Researchers may be underestimating the intensity of Utah's future big earthquakes, study finds
As Utah prepares for an overdue, big earthquake, University of Utah seismologists found that current seismic hazard models may be underestimating the intensity of shaking the Salt Lake Valley could experience in future earthquakes.
That's because sediments in some areas under the valley are thicker than expected, researchers said in a news release — and thicker sediments can lead to stronger shaking during an earthquake.
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'In a basin, seismic shaking is amplified. It's very important to understand the thickness and rigidity of sediment to better assess potential shaking. The sediment is thicker than previously thought — especially in the heavily populated area south of Salt Lake City,' study leader Fan-Chi Lin, an associate professor of geology and geophysics at the U. said in the release.
The state is still rebuilding infrastructure shaken up by the 5.7 magnitude Magna earthquake that happened in 2020. However, often referred to as 'the big one,' a future earthquake of 6.75 or greater magnitude is highly probable at the Wasatch Front in the next 50 years, according to Envision Utah.
With about 80% of the state's population living in the area, experts estimate that could be an exceptionally devastating event.
'Our findings reinforce the idea that a hazard exists in the valley and that shaking could be stronger than expected. Many houses in Salt Lake are unreinforced masonry and could be vulnerable in a big quake,' Lin said. 'Buildings should be reinforced, and people should be prepared.'
After installing an extensive network of seismic data sensors along the valley after the spring of 2020 and analyzing seismic waves from distant earthquakes, Lin's team created a revised and refined three-dimensional seismic velocity model to map the Wasatch Front's geologic structure and identify earthquake hazard sites.
That model allowed the researchers to find thicker sediment deposits than previously estimated, and can provide answers when preparing for 'the big one.'
'If we know the subsurface structure very well, then we can predict how strong the ground motion will be when the big earthquake happens,' Lin said. 'And that will allow us to collaborate with the engineers to determine which buildings are potentially hazardous when the big earthquake hits.'
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Associated Press
7 hours ago
- Associated Press
Belite Bio Reports Second Quarter 2025 Financial Results and Provides a Corporate Update
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With the DRAGON trial on track to complete by the end of this year, we remain focused on advancing Tinlarebant toward key clinical and regulatory milestones.' Second Quarter 2025 Business Highlights and Upcoming Milestones: Clinical Highlights Tinlarebant (LBS-008) is an oral, potent, once-daily, retinol binding protein 4 (RBP4) antagonist that decreases RBP4 levels in the blood and reduces vitamin A (retinol) delivery to the eye without disrupting systemic retinol delivery to other tissues. Vitamin A is critical for normal vision but can accumulate as toxic byproducts in individuals affected with STGD1 and GA, the advanced form of dry age-related macular degeneration (AMD), leading to retinal cell death and loss of vision. Corporate Highlights Second Quarter 2025 Financial Results: Current Assets: As of June 30, 2025, the Company had $149.2 million in cash, liquidity funds, time deposits, and U.S treasury bills. 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Yahoo
6 days ago
- Yahoo
Humans may have untapped 'superpowers' from genes related to hibernation, scientists claim
When you buy through links on our articles, Future and its syndication partners may earn a commission. Hibernating mammals rely on particular genes to adjust their metabolisms as they enter that unique, low-energy state — and humans actually carry that same hibernation-related DNA. Now, early research hints that leveraging this particular DNA could help treat medical conditions in people, scientists say. Hibernation offers "a whole bunch of different biometrically important superpowers," senior study author Christopher Gregg, a human genetics professor at the University of Utah, told Live Science. For example, ground squirrels can develop reversible insulin resistance that helps them rapidly gain weight before they hibernate but starts fading as hibernation gets underway. A better understanding of how hibernators flip this switch could be useful for tackling the insulin resistance that characterizes type 2 diabetes, Gregg suggested. Hibernating animals also protect their nervous systems from damage that could be caused by sudden changes in blood flow. "When they come out of hibernation, their brain is reperfused with blood," Gregg said. "Often that would cause a lot of damage, like a stroke, but they've developed ways to prevent that damage from happening." Gregg and his colleagues think tapping into hibernation-related genes in people could unlock similar benefits. Related: Best-ever map of the human genome sheds light on 'jumping genes,' 'junk DNA' and more A 'hub' of hibernation genes In a pair of studies published Thursday (July 31) in the journal Science, Gregg and his team pinpointed key levers that control genes related to hibernation, showing how they differ between animals that hibernate and those that don't. Then, in the lab experiments, they delved into the effects of deleting these levers in lab mice. Although mice don't hibernate, they can enter torpor — a lethargic state of decreased metabolism, movement and body temperature that typically lasts for less than a day — after fasting for at least six hours. This made mice a suitable genetic model for studying these effects. Using the gene-editing technique CRISPR, the scientists engineered mice with one of five conserved noncoding cis elements (CREs) deactivated, or "knocked out." These CREs act as levers to control genes that, in turn, code for proteins that carry out biological functions. The CREs targeted in the study lie near a gene cluster called the "fat mass and obesity-related locus," or the FTO locus, which is also found in humans. Gene variants found within the cluster have been tied to an elevated risk of obesity and related conditions. Broadly speaking, the FTO locus is known to be important for controlling metabolism, energy expenditure and body mass. By knocking out the CREs, the researchers were able to change the mice's weights, metabolic rates and foraging