountains, they were also more connected to neighboring foxes in Oregon, the Rocky Mountains and Washington Cascades than they are today. This positions them well for genetic rescue should managers decide to pursue it and reconnect the populations.

“Nothing we found disqualifies red foxes from genetic rescue,” said lead author Cate Quinn, who conducted the research as a UC Davis postdoctoral researcher with the Mammalian Ecology and Conservation Unit within the School of Veterinary Medicine. She is now a research biologist with the USDA Forest Service Rocky Mountain Research Station. “The study suggests that genetic rescue could be a viable option for the Lassen population.”

Rescue workers

Genetic rescue is a conservation tool to reverse the effects of inbreeding depression, which is when inbreeding reduces an animal’s fitness and ability to reproduce. Genetic rescue involves bringing new individuals to a population to introduce genetic variation and spur growth.

The tool is not considered lightly, and managers first must understand the severity of inbreeding, the historical baseline genetic rescue seeks to restore, and the deeper evolutionary relationships the foxes share with each other.

To fill those knowledge gaps, the scientists sequenced 28 whole genomes from the four subspecies of montane red foxes. These include small, isolated populations in the Pacific mountains, Oregon Cascades, Lassen Cascades and the Sierra Nevada, as well as a larger population in the Rocky Mountains and a subspecies in the Sacramento Valley. Using genomic technology, the authors could peer back in time to see if a population was always isolated, to what extent, and when that began to change.

Abundant, connected and diverse

The study found high levels of recent inbreeding in Lassen and Sierra Nevada red fox populations, with the Lassen red foxes a high priority for intervention. Only one montane red fox is known to have entered the Lassen population in more than 20 years of monitoring, the study said.

The data also revealed that 10,000 to 12,000 years ago, montane red foxes in the Western United States were abundant, connected and genetically diverse. The Lassen population was likely connected to the Oregon red foxes within the last century, breaking from each other relatively recently, Quinn said.

A hopeful way forward

Combined, these findings point to a hopeful way forward for Lassen’s red foxes, and for other red foxes facing similar challenges.

“We think trapping drove their population down, but we didn’t know what was keeping them small,” said senior author Ben Sacks, director of the Mammalian and Ecology Conservation Unit at the UC Davis School of Veterinary Medicine. “Now we see that what kept them small appears to be inbreeding depression. If what drove their decline is gone, can we bring them back? There is hope here.”

Quinn agrees: “Not too long ago, this was an abundant, connected, diverse population. That diversity still exists. If we were to restore them as a group, these foxes may still have a lot of adaptive potential.”

She cautions, however, that true genetic “rescue” requires reconnecting the whole subspecies — not just growing one population.

“If we only consider each small pocket individually, they’re in trouble, but if we look at the whole montane system, restoration is still possible,” Quinn said.

Additional coauthors include Sophie Preckler-Quisquater of UC Davis and Michael Buchalski of the California Department of Fish and Wildlife.

The study was funded by the U.S. Fish and Wildlife Service, California Department of Fish and Wildlife, and UC Davis.

Researchers working at reefs in Moorea, French Polynesia found that the network of dead coral skeletons left in place by bleaching events caused critical processes to break down, ultimately preventing reefs from recovering. The complex landscape protects seaweed from herbivores, enabling it to quickly colonize the reef and outgrow young coral. The results appear in the journal Global Change Biology.

Dynamic ecosystems

Coral reefs are busy ecosystems undergoing constant change. Every now and again, a larger disturbance will rock the reef, like a storm, an influx of coral predators, or a bleaching event. While all of these can deal a blow to the ecosystem, small nuances can drastically affect the reef’s recovery.

Historically, tropical storms and cyclones have been the biggest disruptors to Moorea’s reefs. “They tend to scrape all the coral off the reef and leave behind a flat surface,” said lead author Kai Kopecky, a former doctoral student in UCSB’s Department of Ecology, Evolution, and Marine Biology. But bleaching and predation are on the rise, and these events kill coral, but leave the reef’s structure intact.

Bleaching occurs when stress — usually heat — causes corals to expel the symbiotic algae that provide them with food. Coral can recover from this if conditions quickly return to their liking, but often the colony simply dies, especially in the presence of other stressors like pollution.

A cyclone walloped Moorea’s reefs in 2010. “It removed basically every single coral colony off the fore reef,” Kopecky said. “But within about five years, it recovered back to the amount of coral it had before the storm had hit.”

