The genomics community’s long wait for 10x Genomics’ highly anticipated news is finally over. On Saturday night, at the Hard Rock Café Hotel in San Diego—across the street from the American Association for Cancer Research (AACR) conference—the company hosted the “Impossible” party to announce its new spatial instrument—the Atera.
Serge Saxonov, PhD, CEO of 10x Genomics, walking onto the stage to thunderous applause, noted that there is “a gap between what we need to see and what we have been able to measure.” The Atera, which enables whole-transcriptome spatial biology at scale, “obliterates the typical trade offs” that come with existing spatial tools, he said.
“This is the biggest launch in our history. I am the most excited I’ve ever been about any product, or any product category, across the board,” Saxonov told GEN. “It has been a long time in development, and it is what we have known the world needs for a long time. I think it will fundamentally change how we measure and understand biology, and it really puts research on a new trajectory. It is really exciting to be at a place now where we can deliver it to the world.”
Nuts and bolts
Atera offers more plex, throughput, and sensitivity than 10x Genomics’ Xenium—enabling whole-transcriptome at scale. More specifically, when compared to Xenium, Atera has four times the throughput, six times higher plex capacity for targeted assays, 3.6x higher plex, and 2–3x sensitivity for whole transcriptome assays.
10x Genomics Atera
The price for Atera is $495,000, and the instrument measures roughly 53” x 36” x 64” or (4.42 ft × 3 ft × 5.33 ft). Orders are currently being taken, and the instrument will be available in the second half of this year.
The instrument can run up to 800 1 cm2 whole transcriptome samples (FFPE and fresh frozen) per year, with flexible run configurations, and a greater than 5 cm² imageable area per slide (for greater than 2,000 mm² total tissue per run when using all four slides.)
There are 18,000-genes on the Atera WTA (whole transcriptome) with stackable customization of 1,000-gene Atera Select panels available now, and optional stacking of up to three 1,000-gene panels coming in the future.
“Spatial genomics with whole-transcriptome profiling capabilities is the ultimate approach to measure single cells in their tissue context,” Holger Heyn, PhD, ICREA professor at the Centro Nacional de Análisis Genómico (CNAG) and member of the Human Cell Atlas, added. “All other lower-plexity approaches have been just a warm-up phase leading to this application.”
Jasmine Plummer, PhD, associate member of the St. Jude Faculty and director of the Center for Spatial OMICs points out that the whole transcriptome, while exciting, can bring a big “sticker shock” for many researchers because it will require a lot more probes in contrast to a sequencing-based platform, where a library accesses all of the genes.
The instrument uses standard glass microscopy slides, which is exciting to Plummer. In the past, she said, slides have posed a challenge when coordinating with other researchers, and using regular slides will be more “pathology friendly.”
An end to tradeoffs?
Existing spatial technologies, which are still relatively nascent in genomics, have been constrained by tradeoffs between plex, resolution, and throughput. Researchers have had to make choices and prioritize.
“In general, with the landscape as it is today, there is a tradeoff,” Nick Banovich, PhD, VP of scientific development at TGen, and professor of bioinnovation and genome sciences division and director of the Center for Spatial Multi-Omics (COSMO), told GEN. “The closer you walk toward whole transcriptome, the lower the per gene sensitivity.”
“The most exciting thing [about Atara],” he continued, “is that there is still quite good sensitivity with whole transcriptome breadth. That’s the huge advantage of this system; there is no tradeoff anymore.”
However, this launch comes just over three years after Xenium’s launch. Purchasing a new instrument so soon may pose a challenge. Plummer notes: “In this economy, with the uncertainty of scientific funding, it is concerning to ask customers—many of whom just landed a machine—to spend another several hundred thousand dollars.”
Why AACR?
Oncology is one of the most exciting, most promising applications of spatial, especially in the near term, noted Saxonov. This is, in large part, because the work exists across the spectrum—from basic discovery to translation to clinical applications. Spatial is unambiguously important, he asserted.
Unveiling at AACR “just made a lot of sense.”
In addition to the party, the company will host a digital launch event on Tuesday, April 21. Within the AACR program, a presentation from the German Cancer Research Center (DKFZ) will include data generated on the platform, highlighting Atera’s ability to uncover cancer biology not accessible with legacy approaches. Researchers distinguished multiple malignant and stem cell states across disease stages, within a single colorectal tumor sample, and mapped how these populations interact with the surrounding immune microenvironment. The data reveal a more complex immune landscape that could inform future therapeutic strategies and drug development. In addition, two posters (#7116, #6216) will include data from Atera.
The future
10x Genomics said that Atera will play a role in advancing large data studies. For example, the company noted that Atera will enable the goal of the Human Cell Atlas (HCA) as it continues its mission to map every cell type in the human body.
