Culture

To investigate humans' impact on freshwater resources, scientists have now conducted the first global accounting of fluctuating water levels in Earth's lakes and reservoirs - including ones previously too small to measure from space.

The research, published March 3 in the journal Nature, relied on NASA's Ice, Cloud and land Elevation Satellite 2 (ICESat-2), launched in September 2018.

ICESat-2 sends 10,000 laser light pulses every second down to Earth. When reflected back to the satellite, those pulses deliver high-precision surface height measurements every 28 inches (70 centimeters) along the satellite's orbit. With these trillions of data points, scientists can distinguish more features of Earth's surface, like small lakes and ponds, and track them over time.

Scientists used these height measurements to study 227,386 water bodies over 22 months and discovered that, from season to season, the water level in Earth's lakes and ponds fluctuates on average by about 8.6 inches (0.22 m). At the same time, the water level of human-managed reservoirs fluctuate on average by nearly quadruple that amount - about 34 inches (0.86 m).

While natural lakes and ponds outnumber human-managed reservoirs by more than 24 to 1 in their study, scientists calculated that reservoirs made up 57% of the total global variability of water storage.

"Understanding that variability and finding patterns in water management really shows how much we are altering the global hydrological cycle," said Sarah Cooley, a remote sensing hydrologist at Stanford University in California, who led the research. "The impact of humans on water storage is much higher than we were anticipating."

In natural lakes and ponds, water levels typically vary with the seasons, filling up during rainy periods and draining when it's hot and dry. In reservoirs, however, managers influence that variation - often storing more water during rainy seasons and diverting it when it's dry, which can exaggerate the natural seasonal variation, Cooley said.

Cooley and her colleagues found regional patterns as well - reservoirs vary the most in the Middle East, southern Africa, and the western United States, while the natural variation in lakes and ponds is more pronounced in tropical areas.

The results set the stage for future investigations into how the relationship between human activity and climate alters the availability of freshwater. As growing populations place more demands on freshwater, and climate change alters the way water moves through the hydrological cycle, studies like this can illuminate how water is being managed, Cooley said.

"This kind of dataset will be so valuable for seeing how human management of water is changing in the future, and what areas are experiencing the greatest change, or experiencing threats to their water storage," Cooley said. "This study provides us with a really valuable baseline of how humans are modulating the water cycle at the global scale."

The researchers' methods relied on a second satellite mission, as well - Landsat, the decades-long mission jointly overseen by NASA and the U.S. Geological Survey. The team used Landsat-derived, two-dimensional maps of bodies of water and their sizes, providing them with a comprehensive database of the world's lakes, ponds, and reservoirs. Then, ICESat-2 added the third dimension - height of the water level, with an uncertainty of roughly 4 inches (10 cm). When those measurements are averaged over thousands of lakes and reservoirs, the uncertainty drops even more.

Although ICESat-2's mission focuses on the frozen water of Earth's cryosphere, creating data products of non-frozen water heights was also part of the original plan, according to Tom Neumann, ICESat-2 project scientist at NASA's Goddard Space Flight Center in Greenbelt, Maryland. Now, with the satellite in orbit, scientists are detecting more smaller lakes and reservoirs than previously anticipated - in this study they detected ponds half the size of the Lincoln Memorial Reflecting Pool.

"We're now able to measure all of these lakes and reservoirs with the same 'ruler,' over and over again," Neumann said. "It's a great example of another science application that these height measurements enable. It's incredibly exciting to see what questions people are able to investigate with these datasets."

Climate change is generally portrayed as an environmental and societal threat with entirely negative consequences. However, some sectors of the global economy may actually end up benefiting.

New economic and philosophical research argues that policymakers must consider both the beneficial effects of climate change to "climate winners" as well as its costs in order to appropriately incentivize actions that are best for society and for the environment.

The study by researchers from Princeton University, University College Cork, and HEC Montréal appears to be the first to develop a systematic, ethical framework for addressing climate winners -- as well as those harmed -- using financial transfers.

Their approach, called "Polluter Pays, Then Receives," requires polluters to first compensate those most harmed by climate change. Subsequently, polluters would be eligible to receive compensation from those who are passively benefiting from climate change.

Published in Economics & Philosophy, the article emphasizes that, through climate change, greenhouse gas emitters affect a variety of individuals and groups both positively and negatively at different regional or sectoral scales, sometimes at the expense of other groups -- what economists call "externalities."

"With a global issue like climate change, it's difficult for people to make decisions that account for the harm or benefit their actions cause, because those effects aren't directly or proportionally felt by that actor," said study co-author Kian Mintz-Woo, a former postdoctoral research associate at the Princeton University Center for Human Values and the Princeton School of Public and International Affairs. "Our research argues that payments are one way to help correct incentives: Harms should be redressed, and then beneficial actions should be rewarded."

Mintz-Woo recently joined the department of Philosophy and the Environmental Research Institute at University College Cork.

While globally the negative consequences of climate change are expected to far outweigh the benefits, some groups or places may experience net benefits. For example, countries at far northern latitudes or specific industries may see improved agricultural conditions, additional tourism, or lower energy costs.

"Not systematically considering or accounting for beneficial climate effects makes it easier for climate impact skeptics to think that climate change discussions are oversimplified or alarmist," said study co-author Justin Leroux, professor of applied economics at HEC Montréal and CIRANO research fellow. "Another motivation of our study was to address the unfairness that arises when some benefit from climate change while others are suffering harm. It's a question of solidarity -- both sharing benefits that weren't truly earned and compensating losses that weren't the fault of those harmed."

The authors say this compensation approach could be experimented with at a regional or national level before being introduced globally. They explore how it might be implemented in a federal nation using the example of Canada. A national carbon tax could be used to collect funds from greenhouse gas emitters. Those revenues would first and foremost be used to compensate victims. In addition, a corporate tax would be levied on the sectors of the economy that gain passively from climate change, like tourism, which could benefit from more tourists taking advantage of longer summers in Arctic regions. Revenue from the additional corporate tax would be shared with the greenhouse gas emitters. Introducing a policy to reward emitters may sound surprising, but the authors emphasize that those emitters would first need to pay for their harms before receiving any benefit payments.

"Payments from passive winners to polluters could either help the polluters more fully compensate the groups that have been harmed by their actions or help fund the polluters' own climate adaptation responses," Mintz-Woo said.

A recent survey of the approximately 274,000 City University of New York (CUNY) students published in the Journal of Urban Health found that the Covid-19 pandemic has taken a toll on their mental health and financial security.

The population-representative survey, conducted by a team of CUNY SPH faculty in collaboration with researchers at Healthy CUNY, found that more than half of CUNY students (54%) reported experiencing depression and/or anxiety in April 2020, at the height of the first wave of the Covid-19 pandemic. Further, they found disturbingly high levels of financial instability and noted that food insecurity and housing worries were strong predictors of anxiety/depression in multivariable models.