The reef experienced a big bleaching event in 2019, a year after Kopecky began working on the island. “It basically just cooked and killed about half the corals on the reef,” he recalled. But unlike the storm, this disturbance left all the dead coral structure in place.

Kopecky and his colleagues at the NSF-funded Long Term Ecological Research (LTER) site at Moorea Coral Reef noticed that the reef didn’t experience the same remarkable recovery in the following years. Instead, coral continued to die, and macroalgae, commonly known as seaweed, began to proliferate. Kopecky was curious how the differences between the two events affected reef recovery processes. In 2023, he and his coauthors published a mathematical model of the system, and this new field study focuses on describing the mechanisms at work.

“This combination of time series data on long term responses of ecosystems, mathematical modeling and field experimentation greatly enriches our scientific understanding and ability to devise practical solutions,” said co-author Professor Russ Schmitt, lead principal investigator at the Moorea Coral Reef LTER site.

“The multi-decadal, site-based research focus makes the LTER network both unique and of immense value in our rapidly changing world,” said LTER co-principal investigator Professor Sally Holbrook, who is also one of the study’s authors.

“The current project was led by Kai, a Ph.D. student at the time, and involved UCSB undergraduate researchers who made important contributions in addition to those of senior ecologists. It is a prime example of how the Moorea Coral Reef project fosters and trains the next generation of environmental scientists,” Schmitt added.

Investigating the reefscape

The team prepared small patches of the reef to create a blank slate for their experiment. They then cemented a controlled number of dead coral skeletons in each patch and plugged healthy young coral into the reef in a way that each could be periodically removed and measured as they grew. They also added trays of macroalgae to compare herbivory within the bleached skeletons to consumption out in the open.

“We found that dead coral skeletons prevent herbivores from being able to remove macroalgae, enabling growth and preventing new corals from being able to settle and survive on the reef,” Kopecky said.

Protection by dead coral skeletons could theoretically help young coral, if new recruits settle on the reef shortly after a bleaching event. Unfortunately, corals tend to spawn only once a year, while many algae reproduce continually, giving the seaweeds the advantage in colonizing the newly available substrate.

Macroalgae compete with coral for space, light and resources. Algae grow faster than coral, so without the balancing effect of herbivory they can easily overrun a reef, preventing new corals from settling and shading out those colonies that do. Young coral recruits are particularly vulnerable to this competition, and once a reef flips from being covered by coral to algae, it can be hard to reverse the change, as the team showed in previous research.

Considering long-term shifts

The authors compared the results in their small-scale experiments to the long-term data from the site, and they’ve seen dramatically different trajectories after the different kinds of disturbances. “Coral cover shot up on the reefs after the cyclone, while macroalgae cover went down,” Kopecky said. “After the bleaching event, it was just the opposite.”

The results find context in the concept of ecological memory, which considers how past events can influence the trajectory of an ecosystem. These shifts can produce misalignments between what an ecosystem is used to and what it’s currently experiencing. “As these disturbance regimes change, ecological memory is also changing,” Kopecky explained. Unfortunately, the ecosystem might not be as adapted to cope with the new regime, where vast stands of dead coral skeletons are left behind after a disturbance. This can alter long-standing relationships, such as those between herbivores, algae and coral.

Kopecky wants to know if removing dead skeletons from the reef could stimulate coral recovery, or at least mitigate the impacts of bleaching. “In coral reefs this is a novel idea and strategy,” he said. “But if you look to other ecosystems — like prescribed burns in forests to remove dead wood — people have been increasingly thinking about manipulating dead stuff in ecosystems for management purposes.”

The finding is confounding researchers searching for an explanation. “We don’t know what’s going on, but it’s just a very exciting finding,” said lead author Alec Lessing of Stanford University. “This means there’s something missing from our understanding of how black hole jets interact with their surroundings.”

A nova erupts in a double-star system where an aging, swelled-up, normal star spills hydrogen onto a burned-out white dwarf companion star. When the dwarf has tanked up a mile-deep surface layer of hydrogen that layer explodes like a giant nuclear bomb. The white dwarf isn’t destroyed by the nova eruption, which ejects its surface layer and then goes back to siphoning fuel from its companion, and the nova-outburst cycle starts over again.

Hubble found twice as many novae going off near the jet as elsewhere in the giant galaxy during the surveyed time period. The jet is launched by a 6.5-billion-solar-mass central black hole surrounded by a disk of swirling matter. The black hole, engorged with infalling matter, launches a 3,000-light-year-long jet of plasma blazing through space at nearly the speed of light. Anything caught in the energetic beam would be sizzled. But being near its blistering outflow is apparently also risky, according to the new Hubble findings.