“With the Human Cell Atlas entering its next phase of generating spatially resolved atlases, whole-transcriptome approaches will be the workhorse for data generation,” Heyn told GEN.
“I am excited to see the Atara platform being launched now,” he added. “It is very timely as we ramp up production for the Human Cell Atlas 2.0 phase.”
Atera’s future
The company presented a roadmap with future plans at the AACR event, highlighting spatial proteomics, automation, base by base sequencing (a de novo sequencing assay) and software improvements.
Atera, Saxonov told GEN, is a fundamental platform that the company will continue enabling. It lays the groundwork for the next decade of research and work. This point in time, he said, feels similar to the early days of next generation sequencing (NGS). And although the company will continue to develop its other platforms and product lines, Atera has “massive amounts of headroom to keep building on top of it. It is the convergence of all these different technology stacks and different fields onto one.”
“What the platform can do right out of the gate is exciting. And all the things that it can do in the future will be really, really exciting,” he asserted.
Background: Wearable devices enabling remote monitoring by surgeons of their patients have gained prominence around total joint arthroplasty (TJA), offering continuous patient data to identify those not meeting postoperative goals, thereby facilitating timely interventions. While multiple studies highlight the utility of these devices in tracking postoperative progress, a standardized approach to their application is lacking. This review aims to synthesize existing literature on the use of wearable device-tracked activity for monitoring TJA outcomes. Objective: We examined the current literature to evaluate how wearable devices are used in monitoring and improving patient rehabilitation and outcomes following TJA. Methods: A systematic review was conducted following Cochrane methodology. A literature search of all available literature was performed in April 2024 and identified 102 studies to undergo full-text review. Systematic reviews, duplicate papers, and theoretical papers were excluded. Ultimately, 35 studies met the selection criteria. Results: The review revealed that 32 of 35 (91.4%) studies used wearable devices to monitor step counts. A total of 21 (60%) studies incorporated joint-specific patient-reported outcome measures, though the specific measures varied. Further, 9 studies used standardized performance-based outcome measures, which also differed across studies. Finally, 7 (20%) studies collected sleep data; however, the methods and outcomes for sleep measurement were inconsistent among these studies. Conclusions: Remote monitoring via wearable devices offers a novel approach to tracking outcomes in TJA patients. Although the use of these devices in perioperative care is expanding, significant variability exists in the data reported across studies. Wearable monitoring is often integrated with patient-reported outcome measures and standardized functional assessments, yet the optimal data parameters that best correlate with established outcome metrics remain undefined. Additionally, data collected by wearables has not yet been shown to predict patient recovery or satisfaction. Further research is essential to refine these data parameters and the development of postoperative protocols that leverage wearable devices to enhance patient compliance and improve clinical outcomes. Trial Registration: PROSPERO CRD420261346230; https://www.crd.york.ac.uk/PROSPERO/view/CRD420261346230
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<strong>Background:</strong> Stress, sleep deprivation, and burnout are significant safety risks for acute care surgeons, negatively impacting performance, well-being, and clinical outcomes. <strong>Objective:</strong> This pilot randomized controlled trial aimed to measure neurophysiological effects of prescribed music (PM) and self-selected music (SSM) on surgeon stress, burnout, and neurophysiological responses using a multimodal protocol that integrated functional magnetic resonance imaging (fMRI), wearable biosensor monitoring, and psychological self-assessments. <strong>Methods:</strong> Full-time attending surgeons at a quaternary care hospital were invited to participate in a 3-armed trial (1:1:1 block allocation). Intervention groups were instructed to listen to 30 minutes (minimum 15 minutes) of either PM or SSM daily at bedtime for 6 weeks, reflecting real-world conditions. PM comprised original compositions based on elements promoting perceived relaxation from a prior study. The control arm avoided music in the 30 minutes before bed. Allocation was concealed from the recruiting investigator; the fMRI technicians, the statistician, and lead investigators were blinded until analyses were completed. Functional connectivity patterns were measured using fMRI at baseline and 6 weeks while participants listened to simulated intensive care unit noise, PM, and SSM. Secondary outcomes included continuous actigraphy for sleep quality and self-reported anxiety, sleep quality, and burnout using validated scales (State-Trait Anxiety Inventory, Pittsburgh Sleep Quality Index, and Maslach Burnout Inventory). <strong>Results:</strong> A total of 22 surgeons were assessed; demands of fMRI and data collection schedule led 3 to decline and 2 (allocated to PM) not to finish baseline measures; 6 PM, 5 SSM, and 6 controls received allocated intervention; 2 PM