"We found concerning levels of financial instability in our student body, with clear effects on CUNY students' mental health and well-being," says Associate Professor Heidi Jones. "Further, over a quarter of CUNY students reported anticipating graduating later than originally planned as a result of the pandemic. CUNY is known to be an important 'equalizer' in terms of the upward social mobility of many of its graduates, and increased time to graduation or drop-out could exacerbate existing inequities."

Fifty percent of CUNY students reported often or sometimes worrying about running out of food before being able to afford more, and 27% reported often or sometimes skipping a meal because they could not afford food. These estimates are considerably higher than reported in an earlier Healthy CUNY survey in 2018.

"Food insecurity continues to burden the lives of too many CUNY students and disrupt their academic and life success," said CUNY SPH Distinguished Professor Nicholas Freudenberg, Executive Director of Healthy CUNY. In response to this problem, Healthy CUNY recently received a $500,000 grant from the Andrew Mellon Foundation to implement a two-year campaign to enroll eligible CUNY students in SNAP, add new services to campus food pantries, and promote student use of community and campus-based food assistance programs.

Parents who reported more hassles using a child car seat or booster seat - such as the child is uncomfortable or having to make multiple trips in a day - were less likely to follow recommendations from the American Academy of Pediatrics (AAP) on child passenger safety, according to a study published in the journal Academic Pediatrics.

Researchers obtained information about transportation safety behaviors and 20 hassles when using child car seats among 238 socioeconomically and racially diverse parents of children 1 to 10 years of age. Eighty percent of parents reported at least a little bit of a problem with one or more of the hassles. On average, parents had a problem with five of the hassles. Parents who were not following the AAP recommendations indicated the hassles were bigger problems.

Half of parents reported at least one behavior that went against the AAP recommendations, such as not always using a child car seat or allowing their child to travel without buckling up. For each additional hassle a parent identified, there was a 14 percent increase in the odds that their child was not consistently using a car seat and an 11 percent increase in the odds of their child traveling unrestrained.

"Our study shows that hassles with car seats are common and associated with unsafe practices," says senior author Michelle Macy, MD, a pediatric emergency medicine specialist at Ann & Robert H. Lurie Children's Hospital of Chicago and Associate Professor of Pediatrics at Northwestern University Feinberg School of Medicine. "Parents need to make car safety a consistent priority. Planning for extra time to be sure everyone is buckled up and not bending the rules helps children know safety isn't negotiable. When kids know that riding in a car seat is a strict rule, they better accept the situation and don't fuss as much."

Injuries sustained in motor vehicle collisions are a leading cause of death for children 1 to 10 years old. There is extensive evidence that young children are best protected against severe injury and death in crashes when they use the recommended child safety seat for their age and size. This evidence serves as the foundation for guidelines published by the AAP.

To optimize safety in passenger vehicles for children, the AAP recommends rear-facing car safety seats as long as possible, forward-facing car safety seats from the time they outgrow rear-facing seats through at least 4 years of age for most children, belt-positioning booster seats from the time they outgrow forward-facing seats until they are tall enough to fit in an adult seat belt, around 4 feet 9 inches and between 8 and 12 years of age for most children, and then lap and shoulder seat belts after booster seats.

The study findings and the child car seat hassles list could serve as basis for developing a risk assessment tool that clinicians could use to identify problems parents face and help them strategize on how to overcome the obstacles to keep their children safe when traveling in a car.

"Meanwhile, clinicians can ask parents about specific hassles with child car seats and offer tips on managing these problems," says Dr. Macy. "It is critically important to reinforce with parents child passenger recommendations and help them achieve consistent safety practices."

UPTON, NY--Physically confined spaces can make for more efficient chemical reactions, according to recent studies led by scientists from the U.S. Department of Energy's (DOE) Brookhaven National Laboratory. They found that partially covering metal surfaces acting as catalysts, or materials that speed up reactions, with thin films of silica can impact the energies and rates of these reactions. The thin silica forms a two-dimensional (2-D) array of hexagonal-prism-shaped "cages" containing silicon and oxygen atoms.

"These porous silica frameworks are the thickness of only three atoms," explained Samuel Tenney, a chemist in the Interface Science and Catalysis Group of Brookhaven Lab's Center for Functional Nanomaterials (CFN). "If the pores were too tall, certain branches of molecules wouldn't be able to reach the interface. There's a particular geometry in which molecules can come in and bind, sort of like the way an enzyme and a substrate lock together. Molecules with the appropriate size can slip through the pores and interact with the catalytically active metal surface."

"The bilayer silica is not actually anchored to the metal surface," added Calley Eads, a research associate in the same group. "There are weak forces in between. This weak interaction allows molecules not only to penetrate the pores but also to explore the catalytic surface and find the most reactive sites and optimized reaction geometry by moving horizontally in the confined space in between the bilayer and metal. If it was anchored, the bilayer would only have one pore site for each molecule to interact with the metal."

The scientists are discovering that the confined spaces modify different types of reactions, and they are working to understand why.

Tenney and Eads are co-corresponding authors on recently published research in Angewandte Chemie demonstrating this confinement effect for an industrially important reaction: carbon monoxide oxidation. Carbon monoxide is a toxic component of engine exhaust from vehicles and thus must be removed. With the help of an appropriate precious metal catalyst such as palladium, platinum, or rhodium, catalytic converters in vehicles combine carbon monoxide with oxygen to form carbon dioxide.

Tenney, Eads, and colleagues at the CFN and Brookhaven's National Synchrotron Light Source II (NSLS-II) showed that covering palladium with silica boosts the amount of carbon dioxide produced by 20 percent, as compared to the reaction on bare palladium.

To achieve this performance enhancement, the scientists first had to get a full bilayer structure across the palladium surface. To do so, they heated a calibrated amount of silicon to sublimation temperatures in a high-pressure oxygen environment. In sublimation, a solid directly transforms into a gas. As the thin film of silica was being created, they probed its structure with low-energy electron diffraction. In this technique, electrons striking a material diffract in a pattern characteristic of the material's crystalline structure.

"We continue heating until we get highly crystalline structures with well-defined pore sizes that we can use to explore the chemistry we're interested in," said Eads.

Here, the team tracked reactants and products and the chemical bonding environment in the 2-D confined space during oxidation of carbon monoxide, incrementally increasing the temperature. To track this information, they simultaneously conducted ambient-pressure x-ray photoelectron spectroscopy (AP-XPS) and mass spectrometry (MS) at the NSLS-II and infrared reflection-absorption spectroscopy (IRAAS) at the CFN.

