The findings suggest restoring the lake to a healthy water level would reduce disparities in harmful dust exposure experienced by different racial/ethnic and socioeconomic groups, along with delivering other ecological and economic benefits.

Exposure to particulate pollution arising from dry portions of the playa is highest among Pacific Islanders and Hispanics and lowest among white people compared to other racial/ethnic groups, according to the findings reported June 21 in the journal One Earth. It was also higher for individuals without a high school diploma. 

This is likely because Salt Lake City’s lower-income neighborhoods are more likely to lie in the path of windblown dust from Great Salt Lake, which has shrunk to less than half its historical size, leaving about 800 square miles of lakebed exposed.

More than two decades of drought and unrelenting upstream diversions have contributed to the decline of the saline terminal lake located immediately west and north of Utah’s main population corridor along the Wasatch Front.

“People here in Utah are concerned about the lake for a variety of reasons — the ski industry, the brine shrimp, the migratory birds, recreation — and this study adds environmental justice and the equity implications of the drying lake to the conversation,” said lead author Sara Grineski, a professor of sociology and environmental studies.

Grineski led an interdisciplinary team of U faculty, largely associated with the Wilkes Center for Climate Science and Policy, from both the College of Social and Behavioral Science (CSBS) and the College of Science. Co-authors are Timothy Collins and Malcolm Araos (geography); John Lin, Derek Mallia and Kevin Perry (atmospheric sciences); and William Anderegg (biology).

The study analyzed data from the Utah Department of Environmental Quality’s air-quality monitoring network, which screens for fine particulate matter, or PM_2.5. Comprised of ultra tiny particles that can penetrate lung tissue, this pollution is linked to myriad health problems, including cardiovascular disease and asthma.

During dust storms, current levels expose residents to 26 micrograms per cubic meter, or μg/m³, of PM_2.5 on average, according to the study, significantly higher than the World Health Organization’s threshold of 15 μg/m³. Were the lake to dry up completely, exposure could rise to 32 μg/m³, while restoring the lake could reduce exposure to 24 μg/m³ during these wind events, according to the study.

The study examined four such events in 2022 on April 19, 20 and 21 and May 7, when spikes of recorded PM_2.5 coincided with high winds.

For the study, which was funded by the National Science Foundation, researcher Derek Mallia developed a model for predicting exposure levels for the three counties abutting the lake’s east and south shores — Salt Lake, Davis and Weber, home to 1.8 million residents — under four different lake level scenarios. It uses a weather model that simulates wind direction and speed, and includes a wind-blown dust model, which measures how much dust is emitted from an erodible surface, such as the Great Salt Lake playa, and is primarily based on the wind speed and soil texture and characteristics.

“We have to use weather models, since we cannot physically go out to the lake and remove/add water to see how much more/less dust it would emit,” Mallia said. “Models like the one that I developed let us run these hypothetical scenarios.”

The study’s scenarios range from a totally dry lake, to very low lake level, to current lake, to ‘healthy’ lake level designated as 4,200 feet above sea level. The lake’s South Arm currently sits at 4,194.4 feet, almost 6 feet higher than the historic low of 4,188.7 registered at the end of 2022.

According to the model, neighborhood disparities in exposure levels would increase when the lake level drops.

“We frame it the converse. Lake levels rise, overall levels of dust go down during the dust events and the gap, especially between Hispanic and Pacific Islander people, narrows with respect to the level of dust exposure for non-Hispanic white people,” Grineski said. “So if we can take better care of the lake, the dust for everyone goes down and the gap in exposure between these groups goes down too.”

Her team’s prior research has previously documented disparities of PM_2.5 exposure generally in the Salt Lake Valley

“There is a really strong pattern of inequality with respect to race and ethnicity,” she added. “It’s sort of a hopeful finding that if we can raise the lake to a ‘healthy’ level we can at least with respect to lake dust we can reduce some of that inequality.”

Most dust from the playa is PM₁₀, pollution comprised of much larger particles that are only measured at a few of Utah’s air quality monitoring stations. Without a robust PM₁₀ monitoring network, researchers and regulators are deprived of a key data source that could give a more complete assessment of the lakebed dust threat, according to co-author Kevin Perry. He said the study points to the need for Utah to expand its network of PM₁₀ monitors since windblown lakebed dust contains about six times more PM₁₀ than PM_2.5.