participants were withdrawn for nonadherence and missing follow-up data and 1 control missed follow-up collection due to scheduling (final analysis set after missing data: PM: n=4, SSM: n=5, control: n=5). One control participant experienced transient vertigo in fMRI. Trends in fMRI data indicated that both intervention groups experienced less negative emotional arousal and anxiety, with physical tension reduced in the PM group. The PM group exhibited reduced stress response in the frontal lobes when exposed to intensive care unit alarms, suggesting diminished attentional response to the high-stress auditory environment, compared to control. However, lack of statistical significance and baseline variability entail cautious interpretation. Observations of sleep quality were mixed, and no statistically significant differences in stress surveys were observed. <strong>Conclusions:</strong> Both music interventions trended toward positive changes in neurophysiological responses, suggesting potential benefits in reducing surgeon stress. However, due to the small sample, mixed or nonsignificant results, and the exploratory nature of this study, findings should be considered preliminary. Further research with larger, diverse cohorts is required to confirm trends, refine both the intervention approach and recruitment strategies, and determine whether objective compositional elements or personally selected music drive the mechanisms of potential positive effects. <strong>Trial Registration:</strong> ClinicalTrials.gov NCT05980429; https://clinicaltrials.gov/study/NCT05980429
ObjectiveTo refine the Chinese version of the Dimensional Anhedonia Rating Scale (DARS) and evaluate the psychometric properties of the Revised Chinese DARS (RC-DARS) in a large sample of first-visit psychiatric outpatients.MethodsThe study was conducted in two sequential phases at a specialized psychiatric hospital. In Phase I (n = 277), the existing Chinese DARS underwent semantic and cultural refinement in accordance with ISPOR and TRAPD guidelines, incorporating cognitive interviews and back-translation procedures. In Phase II (n = 788), the RC-DARS was administered alongside the Self-Rating Depression Scale (SDS), Self-Rating Anxiety Scale (SAS), Pittsburgh Sleep Quality Index (PSQI), and the MMPI Suicide Ideation Subscale (MMPI-SI). Exploratory and confirmatory factor analyses were conducted using common-factor extraction and the WLSMV estimator for ordinal indicators. Internal consistency, gender-based measurement invariance, and convergent validity were evaluated.ResultsExploratory analyses supported a four-factor domain structure. Confirmatory factor analysis demonstrated good model fit for the domain-based model (χ²/df = 3.81, CFI = 0.98, TLI = 0.97, RMSEA = 0.08, SRMR = 0.05), with substantially superior fit relative to an alternative reward-processing model. Internal consistency was excellent (Cronbach’s α = 0.95; McDonald’s ω = 0.96). Multi-group analyses supported configural, metric, and scalar invariance across gender (ΔCFI < 0.01). RC-DARS total scores were significantly negatively correlated with depressive symptoms (r = −0.443), anxiety (r = −0.317), sleep disturbance (r = −0.494), and suicide risk (r = −0.312) (all p <.001). Individuals with severe depressive symptoms exhibited significantly lower RC-DARS scores than those below the clinical threshold.ConclusionsThe RC-DARS demonstrates robust psychometric properties in a first-visit outpatient sample. The revision primarily enhances semantic precision and structural differentiation without materially altering score distributions. The scale may serve as a refined instrument for dimensional assessment of anhedonia in similar clinical contexts, pending longitudinal and multi-site validation.
When the covid-19 pandemic started, Jennifer Phillips thought about the songs of the sparrows.
They were easier to hear, because the world had suddenly become quieter. Car traffic plummeted as people sheltered at home and shifted to remote work. Air travel collapsed. Cities—normally filled with the honking, screeching, engine-gunning riot of transportation—became as silent as tombs.
For years, Phillips has studied how animals react to “anthropogenic noise,” or the racket created by human activity. Most animals really don’t like it, she and her colleagues have learned. Animals constantly listen to the world around them: They’re on the alert for the rustle of approaching predators, or a mating call from a member of their species. As human society has expanded—with sprawling cities, industrial mines, and roads crisscrossing the world—it has gotten noisier too, and animals have trouble hearing one another.
Noise is invisible; there’s no billowing smokestack, no soiled waterway. We just got used to it as it vibrated in the background.
Phillips and her colleagues had spent time in the 2010s in San Francisco recording the sound of white-crowned sparrows in the Presidio. It’s a park that is half peaceful nature and half automobile noise, since it’s filled with thick clumps of trees and grassy fields but also has two highways that slice through it, feeding onto the Golden Gate Bridge. In past recordings, starting in the 1950s, sparrows had sung with complex and lower-pitched melodies and three major “dialects.” But by the 2010s, traffic in the Presidio had exploded, and the hubbub was so loud that the birds began to sing with faster trills—and at a higher pitch—so their fellows could hear them. The two quietest dialects were either dead or on their way to extinction.