behaviors. Some deletions sped up or slowed down weight gain, others turned metabolic rate up or down, and some affected how quickly the mice's body temperatures recovered after torpor, the researchers said in a statement. This finding is "highly promising," particularly given the FTO locus plays a well-known role in human obesity, Kelly Drew, a specialist on hibernation biology at the University of Alaska Fairbanks, told Live Science in an email. Knocking out one CRE — called E1 — in female mice caused them to gain more weight on a high-fat diet than did a comparison group with all of their DNA intact. Deleting a different CRE, called E3, changed the foraging behavior of both male and female mice, specifically changing how they searched for food hidden in an arena. "This suggests that important differences in foraging and decision processes may exist between hibernators and non-hibernators and the elements we uncovered might be involved," Gregg said. Unknowns to address The study authors said their results could be relevant to humans, since the underlying genes don't differ much between mammals. "It's how [the mammals] turn those genes on and off at different times and then for different durations and in different combinations that shape different species," Gregg said. However, "it's definitely not as simple as introducing the same changes in human DNA," Joanna Kelley, a professor who specialises in functional genomics at the University of California, Santa Cruz, told Live Science in an email. "Humans are not capable of fasting-induced torpor, which is the reason why mice are used in these studies," said Kelley, who was not involved in the work. She suggested that future work include animals incapable of torpor, and focus on unpacking all the downstream effects of the deleted CREs. As is, the current study "definitely points the field in a new direction" in terms of how scientists understand the genetic controls driving changes in hibernators throughout the year, she added. Drew also highlighted that torpor in mice is triggered by fasting, while true hibernation is triggered by hormonal and seasonal changes and internal clocks. So while the CREs and genes the study identified are likely critical parts of a metabolic "toolkit" that responds to fasting, they may not be a "master switch" that turns hibernation on or off. RELATED STORIES —Scientists may be able to put Mars-bound astronauts into 'suspended animation' using sound waves, mouse study suggests —'Let's just study males and keep it simple': How excluding female animals from research held neuroscience back, and could do so again —Weight loss may 'rejuvenate' fat tissue in the body "Nevertheless, uncovering these fundamental mechanisms in a tractable model like the mouse is an invaluable stepping stone for future research," Drew said. Gregg emphasized that much remains unknown, including why the effects of some deletions differed in female mice versus male mice or how the changes in foraging behavior seen in mice might manifest in humans. The team also plans to research what would happen if they deleted more than one hibernation-linked CRE at a time in mice. Down the line, Gregg thinks it could be possible to tweak the activity of humans' "hibernation hub genes" with drugs. The idea would be that this approach could yield the benefits of that gene activity — like neuroprotection — without patients having to actually hibernate, he said. Solve the daily Crossword
Yahoo
7 days ago
- Yahoo
Humans may have hibernation ‘superpowers' in untapped genes, scientists say
The 'superpowers' of hibernating animals are also present in human DNA, according to a pair of recent studies that provide clues to unlocking this potential and opening the door for new diabetes and Alzheimer's treatments. Hibernating animals such as squirrels and bears exhibit incredible resilience, going long periods without food and water and withstanding near-freezing temperatures by slowing down metabolism. They avoid muscle and nerve decay and stay healthy despite massive weight fluctuations. When these animals emerge from hibernation, they appear to recover from dangerous symptoms similar to those seen in people suffering from diabetes, Alzheimer's and stroke. 'If we could regulate our genes a bit more like hibernators, maybe we could overcome type 2 diabetes the same way a hibernator returns from hibernation back to a normal metabolic state,' Elliott Ferris, an author of one of the studies, says. The research focuses on a gene cluster called the 'fat mass and obesity locus', which plays an important role in hibernators. DNA regions near the FTO locus regulate the activities of neighbouring genes, tuning them up or down. They enable hibernators to put on weight before cosying up for winter and allow them to slowly use their fat reserves throughout hibernation, researchers say. 'What's striking about this region is that it is the strongest genetic risk factor for human obesity,' says Chris Gregg, a senior author of one of the studies from the University of Utah Health. When researchers mutated the hibernator-specific gene regions in mice, they noticed changes in their metabolism and weight. Some mutations sped up weight gain while others slowed it down under specific dietary conditions. The mutations also affected the ability of mice to recover body temperature after a hibernation-like state. 'When you knock out one of these elements – this one tiny, seemingly insignificant DNA region – the activity of hundreds of genes changes,' Susan Steinwand, another author of the studies, says. Previous studies show that hibernating animals can reverse neurodegeneration, avoid muscle decay, remain healthy despite massive weight fluctuations, and show improved ageing and longevity. The latest studies suggest we possess the necessary genetic code for hibernator-like superpowers, if we can bypass some of our metabolic switches. 'This work provides a genetic framework for harnessing hibernator adaptations to understand human metabolic control,' researchers say. 'Humans already have the genetic framework,' Dr Steinwand says. 'We just need to identify the control switches for these hibernator traits.' Further studies on these genes and their surrounding DNA regions can help confer similar resilience to humans, scientists say. 'There's potentially an opportunity – by understanding these hibernation-linked mechanisms in the genome – to find strategies to intervene and help with age-related diseases,' Dr Gregg says. 'If that's hidden in the genome that we've already got, we could learn from hibernators to improve our own health.'