“We have to use the PM_2.5 data because that’s the network that we have available. It’s not what I would design and not what I would like to do,” he said. “Because of the network being so sparse, I can’t even answer a really basic question, like how many dust events do we have a year that are impacting these communities. And that’s super frustrating.”

A professor of atmospheric science, Perry is known as “Dr. Dust” thanks to his tireless bicycle forays across the vast lakebed gathering sediment samples. These sediments were found to be contaminated with heavy metals in some places.

He noted that potentially harmful dust events typically occur in the spring and fall when cold fronts pass through the Wasatch Front.

“Before a cold front gets here, we have really strong winds from the south that will last for 12 or 18 hours,” Perry said. “And where’s it pushing that dust? It’s pushing it to Layton, Syracuse, Ogden, Brigham City where we have almost no PM₁₀ monitors at all, and then the wind reverses and we’ll get three to four or five hours of stuff coming into Salt Lake Valley where we do have monitors.”

Because of its ability to infiltrate living tissue, PM_2.5 is considered more harmful to human health than PM₁₀, which is also classified as a criteria pollutant under the federal Clean Air Act.

P. aeruginosa is responsible for over 500,000 deaths per year around the world, of which over 300,000 are associated with antimicrobial resistance (AMR). People with conditions such as COPD (smoking-related lung damage), cystic fibrosis (CF), and non-CF bronchiectasis, are particularly susceptible.

How P. aeruginosa evolved from an environmental organism into a specialised human pathogen was not previously known. To investigate this, an international team led by scientists at the University of Cambridge examined DNA data from almost 10,000 samples taken from infected individuals, animals, and environments around the world. Their results are published today in Science

By mapping the data, the team was able to create phylogenetic trees — ‘family trees’ — that show how the bacteria from the samples are related to each other. Remarkably, they found that almost seven in ten infections are caused by just 21 genetic clones, or ‘branches’ of the family tree, that have rapidly evolved (by acquiring new genes from neighbouring bacteria) and then spread globally over the last 200 years. This spread occurred most likely as a result of people beginning to live in densely-populated areas, where air pollution made our lungs more susceptible to infection and where there were more opportunities for infections to spread.

These epidemic clones have an intrinsic preference for infecting particular types of patients, with some favouring CF patients and other non-CF individuals. It turns out that the bacteria can exploit a previously unknown immune defect in people with CF, allowing them to survive within macrophages. Macrophages are cells that ‘eat’ invading organisms, breaking them down and preventing the infection from spreading. But a previously-unknown flaw in the immune systems of CF patients means that once the macrophage ‘swallows’ P. aeruginosa, it is unable to get rid of it.

Having infected the lungs, these bacteria then evolve in different ways to become even more specialised for a particular lung environment. The result is that certain clones can be transmitted within CF patients and other clones within non-CF patients, but almost never between CF and non-CF patient groups.

Professor Andres Floto, Director of the UK Cystic Fibrosis Innovation Hub at the University of Cambridge and Royal Papworth Hospital NHS Foundation Trust, and senior author of the study said: “Our research on Pseudomonas has taught us new things about the biology of cystic fibrosis and revealed important ways we might be able to improve immunity against invading bacteria in this and potentially other conditions.

“From a clinical perspective, this study has revealed important information about Pseudomonas. The focus has always been on how easily this infection can spread between CF patients, but we’ve shown that it can spread with worrying ease between other patients, too. This has very important consequences for infection control in hospitals, where it’s not uncommon for an infected individual to be on an open ward with someone potentially very vulnerable.

“We are incredibly lucky at Royal Papworth Hospital where we have single rooms and have developed and evaluated a new air-handling system to reduce the amount of airborne bacteria and protect all patients.”

Dr Aaron Weimann from the Victor Phillip Dahdaleh Heart & Lung Research Institute at the University of Cambridge, and first author on the study, said: “It’s remarkable to see the speed with which these bacteria evolve and can become epidemic and how they can specialise for a particular lung environment. We really need systematic, pro-active screening of all at risk patient groups to detect and hopefully prevent the emergence of more epidemic clones.”