They’re “screaming at the top of their lungs,” says Phillips. “They really can’t hear the lower frequencies when the traffic noise is present.” Urban noise can even change birds’ bodies; they get thinner and more stressed out. Their mating calls aren’t as effective, because female birds, as researchers have found, generally don’t enjoy high-pitched, high-volume shouting. (It makes them wonder if the males are unhealthy.) The noise can increase bird-on-bird conflict, because when birds can’t hear warning cries they accidentally stumble into enemy territory. Perhaps worst of all, in situations like these biodiversity takes a hit: Entire species that can’t handle urban clamor simply head out of town and never come back.
But as the sudden, eerie silence of the pandemic descended, Phillips sat at home thinking, It’s really quiet. And then she wondered: Would the Presidio birds now be able to hear each other better?
She raced over to the park and started recording. Sure enough, the park was seven decibels quieter—a huge drop. (That’s like the difference between the noise of the average home and whispering.)
And remarkably, the researchers found that the songs of the white-crowned sparrows had transformed. They were singing more quietly, with a richer range of frequencies. A bird could be heard twice as far as before. And the mating calls had gotten more sultry.
“They could sing a higher performance, basically a sexier song, but not have to scream it so loud,” Phillips says.
It was as if time had been reversed and all the damage abruptly repaired. And it proved what Phillips and her peers have been increasingly documenting: that anthropogenic noise is the newest form of pollution we need to tackle. The noise of our relentlessly on-the-move industrial society affects all life on Earth, wildlife and humans, in ways we’re just beginning to grasp. Yet strategies such as electrification and clever urban design could help. As the Presidio showed, noise can vanish overnight—once we figure out how to shut up.
Hidden impacts
Many forms of pollution are obvious to us humans. Dumping toxic goo into lakes? Sure, that’s bad. Coal smokestacks pumping soot and carbon dioxide, plastic bags and sea nets choking whales—we now understand that these, too, are problems. Even an idea as gauzy as light pollution has penetrated the public consciousness to some extent, since it’s why city dwellers can’t see many stars, and we’ve heard it confuses migratory birds.
But noise, mostly from transportation, took longer to hit our radar. This is partly because it’s invisible; there’s no billowing smokestack, no soiled waterway. We just got used to it as it vibrated in the background.
Sparrows in San Francisco’s Presidio began to sing with faster trills—and at a higher pitch—so their fellows could hear them over the noise of nearby traffic.
GETTY IMAGES
The black-chinned hummingbird seems to prefer noisy areas, fledging more chicks than the same species does in quieter areas.
MDF/WIKIMEDIA COMMONS
There were a few studies in the ’70s and ’80s showing that animals were upset by our noise. But the field really began to take off in the ’00s, in part because digital technology made it easier to record long swathes of sound out in nature and analyze them. One early salvo came from the biologist Hans Slabbekoorn, who was studying doves in the city of Leiden and irritatedly noticed that he could rarely get a clean recording because of the background noise. Sometimes he’d see the doves’ throats moving as they cooed but couldn’t hear them. “If I’m having difficulty hearing them,” he thought, “what about them?”
So he and a colleague started recording ambient sound levels in different parts of Leiden. Some were quiet residential areas, which registered a soothing 42 decibels, and others were noisy intersections or areas near highways, which reached 63 decibels, about as loud as background music. Sure enough, he found that birds in the noisy areas were singing at a higher pitch.
Over the next two decades, research in the field bloomed. Noise, the scientists found, has a few common ill effects on animals. It disrupts communication, certainly. But it also generally stresses them, reducing everything from their body weight to their receptivity to mating calls. If an animal nests closer to a road, its reproduction rates can go down; eastern bluebirds, for example, produce fewer fledglings. Truly cacophonous noise—like planes taking off at a nearby airport—can cause hearing loss in birds. And animals can wind up becoming less aware of threats from predators. They’ll wander closer to danger, because they can’t hear it coming. (And sometimes they’ll do the opposite: They’ll develop a rageaholic hair-trigger temper, because they’re constantly on high alert and regard everything as a threat.)
Even in deep rural areas, where things are normally pretty quiet, highways can disrupt wildlife—the noise carries far into the fields nearby. Fraser Shilling, a biologist at the University of California, Davis, has stood up to half a mile from rural highways and recorded sound as loud as 60 decibels, which is at least 20 decibels higher than you’d typically find in the wilderness. “The motorcycles and the 18-wheelers are really the ones that project a lot of noise,” he told me.