The finding of twice as many novae near the jet implies that there are twice as many nova-forming double-star systems near the jet or that these systems erupt twice as often as similar systems elsewhere in the galaxy.

“There’s something that the jet is doing to the star systems that wander into the surrounding neighborhood. Maybe the jet somehow snowplows hydrogen fuel onto the white dwarfs, causing them to erupt more frequently,” said Lessing. “But it’s not clear that it’s a physical pushing. It could be the effect of the pressure of the light emanating from the jet. When you deliver hydrogen faster, you get eruptions faster. Something might be doubling the mass transfer rate onto the white dwarfs near the jet.” Another idea the researchers considered is that the jet is heating the dwarf’s companion star, causing it to overflow further and dump more hydrogen onto the dwarf. However, the researchers calculated that this heating is not nearly large enough to have this effect.

“We’re not the first people who’ve said that it looks like there’s more activity going on around the M87 jet,” said co-investigator Michael Shara of the American Museum of Natural History in New York City. “But Hubble has shown this enhanced activity with far more examples and statistical significance than we ever had before.”

Shortly after Hubble’s launch in 1990, astronomers used its first-generation Faint Object Camera (FOC) to peer into the center of M87 where the monster black hole lurks. They noted that unusual things were happening around the black hole. Almost every time Hubble looked, astronomers saw bluish “transient events” that could be evidence for novae popping off like camera flashes from nearby paparazzi. But the FOC’s view was so narrow that Hubble astronomers couldn’t look away from the jet to compare with the near-jet region. For over two decades, the results remained mysteriously tantalizing.

Compelling evidence for the jet’s influence on the stars of the host galaxy was collected over a nine-month interval of Hubble observing with newer, wider-view cameras to count the erupting novae. This was a challenge for the telescope’s observing schedule because it required revisiting M87 precisely every five days for another snapshot. Adding up all of the M87 images led to the deepest images of M87 that have ever been taken.

Hubble found 94 novae in the one-third of M87 that its camera can encompass. “The jet was not the only thing that we were looking at — we were looking at the entire inner galaxy. Once you plotted all known novae on top of M87 you didn’t need statistics to convince yourself that there is an excess of novae along the jet. This is not rocket science. We made the discovery simply by looking at the images. And while we were really surprised, our statistical analyses of the data confirmed what we clearly saw,” said Shara.

This accomplishment is entirely due to Hubble’s unique capabilities. Ground-based telescope images do not have the clarity to see novae deep inside M87. They cannot resolve stars or stellar eruptions close to the galaxy’s core because the black hole’s surroundings are far too bright. Only Hubble can detect novae against the bright M87 background.

Novae are remarkably common in the universe. One nova erupts somewhere in M87 every day. But since there are at least 100 billion galaxies throughout the visible universe, around 1 million novae erupt every second somewhere out there.

With MS, the body’s immune system attacks myelin, the fatty, white substance that insulates and protects the nerves. People with primary progressive MS experience a steady decline in symptoms. About 10 to 15% of people with the disease have this type of MS.

The study looked at rituximab and ocrelizumab, anti-CD20 infusion therapies that target a protein called CD20 found on some white blood cells called B-cells. Removing these cells from the bloodstream is believed to reduce inflammation and damage that can occur to the myelin. Ocrelizumab is approved by the U.S. Food and Drug Administration (FDA) for primary progressive MS and for people with relapses, but rituximab is not. Rituximab is FDA approved for other diseases like rheumatoid arthritis and prescribed off label for MS.

“MS is a disabling disease, so treatments that slow the progression to worse disability are sorely needed,” said study author Laure Michel, MD, PhD, of Rennes University in France. “Anti-CD20 therapies are widely prescribed, in part because there are few alternate treatments. However, our study suggests they may not slow disability from worsening for people with primary progressive MS.”

The study involved 1,184 people with primary progressive MS who had an average age of 56. They did not take MS medications in the two years prior to the study. For the study, 295 people were treated with rituximab, 131 were treated with ocrelizumab and 728 were untreated. They were followed for an average of four years.

Participants’ level of disability was measured on a scale with scores ranging from zero, meaning no symptoms, to 10 points, meaning death due to MS. At the start of the study, all participants had a score of 6.5 or less.