"AP-XPS tells us what elements are present, whether they're on the surface or in the gas phase," said Tenney. "It can also give us information about the chemical oxidation state or binding geometry of the atoms--whether a carbon is bound to one or two oxygen atoms, for example. MS helps us identify the gas-phase molecules we're seeing evolve in our system on the basis of their weight and charge. IRRAS is a fingerprint of the type of chemical bonds present between atoms and shows the conformation and orientation of carbon monoxide molecules adsorbed on the surface."

According to co-author Dario Stacchiola, leader of the CFN Interface Science and Catalysis Group, one of the team's unique capabilities is the ability to use complementary surface characterization tools to analyze the same sample without exposing it to air, which could cause contamination.

"Reproducibility is often a problem in catalysis," said Stacchiola. "But we have a setup that allows us to prepare a sample in very pristine ultrahigh-vacuum conditions and expose the same sample to industrially relevant pressures of gases."

The experimental results showed a sharp rise in the amount of carbon dioxide above a critical temperature. Below this temperature, carbon monoxide "poisons" the surface, preventing the reaction from proceeding. However, once the temperature threshold is met, molecular oxygen begins to split into two individual oxygen atoms on the palladium surface and form a surface oxide. These oxygen atoms combine with carbon monoxide to form carbon dioxide, thereby preventing poisoning.

"The confined space is changing the energetics and kinetics of the reaction to produce more carbon dioxide," said Eads, who led the recent implementation of this new multimodal surface analysis approach for studying nanoporous films under operational conditions.

"By applying thin films on top of a traditional catalyst that has been studied for decades, we've introduced a "knob" to tailor the chemistry for certain reactions," said Tenney. "Even a one-percent improvement in catalyst efficiency can translate into economic savings in large-scale production."

"We found that a very thin layer of an inexpensive oxide can significantly boost catalytic activity without increasing the amount of the expensive precious metal used as the catalyst," added Stacchiola.

Previously, the team studied the dynamics of the furfuryl alcohol reaction on a palladium surface covered by bilayer silica. Furfuryl alcohol is a biomass-derived molecule that can be converted into biofuel. Compared to carbon monoxide oxidation, which only makes a single product, reactions with larger and more complex biomolecules such as furfuryl alcohol can generate many undesired byproducts. Their preliminary data showed the potential for tuning the selectivity of the furfuryl alcohol reaction with the bilayer silica cover.

"Changing catalytic activity is great--that's what we see in the carbon monoxide oxidation study," said Stacchiola. "The next step is to prove that we can use the oxide covers to tune the selectivity for particular reactions. We think our approach can be applied broadly in catalysis."

Last year, other members of Stacchiola's group--along with colleagues from the CFN Theory and Computation Group, Stony Brook University (SBU), and University of Wisconsin-Milwaukee--published a related study in ACS Catalysis, a journal of the American Chemical Society (ACS). Combining experiment and theory, they discovered why the water formation reaction catalyzed by ruthenium metal is accelerated under confinement with bilayer silica.

"Chemistry in confined spaces is quite a new area of research," said co-corresponding author Deyu Lu, a physicist in the CFN Theory and Computation Group. "In the last decade, there have been many reports that confinement impacts the chemistry, but a mechanistic understanding on the atomic scale has been largely lacking."

In the ACS Catalysis study, the CFN team demonstrated that confinement can change the pathway by which the reaction occurs. Water formation can proceed by two possible reaction pathways: direct hydrogenation and disproportionation. The main difference is how the first hydroxyl group--oxygen bonded to hydrogen--is made. According to calculations by Lu and first author and SBU student Mengen Wang--this reaction step costs the most energy.

In the direct pathway, hydrogen molecules dissociate on the surface into two hydrogen atoms, which combine with a chemically absorbed oxygen on the surface. These hydroxyl groups combine with another hydrogen atom to make water. For the disproportionation pathway, water--which may still initially come from the direct pathway--first needs to be stabilized on the surface. Then, water can combine with a surface oxygen to make two hydroxyl groups on the surface. These hydroxyl groups can join with two hydrogen atoms to form two water molecules. These water molecules can then make more hydroxyl groups, forming a loop in the disproportionation pathway.

In lab-based AP-XPS experiments at the CFN, the team found that the temperature needed to activate the water formation reaction was much lower when silica was covering ruthenium, as compared to the metal by itself.

"The fact that the reaction takes place at lower temperatures in confinement is partially related to its lower activation energy," explained co-corresponding author Anibal Boscoboinik, a chemist in the CFN Interface Science and Catalysis Group. "From the AP-XPS data on surface oxygen, we can indirectly derive the energy required to activate the reaction. We see that this activation energy is much lower when silica is on top of ruthenium."

Applying a popular computational method called density functional theory, the team used supercomputers to study the energetics of the reaction. Initially, the experimentalists hypothesized that the lowered activation energy for the rate-limiting step of the reaction (making the first hydroxyl group) was due to silica pressing down on the reaction complex. However, the calculations showed that the presence of silica didn't change this energy significantly. Rather, it changed the reaction pathway. On the bare ruthenium surface, the direct pathway was favored; in the presence of silica, water molecules stabilized on the surface, activating the disproportionation pathway.

"Without the silica cover, the water molecules desorb, and the reaction follows the direct pathway," said Lu. "Under the silica cover, water needs to cross several kinetic energy barriers in order to leave the surface. These kinetic barriers trap water molecules on the metal surface and activate the disproportionation pathway, enabling the hydroxyl groups to be made at a much lower energy barrier, as compared to the case without the confinement effects."

Though water formation isn't industrially relevant, the scientists say studying this model reaction can help them understand how to leverage the confinement effects to favor certain reaction pathways for more relevant reactions. In other words, the same fundamental principle can be applied to other systems. For example, silica could be coated onto electrodes to evoke particular pathways at liquid-solid interfaces in electrochemical cells. In that case, the reaction would be the opposite--water would be dissociated into oxygen and hydrogen, a clean fuel.

"Understanding this reaction helps us to understand the reverse reaction," said Boscoboinik, who recently published a summary of initial studies on confinement effects with 2-D porous thin films. "If we were guided by experiment alone, we would have attributed the wrong explanation. Theory proved that our initial hypothesis was incorrect and played a key role in revealing the correct reaction mechanism at the microscopic level."

Yet, the scientists have seen other examples where silica has a pressure-related effect. In 2019, they found that bilayer silica presses down on the noble gas xenon at the interface between bilayer silica and ruthenium, inducing stronger bonding between xenon and ruthenium.

"Different effects arise from confinement," said Stacchiola. "It's a very interesting, rich, and mostly unexplored area. We're excited to keep investigating chemistry in confined spaces in the coming years."