Above 55 decibels, many skittish animals get into a fight-or-flight panic. The prevalence of bobcats—an endangered species famously rattled by noise—“starts dropping off the cliff,” says Shilling. Above 65, “you’re really starting to exclude almost all wildlife.”
And that’s not even the upper limit of what wildlife is exposed to. There are roughly a half-million natural-gas wells around the US, and piercingly loud compressors are used to shoot water down into most of them. Up close, the compressors can kick out 95 decibels, a sound as loud as a subway train; at one Wyoming gas well the sound still registered around 48 decibels nearly a quarter-mile away.
Historically, it wasn’t always easy to prove that noise was causing whatever problems the animals were experiencing. Maybe it was other factors; maybe animal populations reduce near a road because some are hit by vehicles?
But several clever experiments have proved that noise—and noise alone—can disrupt wildlife. One was the “phantom road” experiment by the conservation scientist Jesse Barber and his team, then at Boise State University. They went out to a quiet, uninhabited area of the Boise foothills in Idaho, far away from any roads. In this valley in the mountains, thousands of migratory birds stop on their way south each year; they’ll gorge themselves on cherry bushes, gaining weight for the next days of flying. The researchers strapped 15 pairs of speakers to Douglas fir trees, in a half-kilometer line. Then they blasted recordings of highway noise. They played the noise for four days and then turned it off for four days. Then they observed thousands of birds, capturing many to measure their body mass.
The noise truly rattled the birds. When the sound was turned on, nearly a third left the area. Those that stuck around ate less: While birds should be heavier after a day of foraging, these ones didn’t gain much. The noise seemed to have so interrupted their feeding that they weren’t packing on the weight needed for their migratory trip.
Other, similarly nifty A/B tests followed. One was led by David Luther, a biologist at George Mason University (who also worked with Phillips on the covid-19 study in San Francisco). In 2015, these researchers took 17 white-crowned sparrows at birth and raised them in a lab. To teach them their species’ songs, they played the nestlings recordings of adult sparrows singing, at low and high pitches. Six of the nestlings heard the songs without any interference; with the other half, the researchers played the sounds of city noise at the same time.
The results were stark. The lucky birds that were spared the traffic noise learned to perform the quieter, sweeter, more complex songs. But the birds that had traffic noise blasted learned only the higher, faster, more stressed-out songs. From the cradle, noise changed the way they communicated.
Humans hate noise too
You can’t pull the same experiment with humans, raising them in a lab to see how noise affects them. (Not ethically, anyway.) But if we could, we’d likely find the same thing. We, too, are animals—and it appears that we suffer in similar ways from anthropogenic noise, even though we’re the ones creating it.
The sound of traffic is correlated with lousy sleep, higher blood pressure, more heart disease, and higher stress.
Stacks of research in the last few decades have found that noise—most often, as with wildlife, the sound of traffic—is correlated with lousy sleep, higher blood pressure, more heart disease, and higher stress. A Danish study followed almost 25,000 nurses for years and found that an additional 10 decibels hit them hard; over a 23-year period they had an 8% higher rate of death, plus higher rates of nearly every bad thing that could happen to you: cancers, psychiatric problems, strokes. (They controlled for other malign health influences.) As you’d probably predict by now, children fare badly too. When Barcelona researchers followed almost 3,000 elementary school kids for a year, they found that those in noisier schools performed worse on assessments of working memory and ability to pay attention.
“We think of ourselves as being ‘used to it,’” says Gail Patricelli, a professor of evolution and ecology at the University of California, Davis. “We’re not as used to it as we think we are.”
It’s also true that there’s a trade-off. Many people understand that noise from cities and highways is aggravating, but we tolerate it because we get benefits along with the hassles. Cities are crammed with jobs and connections and dating opportunities; cars and trucks bring us the things we need and increase our personal mobility.
It turns out that animals make a similar calculus. Some species appear to benefit in certain ways from proximity to noise, so they move toward it.
Clinton Francis, a biologist at California Polytechnic State University, and a team studied bird populations near noisy gas wells in rural New Mexico. Most species avoided the riot of the well pumps. But Francis was surprised to find that some hummingbirds and finches preferred it, and by one important measure they thrived: They were nesting more in the noisy areas than in the quieter areas. Additionally, several species had more success at fledging chicks in noisier locations.
What was going on? It’s likely that the noise makes it harder for predators to hear the birds and hunt down their nests. “It’s essentially a predator shield,” Francis says. Since his research found that predators can cause as much as 76% of failures of eggs to produce healthy offspring, that’s a significant survival advantage.