Researchers then measured how long it took for people to advance to their first confirmed disability progression. For those whose score was less than 5.5 at the start of the study, advancing one point on the scale was considered progressing in disability. If their score was 5.5 or more, advancing 0.5 points on the scale was disability progression.

After adjusting for possible differences between the treated and untreated groups, researchers found there was no difference in the time it took to progress to the next level of disability between those taking a medication and those taking no medication.

“Medications for MS can be expensive and come with risks of side effects,” said Michel. “Our results indicate that there should be a constant evaluation of MS therapies to determine if the benefits outweigh the risks for people with primary progressive MS.”

A limitation of the study is that it was a look back in time and did not follow people in real time. Also, among those taking medications, most were taking rituximab with fewer people taking ocrelizumab. More research is needed in larger groups of people to confirm the findings.

The study was supported by the France National Research Agency, the French MS registry and the Eugène Devic EDMUS Foundation.

The Rocahepevirus ratti strain is called “rat HEV” because rats are the primary reservoir of the virus. Since the first human case was reported in a person with a suppressed immune system in Hong Kong in 2018, at least 20 total human cases have been reported — including in people with normal immune function.

People infected with rat HEV did not report exposure to rats, leaving the cause of infection undefined. The suspected cause during other human HEV infections, in many cases, is consumption of raw pork — making it a potential route for rat HEV as well.

Researchers at The Ohio State University found that a strain of rat HEV isolated from humans could infect pigs and was transmitted among co-housed animals in farm-like conditions. Rats are common pests in swine barns — suggesting that the pork production industry may be a setting in which rat HEV could make its way to humans.

“We always want to know which viruses might be up and coming, so we need to know the genetics behind this virus in the unlikely event something happens in the United States that would enable rat HEV to expand,” said senior author Scott Kenney, an associate professor of veterinary preventive medicine at Ohio State based in the Center for Food Animal Health at the College of Food, Agricultural, and Environmental Sciences’ Wooster campus.

The study was published recently in PNAS Nexus.

Hepatitis E is the leading cause of the acute viral liver infection in humans worldwide, mostly in developing regions where sanitation is poor. The virus is also endemic in pigs in the United States — though it is present mostly in liver rather than muscle, and is killed when the meat is cooked.

Past studies testing the cross-species infectiousness of rat HEV showed the strain used in experiments did not infect non-human primates.

“It dropped off the radar for six or seven years because it was thought not to be a human pathogen. And now it’s infecting humans, so we need to figure out why,” Kenney said.

One strain linked to human disease is known as LCK-3110. First author Kush Yadav, who completed this work as a PhD student in the Center for Food Animal Health, used the viral genomic sequence to construct an infectious clone of LCK-3110.

The team first showed the cloned virus could replicate in multiple types of human and mammal cell cultures and in pigs. Researchers then injected pigs with an infectious solution containing the LCK-3110 strain or another HEV strain present in pigs in the U.S., as well as saline as a control condition.

Viral particles in the blood and feces were detected one week later in both groups receiving HEV strains, but levels were higher in pigs infected with rat HEV. Two weeks later, co-housed pigs that received no inoculations also began to shed rat HEV virus in their feces — an indication the virus had spread through the fecal-oral route.

Though infected pigs’ organs and bodily fluids were also positive for viral RNA, the animals did not show signs of feeling sick. Previous research suggests rats don’t have clinical symptoms, either.

Even so, the rat HEV virus was detected in cerebrospinal fluid of infected pigs — a finding that aligns with growing concern that various strains of HEV that infect humans can harm the brain. One human death linked to rat HEV was caused by meningoencephalitis.

“HEV is gaining importance for neurological disorders, and a lot of the research now points toward how neuropathology is caused by the hepatitis E virus,” Yadav said. “And even though we have a small number of known human cases, a high percentage of them are immunosuppressed. That means transplant recipients in the United States could be at risk of infection by general HEV as well as rat HEV.

“Research could now focus on whether pork liver products contain rat HEV and explore food safety procedures to block the disease.”

Yadav is now a postdoctoral researcher in the Virginia-Maryland College of Veterinary Medicine at Virginia Tech. Co-authors of the study, all from Ohio State, were Patricia Boley, Carolyn Lee, Saroj Khatiwada, Kwonil Jung, Thamonpan Laocharoensuk, Jake Hofstetter, Ronna Wood and Juliette Hanson.

Conversations encompass continuous exchanges of verbal and nonverbal information. Previous research has demonstrated that gestures and speech synchronize at the individual level. But few studies have investigated how this phenomenon may unfold between individuals.