For nearly a century, improvement in human healthcare has depended heavily on the efficiency with which we can treat bacterial diseases. But today, antibiotic resistance--the ability of certain mutant super-bacteria to block out antibiotics--poses a major threat to healthcare, food security, and overall social development worldwide, threatening to upend much of the progress our civilization has achieved.

Scientists are now urgently attempting to tackle this problem from various angles. Professor Yunho Lee at Gwangju Institute of Science and Technology (GIST), Korea, whose contribution is published in the American Chemical Society's Environmental Science and Technology, is looking at it from the point of view of his field of research--wastewater treatment. "Bacteria, including antibiotic-resistant bacteria and their resistance genes, abound in various aquatic environments. These are therefore dangerous breeding grounds for antibiotic resistance, where through a process called horizontal gene transfer, resistant bacteria could transfer the resistance gene to other bacteria, which could then increase the antibiotic resistance levels among the members of the bacterial community, including pathogens. We could reduce this occurrence, however, if we determined which disinfectants and how much of them could safely and efficiently kill the resistant bacteria and gene in our drinking water and wastewater effluents."

As an initial step towards achieving this, Prof. Lee and his team studied the effects of various amounts of chlorine, ozone, and ultraviolet radiation on the degradation of both extracellular and intracellular (contained within bacteria) methicillin (a type of penicillin) resistance gene, mecA, of the bacteria Staphylococcus aureus in water. Based on high resolution observations using scanning electron microscopy and an analysis of the effect of the disinfectants on the reaction dynamics and cell structure, the scientists developed a reaction kinetics model for each disinfectant versus mecA in addition to a method for measuring the degradation rates. Their experiments verified the effectiveness of their models and method.

"Our findings are a key step in determining the optimal conditions for wastewater disinfection process operations for eliminating mecA and mitigating the spread of antibiotic resistance through our municipal wastewater systems," says Prof. Lee. "In this way, our research significantly contributes to public health protection against infection by antibiotic-resistant bacteria."

Moreover, Prof. Lee is hopeful that their models can be applied to other segments of double stranded DNA as well, such as those of certain viruses. Thus, newer approaches like these could hopefully lead to sustainable solutions to the looming antibiotic resistance problem and more in the near future.

Pesticides used in forestry may threaten species in downstream rivers and estuaries, but little is known about the extent to which this occurs. A new study by researchers at Portland State University found mussels, clams and oysters in watersheds along the Oregon Coast are exposed to pesticides used in managing forests. The results of this study, published in the journal Toxics, have implications for developing better forest management practices that are less likely to negatively affect aquatic life.

The study was led by Kaegan Scully-Engelmeyer, PhD student in the Earth, Environment and Society program at Portland State University, and Elise Granek, professor of Environmental Science and Management at Portland State University. Max Nielsen-Pincus, also faculty in Environmental Science and Management at Portland State University, and researchers at the Oregon Department of Land Conservation and Development, the Oregon Department of Fish and Wildlife, the U.S. Geological Survey and the Oregon Department of Environmental Quality also contributed to the study.

To explore how forest management practices affect downstream coastal ecosystems, Scully-Engelmeyer and Granek collected samples of three species of aquatic bivalves--the Western pearlshell mussel, softshell clam and Pacific oyster--at eight watersheds along the Oregon Coast. These organisms are good indicators of environmental contamination because they are sedentary filter feeders.

The researchers also used special membranes to passively collect pesticides in the water at 15 watershed sites over a span of 45 days.

"During a rainfall event, you have pulses of pesticides washed from the land that move through the water," Scully-Engelmeyer said. "Passive water samplers are a way to monitor for these types of exposure."

The researchers tested both the bivalve tissue samples and the filtered water samples for the presence of dozens of different pesticides, including herbicides, fungicides and insecticides. They detected 16 different compounds in bivalve and passive water samples, five of which are currently used in forestland management. They also collected data from the state's public notification system, which reports pesticides used in state-regulated forestlands, to see if there were relationships between these notifications and the presence of different pesticides.

"The system provides notified activities so you don't know with 100% accuracy which chemicals were used and at what date," Scully-Engelmeyer said. "We can't say it's directly related to these specific activities, but we did find that it's related to notified activity upstream."

The team found pesticides in 38% of the bivalve samples, showing that compounds used on land were present at sufficient enough levels to accumulate in the tissues of mussels, clams and oysters. Indaziflam, an herbicide currently used in Oregon forestry, was found in 7% of the bivalve samples. Contaminants also included pesticides used in orchards, Christmas tree farms, and homes as well as previously used -- and now banned -- pesticides, including DDT byproducts.

The types and amounts of pesticides varied by site, but all watersheds had at least one of the 12 chemicals detected in sampled bivalves. The most contaminated organisms were collected along the Central Oregon Coast, in the Siuslaw and Smith watersheds.

"The levels of the particular compounds we detected are not something that federal guidelines consider harmful to human health, however, they may be harmful to animals in aquatic and marine environments," Granek said. "Additionally, we were just looking at a handful of compounds, yet aquatic organisms and their consumers are likely exposed to many more contaminants including microplastics and heavy metals, among others. How the exposure we detected -- paired with other contaminants they may encounter in their waters -- affect the animals sampled or their predators is a really interesting question and unfortunately we don't have regulatory guidelines that consider exposure to multiple stressors."

The results of this study -- and subsequent studies -- may help guide evidence-based forest management practices to reduce the amounts of forestry chemicals entering aquatic ecosystems.

Forestry management has long been a contentious issue in Oregon with the timber industry and environmental groups frequently struggling to find common ground, however there are signs this is changing:

-In June, Senate Bill 1602, which changes some of Oregon's non-federal forestland protections, including the size of helicopter pesticide spray buffers along streams, passed almost unanimously.
-And last February, Governor Kate Brown announced the Private Forest Accord, an agreement that 13 timber and forest products entities and 13 environmental organizations will work together to determine recommendations for changing how forests are managed.

Granek has been contacted by this working group about the study. "This work is really timely," she said. "I hope it will inform some of their process."

Granek and others in her lab are currently studying how individual pesticide compounds -- and combinations of these compounds -- affect the health, growth and survival of softshell clams. She hopes results of this work will also be shared with the Private Forest Accord working group.

Healthcare sex discrimination protections for the LGBTQ community may be expanded under the Biden Administration, including safeguards against verbal abuse, physical abuse and the denial of bedside care, according to West Virginia University College of Law experts.

In a report published in California Law Review, Professor Valarie Blake and students Ashley Stephens and Amy Post examined whether gender identity and sexual orientation should be included in healthcare sex discrimination laws, on the heels of the historic 2020 Supreme Court case Bostock v. Clayton County.

In that case, the Court ruled that sex discrimination includes gender identity and sexual orientation when it comes to employment standards. Yet the interpretation of whether it extends into healthcare access is vague.

