The paper is published in the journal Atmospheric Chemistry and Physics.

The research team, led by Joannes Maasakkers, a former graduate student at SEAS, developed a method to trace and map total emissions from satellite data to their source on the ground.

“This is the first country-wide evaluation of the emissions that the EPA reports to the United Nations Framework Convention on Climate Change (UNFCC),” said Maasakkers, who is currently a scientist at the SRON Netherlands Institute for Space Research.

Currently, the EPA only reports total national emissions to the UNFCC. In previous research, Maasakkers and his collaborators, including Daniel Jacob, the Vasco McCoy Family Professor of Atmospheric Chemistry and Environmental Engineering at SEAS, worked with the EPA to map regional emissions of methane from different sources in the US. That level of detail was used to simulate how methane moves through the atmosphere.

In this paper, the researchers compared those simulations to satellite observations from 2010-2015. Using a transport model, they were able to trace the path of emissions from the atmosphere back to the ground and identify areas across the US where the observations and simulations didn’t match up.

“When we look at emissions from space, we can only see how total emissions from an area should be scaled up or down, but we don’t know the source responsible for those emissions,” said Maasakkers. “Because we spent so much time with the EPA figuring out where these different emissions occur, we could use our transport model to go back and figure out what sources are responsible for those under- or over-estimations in the national total.”

The biggest discrepancy was in emissions from oil and natural gas production.

The EPA calculates emission based on processes and equipment. For example, the EPA estimates that a gas pump emits a certain amount of methane, multiplies that by how many pumps are operating across the country, and estimates total emissions from gas pumps.

“That method makes it really hard to get estimates for individual facilities because it is hard to take into account every possible source of emission,” said Maasakkers. “We know that a relatively small number of facilities make up most of the emissions and so there are clearly facilities that are producing more emissions than we would expect from these overall estimates.”

The researchers hope that future work will provide more clarity on exactly where these emissions are coming from and how they are changing.

“We plan to continue to monitor U.S. emissions of methane using new high-resolution satellite observations, and to work with the EPA to improve emission inventories,” said Jacob.

“It’s important to understand these emissions better but we shouldn’t wait until we fully understand these emissions to start trying to reduce them,” said Maasakkers. “There are already a lot of things that we know we can do to reduce emissions.”

This paper was co-authored by Daniel Jacob, Melissa Sulprizio, Tia R. Scarpelli, Hannah Nesser, Jianxiong Sheng, Yuzhong Zhang, Xiao Lu, A. Anthony Bloom, Kevin Bowman, John Worden, and Robert Parker.

The research was funded by the NASA Carbon Monitoring System (CMS) program.

“We found that the large spin-orbit coupling and strong electronic correlations in a system of uranium-cobalt-aluminum doped with ruthenium resulted in a colossal anomalous Nernst conductivity,” said Filip Ronning, lead investigator on the paper published today in Science Advances. Ronning is director of the Institute for Materials Science at Los Alamos National Laboratory. “It illustrates that uranium and actinide alloys are promising materials to study the interplay among a material’s topology and strong electron correlations. We’re very much interested in understanding, tuning and eventually controlling this interplay, so hopefully one day we can exploit some of these remarkable responses.”

The Nernst response occurs when a material converts a flow of heat into an electric voltage. This thermoelectric phenomenon can be exploited in devices that generate electricity from a heat source. The most notable current example is the radioisotope thermoelectric generators (RTGs) that were developed in part at Los Alamos. RTGs use heat from the natural radioactive decay of plutonium-238 to generate electricity — one such RTG is currently powering the Perseverance rover on Mars.

“What’s exciting is that this colossal anomalous Nernst effect appears to be due to the rich topology of the material. This topology is created by a large spin-orbit coupling, which is common in actinides,” Ronning said. “One consequence of topology in metals is the generation of a transverse velocity, which can give rise to a Nernst response as we observe. It can also generate other effects such as novel surface states that may be useful in various quantum information technologies.”

The uranium system studied by the Los Alamos team generated 23 microvolts per kelvin of temperature change — four times bigger than the previous record, which was discovered in a cobalt-manganese-gallium alloy a couple of years ago and also attributed to these sorts of topological origins.

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The team studied fruit flies and cutting-edge brain cell models called organoids. They focused on the signals muscles send when stressed. The researchers found that stress signals rely on an enzyme called Amyrel amylase and its product, the disaccharide maltose.

The scientists showed that mimicking the stress signals can protect the brain and retina from aging. The signals work by preventing the buildup of misfolded protein aggregates. Findings suggest that tailoring this signaling may potentially help combat neurodegenerative conditions like age-related dementia and Alzheimer’s disease.

“We found that a stress response induced in muscle could impact not only the muscle but also promote protein quality control in distant tissues like the brain and retina,” said Fabio Demontis, PhD, of St. Jude Developmental Neurobiology. “This stress response was actually protecting those tissues during aging.”

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“The demonstration of high single-photon purity in the infrared has immediate utility in areas such as quantum key distribution for secure communication,” said Victor Klimov, lead author of a paper published today in Nature Nanotechnology by Los Alamos National Laboratory scientists.

The Los Alamos team has developed an elegant approach to synthesizing the colloidal-nanoparticle structures derived from their prior work on visible light emitters based on a core of cadmium selenide encased in a cadmium sulfide shell. By inserting a mercury sulfide interlayer at the core/shell interface, the team turned the quantum dots into highly efficient emitters of infrared light that can be tuned to a specific wavelength.