To fill this knowledge gap, Fauviaux and colleagues used an online dataset consisting of 14 sessions of two people engaged in unstructured face-to-face conversations during which they were free to talk about specific topics. Each of these sessions contained between one and four discussions, and the conversations lasted from 7 to 15 minutes. The researchers analyzed both audio and motion data, and measured speech and gesture synchronization at different timescales. Specifically, they focused on vocal properties through the speech amplitude envelope and movement properties through head and wrist gestures.

The results supported previous research on speech and gesture coordination at the individual level, revealing synchronization at all timescales of the conversation. That is, there was higher-than-chance synchronization between a given participant’s wrist and head movements, and similar synchronization between these movements and vocal properties.

Extending the literature, the researchers also found that gestures and speech synchronize between individuals. In other words, there was coordination between the voices and the bodies of the two speakers. Taken together, the findings suggest that this type of synchronization of verbal and nonverbal information likely depends on the turn-taking dynamics of conversations.

According to the authors, the study enriches our understanding of behavioral dynamics during social interactions at both the intrapersonal and interpersonal levels, and strengthens knowledge regarding the importance of synchrony between speech and gestures. Future research building on this study could shed light on prosocial behaviors and psychiatric conditions characterized by social deficits.

The authors add: “How do my speech and behaviors influence, or respond to, the speech and behaviors of the person I’m conversing with? This study answers this question by investigating the multimodal dynamic between speech and movements, both at the individual’s level and the dyadic level. Our findings confirm intrapersonal coordination between speech and gestures across all temporal scales. It also suggests that multimodal and interpersonal synchronization may be influenced by the speech channel, particularly the dynamics of turn-taking.”

Abdominal aortic aneurysms occur when the main artery, the aorta, swells and potentially ruptures, causing life-threatening internal bleeding. Obstructive sleep apnea is typically a chronic condition where people repeatedly stop and start breathing while sleeping and can increase the risk of developing cardiovascular problems. Citing studies that indicate a higher prevalence of abdominal aortic aneurysms in patients with obstructive sleep apnea, MU researchers examined the link between the two using mouse models.

The research team found that intermittent hypoxia — when the body isn’t getting enough oxygen for a given period of time — caused by obstructive sleep apnea increased the susceptibility of mice to develop abdominal aortic aneurysms.

“Chronic intermittent hypoxia by itself is not enough to cause abdominal aortic aneurysms, but for a patient with obstructive sleep apnea who also has additional metabolic problems like obesity, our findings suggest it may help degrade aortic structures and promote aneurysm development,” said Luis Martinez-Lemus, study author and a professor of medical pharmacology and physiology.

Intermittent hypoxia happens during obstructive sleep apnea when throat muscles relax and block the flow of air into the lungs. According to the research, the loss of oxygen triggers certain enzymes called MMPs. The increased enzyme activity can degrade the extracellular matrix, which acts like a cell scaffolding network, weakening the aorta.

“Patients with abdominal aortic aneurysms usually don’t notice any symptoms, except for some back and belly pain, until the aneurysm bursts. Once that happens, it’s crucial to get the patient to surgery quickly so doctors can repair the aorta,” said Neekun Sharma, the lead author of the study. “Learning how these aneurysms develop can help us find ways to monitor or slow down their progression, especially for patients who have obstructive sleep apnea.”

Luis Martinez-Lemus is a professor of medical pharmacology and physiology, the James O. Davis Distinguished Professorship in Cardiovascular Research, and a NextGen Precision Health investigator. He earned his PhD at Texas A&M University and is a Doctor of Veterinary Medicine. Neekun Sharma is an assistant research professor in the Division of Endocrinology and Metabolism in the Department of Medicine.

“Chronic Intermittent Hypoxia Facilitates the Development of Angiotensin II-Induced Abdominal Aortic Aneurysm in Male Mice” was recently published in the Journal of Applied Physiology. In addition to Martinez-Lemus and Sharma, MU study authors include Abdelnaby Khalyfa, associate research professor in the Department of Pediatrics; Dunpeng Cai, assistant professor of surgery; Mariana Morales-Quinones, senior research specialist; Shi-You Chen, Division Chief of Surgical Research; Jaume Padilla, associate professor of Nutrition and Exercise Physiology; Camila Manrique-Acevedo, MU Health Care endocrinologist; and Bysani Chandrasekar, a professor of medicine in the Department of Cardiology. Rogerio Soares, Yusuke Higashi and David Gozal also contributed.