Bostock's reach will be litigated frequently in the coming months, Blake said, and the Biden administration will likely introduce a new rule broadening LGBTQ rights that will inevitably lead to further legal challenges.

Ultimately, the Supreme Court may need to decide the matter, Blake and her co-authors wrote. Bostock necessitates the view that health care entities receiving federal funds cannot discriminate against individuals on the basis of LGBTQ identity, they said.

The Bostock decision had prompted Stephens and Post to discuss those implications in the West Virginia Medical Journal. Blake then partnered with the students to produce a deeper dive into the issues surrounding sex discrimination in the California Law Review paper.

"In any context, he (Justice Neil Gorsuch) basically says that if you discriminate on sex, you are always discriminating based on sexual orientation or transgender status, because those are intrinsically linked with sex," Blake said. "And so looking at that, the Court only decided on employment law, but we have other areas - like healthcare - where sex discrimination has still been not defined. And in which Gorsuch's opinion appears to resolve any uncertainty that LGBTQ discrimination is sex discrimination and must be forbidden under the law."

The authors believe discrimination in a healthcare setting can have a lasting impact on an LGBTQ person. Someone with a negative experience at a care facility is likely to avoid seeking medical help in the future, they said.

Healthcare protections were first introduced under the Obama Administration in 2010 with Section 1557 of the Affordable Care Act, banning sex discrimination. However, they weren't solidified for the LGBTQ community until 2016 when the Department of Health and Human Services stated that the statute included the community in a broad sense.

The inclusion of gender identity and sexual orientation sparked backlash among several religious organizations and some states that argued that healthcare professionals could deny services based on religious exemptions.

Additionally, in 2020 the Trump Administration stripped gender identity and sexual orientation from Section 1557, leaving the LGBTQ community unprotected. However, according to Post, the Bostock case essentially challenges this action by the Trump administration.

"Those things shouldn't preclude you from receiving healthcare and it's kind of just like the way that we may think it's inherently obvious that a doctor shouldn't say, well, they're male, so I'm not going to help them out because I don't like men," Blake said.

"We think it should also be as inherently obvious that it doesn't matter if you identify as LGBTQ-plus, you are deserving of the care that everybody else is."

Moving forward, Stephens suggests that legislation should be explicitly written and include gender identity and sexual orientation to ensure that the LGBTQ community is covered on all platforms.

Additionally, the researchers emphasized patient advocacy and said that in order to avoid any discriminatory practices, a patient can ask if a care facility is LGBTQ friendly. This helps to ensure a positive experience and relationship between patient and provider, they said.

"What I would say is to those people who feel that they've been discriminated against, you know, show up, get your care met," Blake said. "Take care of yourself and expect that you will get that care met because you have rights and you deserve them."

Since early in the pandemic, COVID-19 has been associated with heart problems, including reduced ability to pump blood and abnormal heart rhythms. But it's been an open question whether these problems are caused by the virus infecting the heart, or an inflammatory response to viral infection elsewhere in the body. Such details have implications for understanding how best to treat coronavirus infections that affect the heart.

A new study from Washington University School of Medicine in St. Louis provides evidence that COVID-19 patients' heart damage is caused by the virus invading and replicating inside heart muscle cells, leading to cell death and interfering with heart muscle contraction. The researchers used stem cells to engineer heart tissue that models the human infection and could help in studying the disease and developing possible therapies.

The study is published Feb. 26 in the Journal of the American College of Cardiology: Basic to Translational Science.

"Early on in the pandemic, we had evidence that this coronavirus can cause heart failure or cardiac injury in generally healthy people, which was alarming to the cardiology community," said senior author Kory J. Lavine, MD, PhD, an associate professor of medicine. "Even some college athletes who had been cleared to go back to competitive athletics after COVID-19 infection later showed scarring in the heart. There has been debate over whether this is due to direct infection of the heart or due to a systemic inflammatory response that occurs because of the lung infection.

"Our study is unique because it definitively shows that, in patients with COVID-19 who developed heart failure, the virus infects the heart, specifically heart muscle cells."

Lavine and his colleagues -- including collaborators Michael S. Diamond, MD, PhD, the Herbert S. Gasser Professor of Medicine, and Michael J. Greenberg, PhD, an assistant professor of biochemistry and molecular biophysics -- also used stem cells to engineer tissue that models how human heart tissue contracts. Studying these heart tissue models, they determined that viral infection not only kills heart muscle cells but destroys the muscle fiber units responsible for heart muscle contraction.

They also showed that this cell death and loss of heart muscle fibers can happen even in the absence of inflammation.

"Inflammation can be a second hit on top of damage caused by the virus, but the inflammation itself is not the initial cause of the heart injury," Lavine said.

Other viral infections have long been associated with heart damage, but Lavine said SARS-CoV-2, the virus that causes COVID-19, is unique in the effect it has on the heart, especially in the immune cells that respond to the infection. In COVID-19, immune cells called macrophages, monocytes and dendritic cells dominate the immune response. For most other viruses that affect the heart, the immune system's T cells and B cells are on the scene.

"COVID-19 is causing a different immune response in the heart compared with other viruses, and we don't know what that means yet," Lavine said. "In general, the immune cells seen responding to other viruses tend to be associated with a relatively short disease that resolves with supportive care. But the immune cells we see in COVID-19 heart patients tend to be associated with a chronic condition that can have long-term consequences. These are associations, so we will need more research to understand what is happening."

Part of the reason these questions of causation in heart damage have been hard to answer is the difficulty in studying heart tissue from COVID-19 patients. The researchers were able to validate their findings by studying tissue from four COVID-19 patients who had heart injury associated with the infection, but more research is needed.

To that end, Lavine and Diamond, are working to develop a mouse model of the heart injury. To emphasize the urgency of the work, Lavine pointed to the insidious nature of the heart damage COVID-19 can cause.

"Even young people who had very mild symptoms can develop heart problems later on that limit their exercise capacity," Lavine said. "We want to understand what's happening so we can prevent it or treat it. In the meantime, we want everyone to take this virus seriously and do their best to take precautions and stop the spread, so we don't have an even larger epidemic of preventable heart disease in the future."

They can hear well up to about forty years old, but then suddenly deafness strikes people with DFNA9. The cells of the inner ear can no longer reverse the damage caused by a genetic defect in their DNA. Researchers at Radboud university medical center have now developed a "genetic patch" for this type of hereditary deafness, with which they can eliminate the problems in the hearing cells. Further research in animals and humans is needed to bring the genetic patch to the clinic as a therapy.