Cities can offer the same protections to certain species. Consider the case of Flaco, a Eurasian eagle-owl that escaped from the Central Park Zoo in February of 2023 and found he was in a terrific place to hunt. The incessant traffic ought to have caused him trouble. “An owl like this is among the most vulnerable species to intrusions from noise pollution. They’re listening for extremely faint signals or cues that their prey provide,” Francis notes. But New York has its compensations, because prey animals abound. They’re also naïve and unguarded, never expecting an owl with a six-foot wingspan to swoop down and devour them.
EDDIE GUY
Granted, these upsides don’t cancel out the negatives. Human noise may shield some birds from predators, but in other ways it leaves them faintly miserable, with high levels of stress hormones and lower weight.
Worse, the species that manage to thrive in cities or near highways are often the same ones all over the country. And they represent only a minority of species; most are driven further away, with less and less land to live on as civilization spreads ever outward.
“Overall, it’s kind of a nightmare for diversity,” says Luther.
How to silence the world
In the early ’00s, the village of Alverna in the Netherlands began to get louder. A major intercity road cut straight through the town, and traffic had gone up by two-thirds in the previous decade. Facing complaints about the din, the town offered to put up some 13-foot walls on either side of the route. Residents hated the idea. Who wants to look out the window at massive walls?
So instead town planners redesigned the road in subtle ways. They lowered it by half a meter, slightly blocking the tire sounds. They built wedges that rise up three feet on either side, and surfaced them with attractive antique stone; that blocked even more sound. They planted sound-absorbing trees. And as a final coup de grâce, they reduced the speed limit from about 50 to 30 miles per hour. When a car is moving slowly, the engine is producing most of the roar—but once it’s going 45 mph or faster, the rumble of tires on the pavement takes over and is much louder. Each intervention had only a small effect, but cumulatively they made the road a blessed 10 decibels quieter.
This tale illustrates one curious upside of noise. Compared with other forms of pollution, it can be ended quickly. Toxic pollutants or CO2 can hang around for tens of thousands of years; the microplastics in your pancreas are probably never coming out. But with noise, the instant you reduce the source, the benefits are immediate.
Plus, most of what works is “not rocket science,” Shilling says. A tall wall at the side of a highway will cut noise by 10 decibels; fill a double-sided wall with rubble and it’s even better. That could cut the traffic noise to below 55 decibels, he notes, which would help particularly skittish forms of wildlife. Walls can block animal movement, though, so in animal-heavy areas it’s better to build berms—small hills on either side of a highway. Areas of high ecological importance could be prioritized to keep costs down.
“If there’s a great chunk of wetland habitat and it’s the only one around for 50 miles in any direction? Well, then we should build noise walls around it,” he says. We should also build overpasses and underpasses to help animals get around. And to quiet the din of gas wells out in the countryside, states could require companies to build walls around them. (They’ll likely only do that, though, when human neighbors complain or launch lawsuits; animals don’t have lawyers.)
Cities, too, can learn to shut up, as Alverna proved. At the most ambitious, some have buried noisy highways that once cut through the downtown core. Boston put a massive elevated highway underground in its “Big Dig”; in Slabbekoorn’s hometown of Amstelveen—a suburb of Amsterdam—they’re currently enclosing the A9 highway in a tunnel and turning the surface into a verdant park with new buildings. “That’s amazing, getting back a lot of the space as well,” he says.
Granted, this sort of reengineering can be brutally expensive, which is why politicians blanch when they’re asked to reduce road noise. The Big Dig cost $15 billion, and with interest up to $24 billion. When I mentioned cost to Shilling, he sighed. “It’s not as expensive as a B-1 bomber or tax cuts for rich people,” he says. “Environmental stuff is considered expensive just because our expectations are low, not because we can’t afford to do it.”
There are cheaper and more politically palatable fixes, though. Reducing urban speed limits is one; Paris recently cut the top speed on its ring roads from 70 to 50 kilometers per hour (43 to 31 mph), and noise at night went down by an average 2.7 decibels—a noticeable drop. Planting more trees and vegetation all around roads and cities can cut a few decibels more, and residents love it.
Growing adoption of electricity would also bring down the volume. “Electric vehicles of all kinds have the potential to make a big difference,” Patricelli says; when the light turns green and an EV next to you accelerates away, it’s up to 13 decibels quieter than a comparable gas-powered vehicle. These benefits won’t be felt as much on highways, because EVs still make tire noise at high speeds. But in the slower stop-and-go traffic of urban life, they are far more pleasant to the ears, both animal and human. Indeed, the electrification of everything that currently uses a gas-powered motor will make urban life quieter. Cities like Alameda, California, and Alexandria, Virginia, are increasingly banning gas-powered leaf blowers and lawn mowers, which operate at hair-raising volume while electric ones whisper along.
We’ve engineered a civilization that roars, but the next phase is making it purr. The animals will thank us.