The research was funded by Wellcome and the UK Cystic Fibrosis Trust.

Selective schools are government-funded schools that enrol only the highest performing students. Pupils take a standardized entrance exam, from which the best-scoring are enrolled.

Some argue that selective schools are necessary for bright pupils to reach their full academic potential. Selective schools can outperform or perform just as well as elite schools in final year exams, but without the high fees charged to parents. Hence, selective schools can offer a means for children from low socioeconomic backgrounds to receive a first-class education.

However, others argue that selective schools disproportionately benefit high socioeconomic children whose parents can afford private tutoring to prepare them for the entrance exams.

“Studies show that parents wish to enrol their children into selective schools, because they believe it will increase the chances of their children getting into a prestigious university, and securing a well-paid and high-status job,” says Melissa Tham, a research fellow at the Mitchell Institute at Victoria University, Melbourne, Australia.

To find out whether there are benefits associated with selective schools, Tham and her colleagues Shuyan Huo, and Andrew Wade tracked almost 3000 pupils from the Longitudinal Surveys of Australian Youth (LSAY), a nationally representative survey program that follows young Australians over an 11-year period. The survey started when respondents were aged 15 in 2009.

As expected, the selective schools featured in the study had a higher proportion of academically high-achieving students, as measured by mathematics and reading scores.

However, at ages 19 and 25 there was little difference between the educational and employment outcomes of children who attended selective schools versus non-selective schools. For example, the study found that while 81% of selective school students went on to secure a job or university place at 19 compared to 77.6% of pupils from non-selective schools, this difference disappeared when the students were matched on key characteristics, including socioeconomic background, gender, and geographical location.

At age 25, all outcomes between selective and non-selective school students were not significant, except general life satisfaction. Attending a selective school increased a student’s general life satisfaction score by just 0.19 points. Meanwhile, students who attended non-selective school were just as likely to go on to study at university or secure a job as their peers who attended selective schools.

“These very modest findings indicate that attending an academically selective school does not appear to pay off in large benefits for individuals,” says Andrew Wade, co-author of the study.

“We argue that academically selective schools in the government sector therefore contradicts the principles of inclusive and equitable education which underpin Australia’s school system.”

According to the authors, the findings suggest that more research is needed to determine whether selective schools offer any benefit to academically able students.

“Rather than tweak some aspects of the enrolment processes, we see greater value in conducting a thorough and critical examination of fully and partially selective schools, and scaling back selectivity if the supposed benefits are not found,” says Huo.

How RNAP accomplishes this feat is largely unknown. A snapshot of RNAP in the act of opening that bubble would provide a wealth of information, but the process happens too quickly for current technology to easily capture visualizations of these structures. Now, a new study in Nature Structural & Molecular Biology describes E. coli RNAP in the act of opening the transcription bubble.

The findings, captured within 500 milliseconds of RNAP mixing with DNA, shed light on fundamental mechanisms of transcription, and answer long-standing questions about the initiation mechanism and the importance of its various steps. “This is the first time anybody has been able to capture transient transcription complexes as they form in real time,” says first author Ruth Saecker, a research specialist in Seth Darst’s laboratory at Rockefeller. “Understanding this process is crucial, as it is a major regulatory step in gene expression.”

An unprecedented view

Darst was the first to describe the structure of bacterial RNAP, and teasing out its finer points has remained a major focus of his lab. While decades of work have established that RNAP binding to a specific sequence of DNA triggers a series of steps that open the bubble, how RNAP separates the strands and positions one strand in its active site remains hotly debated.

Early work in the field suggested that bubble opening acts as a critical slowdown in the process, dictating how quickly RNAP can move onto RNA synthesis. Later results in the field challenged that view, and multiple theories emerged about the nature of this rate-limiting step. “We knew from other biological techniques that, when RNAP first encounters DNA, it makes a bunch of intermediate complexes that are highly regulated,” says coauthor Andreas Mueller, a postdoctoral fellow in the lab. “But this part of the process can happen in less than a second, and we were unable to capture structures on such a short timescale.”

To better understand these intermediate complexes, the team collaborated with colleagues at the New York Structural Biology Center, who developed a robotic, inkjet-based system that could rapidly prepare biological samples for cryo-electron microscopy analysis. Through this partnership, the team captured complexes forming in the first 100 to 500 milliseconds of RNAP meeting DNA, yielding images of four distinct intermediate complexes in enough detail to enable analysis.