Hereditary deafness can manifest itself in different ways. Often the hereditary defect (mutation) immediately causes deafness from birth. Sometimes, as with DFNA9, you experience the initial problems in hearing after forty, fifty, sixty years. This has everything to do with the way DFNA9 mechanistically works. Every person gets half of his genes from his father and the other half from his mother. If you have two healthy copies of the DFNA9 gene, your inner ear works normal. If you receive a mutated copy of the gene from either your father or mother, deafness will develop later in life.

Protein spaghetti

Erik de Vrieze and Erwin van Wijk, both researchers at Hearing & Genes of the department of Ear, Nose and Throat, have conducted extensive research into the condition. De Vrieze: "We now know that you actually produce enough of the associated DFNA9 protein with just one healthy gene copy to be able to hear well for life. But there is a catch with this condition. The mutated protein is, in a way, disturbing the function of the healthy protein. It sticks to it, so that the healthy protein can also no longer do its job. This clumped protein spaghetti is constantly being removed by the cells of the inner ear, but after decades the clean-up service in these cells is reaching its limit and can no longer cope with these protein clumps. A threshold value is exceeded. As a result, the waste accumulates, the hearing cells start to function poorly and even die over time. After years of normal hearing, DFNA9 patients suddenly notice that their hearing is deteriorating, and sometimes deteriorating very quickly. Until at some point they will become deaf. "

Enough time for treatment

The specific DFNA9 mutation seems to originate from a common ancestor in the Southern Netherlands, somewhere at the end of the Middle Ages. This can more or less be deduced from the spread of the fairly unique clinical manifestation, which is now estimated to occur in about 1500 people in the (southern) Netherlands and Belgium. Perhaps even more important than the origin of the disease is whether or not anything can be done about it. Van Wijk: "This condition has two favorable characteristics for therapy development. Firstly, it is a hereditary condition that only manifests itself after a few decades in life. In case an effective treatment will become available for this disease, a sufficiently large timeframe is available to apply it before the hearing loss really strikes. "

Turning off mutant gene

The other point - developing an effective therapy - is a bit more complicated, but offers good starting points. Van Wijk: "The idea is that by specifically turning off the mutated gene copy you can prevent deafness. Without this mutated gene copy, no mutant protein will be produced and protein clumping will no longer take place. In addition, one healthy gene copy alone produces enough protein to maintain good hearing. "

Genetic patch

De Vrieze and Van Wijk further developed this idea. Together with colleagues, they have now published the research results in the scientific journal Molecular Therapy - Nucleic Acids. "Genes, that reside on our DNA, provide the genetic code for the translation process into proteins," says De Vrieze. "To get from a gene to a protein, you always need a translation process via so-called messenger RNA. And that is exactly the process we focused on. The unique DNA error in the DFNA9 gene is also reflected in the RNA. We developed a small piece of RNA that specifically binds to the messenger RNA derived from the mutated DFNA9 gene. As a result, the entire mutated messenger RNA is targeted for degradation. In this way, an essential link is lost and the mutant DFNA9 protein is no longer or hardly produced. The piece of RNA that we stick on the mutated DFNA9 messenger RNA is named an antisense oligonucleotide or "genetic patch".

Perspective!

In recent years, De Vrieze and Van Wijk have not only developed this genetic patch, but also investigated its effect in cultured cells. Their current article is mainly describing these results, as the approach works in cultured cells. So there is a "proof of concept", as it is called in science. In short, the research shows that the approach works at the cellular level.

Arthur Robbesom of the "The Ninth of ..." DFNA9 Foundation is delighted with the study. "This offers a real perspective for about 1,500 people in the Netherlands and Belgium who are suffering from this condition. "The foundation is also closely involved in this research. Robbesom:" Now it is important to take the next necessary steps in the research as soon as possible. We will wholeheartedly support you."

Philadelphia, March 2, 2021--Taking the first deep dive into how the immune system is behaving in patients with multisystem inflammatory syndrome in children (MIS-C), researchers at Children's Hospital of Philadelphia (CHOP) and the Perelman School of Medicine at the University of Pennsylvania have found that children with this condition have highly activated immune systems that, in many ways, are more similar to those of adults with severe COVID-19. The results, published today in Science Immunology, show that better understanding the immune activation in patients with MIS-C could not only help better treat those patients but also improve treatment for adults with severe COVID-19.

"This study shows that children with MIS-C are tremendously immune activated, particularly when it comes to CD8 T cells, but that this activation subsides once patients begin to improve clinically," said Laura Vella, MD, PhD, attending physician in the Division of Infectious Diseases at CHOP and first author of the study. "Our findings provide a broad immunologic foundation for understanding pathogenesis and recovery in this novel SARS-CoV-2-associated inflammatory syndrome, with potential implications for adult disease."

Pediatricians first recognized MIS-C in April 2020, when pediatric patients began presenting with symptoms involving hyperinflammation, including fever, gastrointestinal distress and cardiogenic shock. The syndrome, thought to be a post-infectious complication of SARS-CoV-2 infection, has similarities in clinical presentation to Kawasaki disease, especially the vascular involvement, but it differs from Kawasaki disease in key ways, including unique clinical, inflammatory, and autoantibody signatures. The syndrome also lacks the respiratory complications typical of adult and pediatric COVID-19. However, until this point, the immunologic features driving MIS-C remained poorly understood.

To better understand the immunology behind MIS-C, the researchers collected blood samples from patients admitted to CHOP with COVID-19 or MIS-C between April and June of 2020. They analyzed more than 200 immune parameters, including serologic and plasma cytokine data, and compared these data with samples from adult COVID-19 patients, recovered adult COVID-19 subjects, and healthy adults.

The researchers found that children with MIS-C had highly elevated T cells, particularly CD8 T cells and a highly activated vascular patrolling CD8 T cell subset. These vascular patrolling CD8 T cells have a proposed role in the control of persisting or reactivating viral infection and have also been implicated in cardiovascular disease, which could have relevance to the vascular symptoms observed in these patients. The researchers found patients with MIS-C, who all had high vascular patrolling CD8 T cells, also required vasoactive support, had elevated D-dimer, and had decreased platelets. The elevation of CD8 T cells far exceeded what the researchers observed in pediatric patients with acute COVID-19 and most adults with COVID-19, but the level of CD8 T cells dropped in MIS-C patients in conjunction with clinical improvement.

The study also highlighted a skewed B cell response in patients with MIS-C compared to acute pediatric COVID-19 and resolved adult disease. Patients with MIS-C are almost universally seropositive for SARS-CoV-2, meaning enough time had passed since infection for an antiviral antibody to develop and be detected. Pediatric and adult patients with acute COVID-19 were not seropositive, consistent with the belief that that MIS-C is a delayed event following SARS-CoV-2 infection. Yet despite MIS-C being a delayed event, the researchers found that MIS-C patients had elevated plasmablasts, or immature plasma B cells, whereas plasmablasts in adults who recover from COVID-19 return to baseline two to three weeks after symptoms resolve, although a subset of hospitalized adult patients with COVID-19 did have a sustained elevation of plasmablasts.