Clive Thompson is a science and technology journalist based in New York City.
Timing exercise according to a person’s natural propensity towards being a “morning lark” or an “night owl” could maximize its cardiovascular benefits, a randomized trial suggests.
Matching exercise according to individual body clocks maximized the sleep quality and several parameters of cardiovascular health of middle-aged adults with preclinical risk factors.
The findings highlight the added value of incorporating circadian biology into exercise plans to optimize health outcomes.
Reporting their findings in Open Heart, the researchers suggest that assessing for chronotype—the predisposition towards morningness or eveningness—should be considered when prescribing exercise for those at risk of cardiometabolic disease.
“Our study shows that when you exercise may be just as important as how you exercise,” researcher Arsalan Tariq, PhD, from the University of Lahore, explained to Inside Precision Medicine.
“Aligning workouts with an individual’s biological clock significantly amplifies cardiovascular and metabolic benefits, offering a simple way to personalize prevention and improve adherence.”
A person’s chronotype affects their sleeping patterns, hormonal secretion, and energy levels during the day through an internal timing mechanism.
This is regulated by the circadian clock in a system that influences various physiological processes including blood pressure, heart rate, glucose metabolism, and vascular function.
Tariq and team examined how timing exercise affected key indicators of cardiovascular health among at-risk middle-aged adults.
Participants were aged 40 to 60 years and had at least one cardiovascular risk factor, such as high blood pressure, overweight, or obesity. The group also included those with a family history of premature cardiovascular disease.
Participants were randomly assigned to exercise at a time that either matched or did not match their chronotype, between 8am and 11am or between 6pm and 9pm.
This consisted of five, 40-minute sessions per week of supervised moderate intensity aerobic exercise such as brisk or treadmill walking for 12 weeks.
Of the 134 participants who completed the 60 sessions, 70 were larks—34 of whom had exercise matched with chronotype—and 64 were owls, with 30 matched to chronotype.
Measurements taken at the start of the trial and three days after it finished showed particular improvements in sleep and systolic blood pressure among those matched with chronotype.
Sleep quality improved by 3.4 points in matched participants versus 1.2 in the unmatched on the Pittsburgh Sleep quality Index. Systolic blood pressure dropped by 10.8 mmHg compared with 5.5mmHg in matched versus unmatched groups, respectively.
Chronotype-aligned exercise also led to significantly greater improvements in diastolic blood pressure, heart rate variability, peak oxygen consumption, low-density lipoprotein, and fasting glucose compared with misaligned exercise.
“Personalized, time-matched exercise interventions may become a practical strategy in clinical and public health settings, potentially leading to better outcomes and improved engagement,” the researchers reported.
“Future research and guidelines may consider circadian factors as a core component of lifestyle-based disease prevention.”
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Studying mice, researchers at Toronto’s Sinai Health have found that semaglutide—the active ingredient in popular weight loss drugs that mimic the gut hormone GLP-1—acts directly on a subset of liver cells to improve organ function, and does so independently of weight loss. The finding challenges long-held assumptions about how GLP-1 medicines work in the liver and could reshape how physicians treat metabolic liver disease.
For years, the liver benefits of semaglutide have puzzled scientists. “Glucagon-like peptide-1 (GLP-1) medicines improve metabolic liver disease through weight-loss-dependent and -independent actions,” the authors wrote. The drug was known to lower blood sugar and promote weight loss, but patients’ livers were improving in ways that those effects alone could not explain. And as the authors further noted, “The therapeutic scope of GLP-1 medicines extends beyond glycemic control and weight loss, with benefits evident in people with atherosclerotic heart disease, heart failure with preserved ejection fraction (HFpEF), peripheral artery disease, diabetic kidney disease, knee osteoarthritis, and obstructive sleep apnea (OSA).” However, as the team further pointed out, “… the mechanisms by which GLP-1 medicines improve organ dysfunction remain incompletely understood.”
Drucker has been at the forefront of GLP-1 research since the 1980s when his pioneering discoveries helped lay the groundwork for the development of GLP-1 medicines. After transforming treatment of type 2 diabetes and obesity, semaglutide and other GLP-1 medicines have been approved for other conditions including MASH (metabolic dysfunction-associated steatohepatitis). MASH is a severe form of fatty liver disease in which fat build-up, inflammation, and tissue scarring can lead to cirrhosis and liver failure. It affects about 25% Canadian adults and because it is closely linked with obesity and type 2 diabetes, treatment typically includes lifestyle interventions to reduce weight. “The approval of semaglutide for MASH highlights the importance of understanding the hepatoprotective mechanisms of GLP-1 action,” the investigators stated.