For the first time, a clear picture of the structural changes and intermediates that form during the initial stages of RNA polymerase binding to DNA snapped into focus. “The technology was extremely important to this experiment,” Saecker says. “Without the ability to mix DNA and RNAP quickly and capture an image of it in real-time, these results don’t exist.”

Getting into position

Upon examining these images, the team managed to outline a sequence of events showing how RNAP interacts with the DNA strands as they separate, at previously unseen levels of detail. As the DNA unwinds, RNAP gradually grips one of the DNA strands to prevent the double helix from coming back together. Each new interaction causes RNAP to change shape, enabling more protein-DNA connections to form. This includes pushing out one part of a protein that blocks DNA from entering RNAP’s active site. A stable transcription bubble is thus formed.

The team proposes that the rate-limiting step in transcription may be the positioning of the DNA template strand within the active site of the RNAP enzyme. This step involves overcoming significant energy barriers and rearranging several components. Future research will aim to confirm this new hypothesis and explore other steps in transcription.

“We only looked at the very earliest steps in this study,” Mueller says. “Next, we’re hoping to look at other complexes, later time points, and additional steps in the transcription cycle.”

Beyond resolving conflicting theories about how DNA strands are captured, these results highlight the value of the new method, which can capture molecular events happening within milliseconds in real-time. This technology will enable many more studies of this kind, helping scientists visualize dynamic interactions in biological systems.

“If we want to understand one of the most fundamental processes in life, something that all cells do, we need to understand how its progress and speed are regulated,” says Darst. “Once we know that, we’ll have a much clearer picture of how transcription begins.”

Young adults who have higher levels of inflammation, which is associated with obesity, physical inactivity, chronic illness, stress and smoking, may experience reduced cognitive function in midlife, a new study out of UC San Francisco has found.

Researchers previously linked higher inflammation in older adults to dementia, but this is one of the first studies to connect inflammation in early adulthood with lower cognitive abilities in midlife.

“We know from long-term studies that brain changes leading to Alzheimer’s disease and other dementias may take decades to develop,” said first author Amber Bahorik, PhD, of the UCSF Department of Psychiatry and Behavioral Sciences and the Weill Institute for Neurosciences. “We wanted to see if health and lifestyle habits in early adulthood may play a part in cognitive skills in midlife, which in turn may influence the likelihood of dementia in later life.”

In their study, publishing in Neurology on July 3, researchers found that only 10% of those with low inflammation performed poorly on testing of processing speed and memory, compared to 21% and 19%, respectively, of those with either moderate or higher levels of inflammation.

When researchers adjusted for factors like age, physical activity and total cholesterol, disparities remained in processing speed; and the researchers also found differences in executive functioning, which includes working memory, problem solving and impulse control.

The study followed 2,364 adults in the CARDIA study, which aims to identify the factors in young adulthood that lead to cardiovascular disease two-to-three decades later.

Participants were 18 to 30 years old when they entered the study and were tested four times over an 18-year period for the inflammatory marker C-reactive protein (CRP). They took the cognitive tests five years after their last CRP measurement, by which time most participants were in their forties and fifties.

About half the participants were female; a little under half were Black, and the rest were white. Some 45% had lower stable inflammation, while 16% had moderate or increasing inflammation; 39% had higher levels.

A link between inflammation and health risks

The researchers also linked higher levels of inflammation with physical inactivity, higher BMI and current smoking.

“Inflammation plays a significant role in cognitive aging and may begin in early adulthood,” said senior author Kristine Yaffe, MD, a professor of psychiatry and behavioral sciences, neurology, and epidemiology and biostatistics at UCSF. “There is likely a direct and indirect effect of inflammation on cognition.”

Yaffe is a member of the first team of experts to determine that 30% of dementia risk is preventable. Her recent research has looked at the association in midlife between fragmented sleep and lower cognition and the effects of personalized health and lifestyle changes in preventing memory loss in higher-risk older adults.

“Fortunately, there are ways to reduce inflammation — such as by increasing physical activity and quitting smoking — that might be promising paths for prevention,” Yaffe said.