The researchers proposed three possible drivers of the immune pathogenesis in MIS-C: (1) continued activation of adaptive immune responses, driven by persisting SARS-CoV-2 antigen; (2) an additional trigger, such as the virus localizing to a new tissue type or a secondary infection, occurring two to three weeks after the initial infection with SARS-CoV-2; or (3) an autoimmune response. More research is needed to investigated these potential scenarios.

"SARS-CoV2 infection can lead to a broad spectrum of clinical and immunological outcomes," said E. John Wherry, PhD, Director of the Institute for Immunology and senior author of the study. "The use of an 'Immune Health' profiling approach for pediatric COVID-19 patients not only identified distinct features of the pediatric MIS-C presentation of disease, but the insights gained by studying MIS-C patients may reveal new therapeutic opportunities for pediatric and adult COVID-19 patients."

A new study of patients with Multisystem Inflammatory Syndrome in Children (MIS-C), a rare but severe complication of COVID-19 in children, reveals distinct immune features of COVID-19 not seen in adults that may clue scientists in to why SARS-CoV-2 infection manifests differently in children compared with adults. Their results showed that although the immune landscape in pediatric COVID-19 was similar to that in adults, MIS-C patients uniquely exhibited increased activation of a blood vessel-patrolling CD8+ killer T cell subset, and all pediatric COVID-19 patients harbored greater B cell frequencies for a more prolonged period of time than observed in healthy adults. MIS-C is characterized by pervasive inflammation, an array of symptoms ranging from fever to vomiting, and insufficient blood flow throughout the body that can lead to shock. To home into the immune features of MIS-C, Laura Vella and colleagues analyzed immune responses in blood taken from 30 hospitalized SARS-CoV-2-infected pediatric patients - 14 of whom were diagnosed with MIS-C. They compared results of this analysis with samples from adult COVID-19 patients, recovered adult COVID-19 subjects, and healthy adults. While MIS-C patients exhibited patterns of decreasing T cell count and activation similar to adults with severe COVID-19, they also exhibited robust activation of a killer T cell subset that patrols and interacts with the vasculature to control viral persistence. This feature was not observed in either adult or non-MIS-C pediatric COVID-19 patients. In addition, while children with COVID-19-driven acute respiratory distress syndrome had sustained immune activation, overall immune activation in MIS-C patients decreased over time, paralleling clinical improvement. All pediatric COVID-19 patients had substantially elevated B cell frequencies compared to healthy adults, but future work will be necessary to dissect how this impacts disease. Together, these findings portray the variability in immune responses to SARS-CoV-2 across ages and patient populations and may help inform treatments for severe COVID-19 in children.

Orange, Calif. - Even before the COVID-19 pandemic, college students were reporting record levels of stress and anxiety. According to the American College Health Association Fall 2018 National College Health Assessment, 63% of U.S. college students experienced overwhelming anxiety throughout the year. Plus, stress can impact students' academic performance, and students with higher stress levels are more at-risk of withdrawing from college--often permanently. Given these complex mental health issues, all hands are needed on deck to support student success.

A new review from Chapman University's Schmid College of Science and Technology and Grand Challenges Initiative provides actionable and evidence-based strategies for instructors to help combat the ongoing epidemic of stress and anxiety among college and university students, with a focus on students in STEM disciplines. The strategies can be implemented by new and experienced instructors in order to reduce student stress and anxiety and ultimately improve students' academic performance and quality of life. The role that higher education instructors can play in alleviating students' stress and anxiety has been largely underexplored in previous studies, in favor of proposals for broad programmatic approaches at the institutional level.

Led by Chapman professors Jeremy Hsu and Gregory Goldsmith, the review covers specific and highly practicable actions. From learning about the university's available campus mental health programs, to arriving a few minutes prior to the start of class to allow student check-ins and greetings, to sharing relevant personal stories, the approaches in the paper directly equip the instructors who see and interact with students on a daily basis to improve the classroom experience.

We asked the authors five questions about their new review, published this week in the journal CBE--Life Sciences Education: https://www.lifescied.org/doi/10.1187/cbe.20-08-0189

Five Questions with the Authors

1.What motivated you to review best practices for reducing student stress and anxiety in the classroom?

We have always been concerned about stress and anxiety in our students and have seen how much the pandemic has exacerbated these issues. To address our concerns, we have looked for evidence-based practices to try to mitigate stress and anxiety in our classrooms and to best support our students. We wanted to bring together this research as a guide for instructors to highlight practical approaches to alleviating student stress and anxiety as they navigate these challenging circumstances.

2. You lay out a framework for instructors to alleviate stress and anxiety with five overarching approaches: learning and preparing to act; connecting with students; building an empowering classroom culture; reducing testing anxiety; and promoting effective academic skills. If you had to choose one for instructors to focus on, which would you choose and why?

Our review highlights that instructors can make a difference in alleviating student stress and anxiety through many types of interactions. For instance, it is important that instructors know and advertise the mental health resources and professional support that are available to students. Another approach involves the simple act of instructors taking a few minutes before each class to chat informally with students. Instructors can also reduce student stress and anxiety by changing the structure of their exams. Cumulatively, these small acts can add up to big improvements for students' performance in the classroom.

3. How do the approaches you identify intersect with our renewed interest in diversity, equity, and inclusion in STEM?

One of the things that stood out to us was that classroom practices that are not sensitive to equity and inclusion can disproportionately increase stress and anxiety among certain identities. Sometimes, the words or actions that seem trivial to an instructor can increase stress among certain students, and this is likely to impact their ability to learn. For instance, instructors can sometimes make statements that make students question whether they belong in the classroom and this can be a source of stress. In turn, one can also imagine that this affects whether or not a student chooses to persist in a STEM major.

4. What can universities do to support instructors in their efforts to reduce stress and anxiety in the classroom?

We are always in favor of increasing the training and support for instructors, so that they are prepared to support their students. More fundamentally, we need to normalize conversations where we talk about stress and anxiety and how we can work together so that all of our students can thrive.

5. At the end of the paper, you identify a number of areas for future research. Were there any surprises?

We have known for a while that students consistently identify stress and anxiety as barriers to their success, so in some ways, the biggest surprise was that the research on best practices in the classroom is so limited. It is also not yet clear that what works in some disciplines, or for some student demographics, will work for others. There are clearly some very exciting opportunities for experts in education and psychology to come together and provide important insights into how to improve outcomes for all of our students.

The Deepwater Horizon disaster began on April 20, 2010 with an explosion on a BP-operated oil drilling rig in the Gulf of Mexico that killed 11 workers. Almost immediately, oil began spilling into the waters of the gulf, an environmental calamity that took months to bring under control, but not before it became the largest oil spill in the history of the petroleum industry.