Drucker and colleagues have now found that semaglutide acts directly on the liver to reduce inflammation and scarring and improve organ function in a way that is independent of weight loss. Their finding overturns a prevailing assumption in the field that liver cells do not carry the receptor that semaglutide binds to, meaning the drug had no direct route to the organ.
Postdoctoral researcher Maria Gonzalez-Rellan, PhD, spearheaded the work that combined sophisticated mouse models of MASH with deep molecular analyses of liver cells. Her work identified two cell types carrying semaglutide receptors: liver sinusoidal endothelial cells (LSECs) and immune T cells. Although LSECs account for only about 3% of liver cell volume, they proved to be the key driver of semaglutide’s liver benefits.
A pioneer in GLP-1 biology, Daniel Drucker, MD, has dedicated his career to understanding how the GLP-1 hormone, and the therapies derived from it, function in the body. His early discovery that GLP-1 stimulates insulin secretion in a glucose-dependent manner paved the way for today’s widely popular medications for type 2 diabetes and obesity. Drucker’s ongoing research continues to shine light on the less understood aspects of GLP-1 biology including its effects on the liver and in regulating inflammation. [Colin Dewar, Sinai Health]
LSECs line the tiniest blood vessels in the liver and are studded with pores that allow them to act as a molecular sieve, filtering substances passing between the liver and the bloodstream. Gonzalez-Rellan showed that semaglutide reversed MASH in mice that lacked the brain receptors controlling appetite, demonstrating that weight loss is not required for liver benefits. “Unexpectedly. semaglutide improves hepatic inflammation, fibrosis, and immune remodeling through actions on Glp1r+ pericentral liver sinusoidal ECs (LSECs) independent of changes in body weight (BW),” the team reported. “… we leveraged a unique model of GLP-1R deficiency, Glp1rWnt1-/- mice, which are resistant to GLP-1RA-induced weight loss. Remarkably, semaglutide markedly improved hepatic steatosis, fibrosis, and immune remodeling in the absence of weight reduction.”
In a further test, mice lacking LSEC receptors showed no liver improvement on semaglutide even after losing 20% of their body weight. Detailed molecular analyses of liver cell types showed that semaglutide shifts gene activity in LSCEs, prompting them to release anti-inflammatory molecules that act on the broader liver environment, pushing it toward a state more closely resembling a healthy, disease-free liver. “Together, the data using mouse models of MASH reveal an EC-specific, weight-loss-independent, semaglutide-regulated, GLP-1R-dependent intrahepatic network for improving liver health,” the scientists said.
“It turns out that the receptor responsible for these benefits is in a very specialized population of liver cells,” commented Drucker, who is also a professor of medicine at the University of Toronto. “And this receptor orchestrates the production of molecules that talk to many different types of liver cells to calm down the inflammatory environment that is the problem in metabolic disease.”
The findings carry practical implications. GLP-1 medicines have become widely prescribed, yet their mechanism of action in the body, beyond appetite suppression and blood sugar control, have remained incompletely understood. Knowing that semaglutide improves liver health independently of weight loss could influence prescribing decisions. “We’ve seen in clinical trials that patients who lose very little weight see the same reductions in liver inflammation, scarring and enzyme levels as those who lose a great deal of weight. Now we know why,” Drucker pointed out. In their paper the team concluded “Hence, semaglutide produces a broad proteomic remodeling of the liver, enabling restoration of metabolic homeostasis and suppression of fibrogenic and inflammatory programs. The strong concordance between single-cell transcriptional changes, bulk tissue proteomics, and biomarker signatures underscores the breadth of GLP-1R-mediated hepatic reprogramming.”
Physicians may choose lower doses that avoid the side effects associated with the higher doses needed for significant weight loss, potentially also lowering costs for patients, Drucker suggested adding “We’re not saying weight loss isn’t important because many things improve when patients lose weight. But we now know that weight shouldn’t be the only measure of success, because GLP-1 medicines will improve liver health whether or not the patient loses weight.”
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Listed below are links to the GEN stories referenced in this episode of Touching Base:
![A pioneer in GLP-1 biology Dr. Daniel Drucker has dedicated his career to understanding how the GLP-1 hormone, and the therapies derived from it, function in the body. His early discovery that GLP-1 stimulates insulin secretion in a glucose-dependent manner paved the way for today's widely popular medications for type 2 diabetes and obesity. Dr. Drucker's ongoing research continues to shine light on the less understood aspects of GLP-1 biology including its effects on the liver and in regulating inflammation. [Colin Dewar, Sinai Health]](https://www.genengnews.com/wp-content/uploads/2026/04/Low-Res_Drucker_LTRI_Colin_Dewar-225x300.jpeg)