Nearly 10 years have passed since then, and the oil slick has long since dispersed. Yet, despite early predictions, area wildlife are still feeling the effects of that oil, and research published in Environmental Toxicology and Chemistry has shown that negative health impacts have befallen not only dolphins alive at the time of the spill, but also in their young, born years later.

A team of researchers, including UConn Department of Pathobiology Professor and Director of the Connecticut Sea Grant College Program Sylvain De Guise, is part of a network conducting a long-term study on the health of bottlenose dolphins living in Louisiana's Barataria Bay, in the vicinity of the disaster. This population of dolphins includes individuals who lived through the disaster and some born afterwards.

"We were on the ready and as soon as we could, and in 2011 we initiated a comprehensive health assessment where 60 to 80 people in the field worked together to find and safely pursue a multi-disciplinary, multi-expertise sample collection and study effort to assess the dolphins' health," says De Guise.

De Guise explains that after collection, samples were processed in 60 to 80 different specialized labs, and the researchers then regrouped to put the information together. De Guise's research group specializes in studying the immune system, and from the very first set of samples they started to see consistent and abnormal immune responses in the Barataria Bay dolphins, compared with a similar control group of dolphins from Sarasota Bay who were not exposed to oil.

For the Barataria Bay dolphins, the researchers observed immune cells called T-cells that were overly responsive to stimulation. The body uses T-cells to respond to a stimulus, or something recognized as foreign. In particular, there were increased numbers of cells called regulatory T cells, or Tregs, which De Guise describes as the cells that help put the brakes on during an immune response to prevent the body from over-responding and doing more harm than good.

Despite the elevated numbers, De Guise says they were surprised to find the Barataria Bay dolphin Tregs appear to be functionally defective.

In some ways, the immune response can be looked at almost like a relay race, with cells signaling others to respond and join in the effort. In the case of T-helper (Th) cells, important signals called cytokines determine which type of T-helper will be next in the relay, and for the Barataria Bay dolphins, the signals are not relayed as expected.

"T-helper cells decide which direction your immune system will respond. If you have a pathogen that invades cells, a virus for example, you need a T-helper1 (Th1) response that will destroy the affected cells. If you have a pathogen that does not invade cells, like most types of bacteria, you need to generate antibodies to bind to those bacteria and help eliminate them with a Th2 response," says De Guise.

In the lab, the researchers studied the immune cells from both dolphin populations by exposing them to proteins called cytokines which elicit predictable responses from the T-cells. The researchers also exposed T-cells from the control group dolphins to oil to see what would happen. In all samples of T-cells exposed to oil, Th2 responses were exaggerated compared to the control group.

"We were able to demonstrate that there was a difference in responsiveness between the populations, in both real-life and in-vitro tests which resulted in an increase in Th2 response in the Barataria Bay dolphins," says De Guise.

The researchers went one step further by conducting a mouse study to see if a similar immune response could be seen in mice exposed to oil, and they did.

"The effects on the mouse immune system that we found were strikingly similar to what we saw in the dolphins," says De Guise. "We want to show the likelihood of a cause and effect relationship and add to the weight of evidence that oil impacts the immune system in a way that is very reproducible across species. The changes that we found in the Barataria Bay dolphins is specific to oil and not related to something else."

Though the researchers are not sure if the abnormal immune response is due to the initial exposure or continued exposure to oil still present in sediments, De Guise says the result may lead to the dolphins being more susceptible to pathogens like viruses, due to dysfunctional T-reg cells. Only future studies can shed light, and De Guise says now that images of oil slicks are no longer capturing attention, funding is harder to come by.

However, for this study, De Guise notes it is very rare to have such a long-term, detailed follow-up on a wild population of animals, and the researchers were very surprised to see effects in a second generation who did not live through the disaster.

"The outcome of this work is that we are not sure if these effects are reversible or not. The longer we look, they are still around. I think it is the first time we find such evidence across generations in a wild animal population, and that is scary. It raises concern for the long-term recovery of these dolphins," says De Guise. "These are long-lived mammals and, in many ways, not unlike humans who live in the area and depend on natural resources. It is interesting science, but it is very scary."

Disruptions in the circadian rhythms in lung cells may explain why adults who survived premature birth are often more at risk of severe influenza infections, suggests a study in mice published today in eLife.

Dramatic improvements in the care of infants born prematurely have allowed many more to survive into adulthood. Yet ex-preemies can face several long-term side effects of the life-saving care they received. The study suggests potential new approaches to treating lasting lung problems in those born prematurely.

Many premature infants are not able to breathe on their own and require oxygen to survive. But receiving too much oxygen may cause lasting damage to the lung that makes them more prone to severe flu infection later in life. In a previous study*, senior author and neonatologist Shaon Sengupta, and her colleagues at the Children's Hospital of Philadelphia Research Institute, Pennsylvania, US, found that susceptibility to flu in mice depended on the time of day when they caught the infection. Mice that caught the infection when they became active at dusk were more likely to die, while those infected as they went to sleep at dawn were more likely to survive. This suggests that the circadian clock, which controls the daytime and nighttime activities of the body, may offer some protection against flu.

"Given these previous findings, we wanted to see if the severity of flu infection in former premature infants may be caused by disruptions to their circadian clock," says Yasmine Issah, a former Research Technician at the Children's Hospital of Philadelphia Research Institute, and co-first author of the current study alongside Postdoctoral Research Fellow Amruta Naik.

The team began by showing that the time of day when exposure to flu occurred did not affect susceptibility to infection in adult mice that were exposed to high levels of oxygen as newborns. This suggests that these mice had lost their circadian clock-based flu protection.

But when the team tested the ability of the animals to readjust to a normal day-night schedule after living in dim light for several weeks, they found the animals had no problems - suggesting that their central circadian clock in the brain, which is regulated by exposure to daylight, was working normally.

To find out if the circadian problems were restricted to lung cells, which have their own circadian clocks separate from the brain clock, the team removed a key circadian clock gene called Bmal1 in the lung cells of normal adult mice. They eliminated the gene in the same lung cells that are damaged in newborn mice given high levels of oxygen. As with the mice that had been exposed to high oxygen as newborns, the adult animals with the deleted gene were equally susceptible to flu at dawn or dusk.

"Our findings suggest that adverse early-life exposures can disrupt the lung circadian clock," concludes Sengupta, an attending neonatologist at the Children's Hospital of Philadelphia Research Institute. "Those born prematurely are uniquely vulnerable to this faulty development of their circadian network, and this is a new paradigm for understanding the lung problems that persist into adulthood in ex-preemies. These findings could pave the way for potential new treatments that work by improving the circadian health in adults born prematurely."