“This new synthesis allows for highly accurate, atomic-level control of the thickness of the emitting mercury sulfide interlayer. By changing it in increments of a single atomic layer, we can tune the wavelength of the emitted light in discrete quantized jumps, and further adjust it in a more continuous fashion by tuning the cadmium selenide core size,” said Vladimir Sayevich, the lead chemist on this project.

Far superior to existing near-infrared quantum dots, these new structures show “blinking-free” emission at a single-dot level, nearly perfect single-photon purity at room temperature (which produces “quantum light”), and fast emission rates. They behave extremely well with both optical and electrical excitation.

Single photons can be used as qubits in quantum computing. In a cybersecurity application, single photons can protect a computer network through quantum key distribution, which provides ultimate security through “unbreakable” quantum protocols.

Bio-imaging is another important application. The emission wavelength of the newly developed quantum dots is within the near-infrared bio-transparency window, which makes them well suited for deep tissue imaging.

People can’t see infrared light, but many modern technologies rely on it, from night-vision devices and remote sensing to telecommunications and biomedical imaging. Infrared light is also a big player in emerging quantum technologies that rely on the duality of light particles, or photons, which can also behave as waves. Exploiting this quantum property requires sources of “quantum light” that emit light in the form of individual quanta, or photons.

“There is also a cool chemical element in achieving single-atomic layer accuracy in making these dots,” said Zack Robinson, the project member focusing on quantum dot spectroscopy. “The thickness of the emitting mercury sulfide interlayer is identical across all dots in the samples. That’s very unique, especially for a material made chemically in a beaker.”

Klimov added, “However, this is just the first step. In order to take full advantage of ‘quantum light’ one needs to achieve photon indistinguishability, that is, to make sure that all emitted photons are quantum-mechanically identical. This is an extremely difficult task, which we will tackle next in our project.”

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The novel active ingredient is a so-called aptamer. These are short chains of DNA, the chemical compound that also makes up chromosomes. DNA chains like to attach themselves to other molecules; one might call them sticky. In chromosomes, DNA is therefore present as two parallel strands whose sticky sides face each other and that coil around each other like two twisted threads.

Aptamers, on the other hand, are single-stranded. This allows them to form bonds with molecules to which conventional DNA would not normally bind and to influence their function. This makes them interesting for research into active ingredients, especially since it is now very easy to produce huge libraries of different aptamers. Some of these libraries contain millions of times more potential active ingredients than there are people living on Earth. “We used such a library to isolate aptamers that can attach to the spike protein of SARS coronavirus 2,” explains Prof. Dr. Günter Mayer of the LIMES Institute (the acronym stands for “Life and Medical Sciences”) at the University of Bonn.

Spike is essential for the infection

The spike protein is essential for the virus: It uses it to dock onto the cells it attacks. In the process, the protein binds to a molecule on the surface of its victims called ACE2, which effectively locks into the spike protein, much like a ski boot in a ski binding. The virus then fuses with the cell and reprograms it to produce numerous new viruses. “The vast majority of antibodies we know today prevent docking,” Mayer explains. “They attach to the part of the spike protein responsible for recognizing ACE2, which is the receptor binding domain, or RBD.”

The now isolated aptamer with the abbreviation SP6 also binds to the spike protein, but at a different site. “SP6 does not prevent viruses from docking to target cells,” explains Prof. Dr. Michael Famulok of the LIMES Institute, who also works at the caesar research center in Bonn. “Nevertheless, it reduces the level of cell infection by the virus; we do not yet know which mechanism is responsible for this.” The researchers did not use real coronaviruses in their experiments, but so-called pseudoviruses. These carry the spike protein on their surface; however, they cannot cause disease. “We now need to see if our results are confirmed in real viruses,” Famulok therefore emphasizes.

New Achilles heel of coronavirus?

If so, in the medium term the work could for instance result in a kind of nasal spray that protects against coronavirus infection for a few hours. The necessary studies will certainly take months to complete. Irrespective of this, however, the results may help to better understand the mechanisms involved in infection. This is all the more important because the existing active ingredients mainly target the receptor domain. In the so-called “British mutation,” this domain is altered so that it binds more strongly to ACE2. “The more such mutations accumulate, the greater the risk that the available drugs and vaccines will no longer work,” stresses Günter Mayer. “Our study may draw attention to an alternative Achilles’ heel of the virus.”

The results are also evidence of successful cooperation: Mayer and his postdoctoral researcher Dr. Anna Maria Weber were primarily responsible for characterizing the aptamer. Prof. Famulok’s group at the caesar research center was responsible for conducting the pseudovirus experiments, which were led by his colleague Dr. Anton Schmitz. Famulok and Mayer are members of the Transdisciplinary Research Areas “Life & Health” and “Building Blocks of Matter and Fundamental Interactions.” Mayer also heads the Center of Aptamer Research and Development (CARD) at the University of Bonn.

The study was funded by the German Federal Ministry of Education and Research (BMBF) and the German Research Foundation (DFG).

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“We are looking at water scarcity as a globally connected and multi-sector phenomenon,” said Jonathan Lamontagne, assistant professor of civil and environmental engineering at Tufts University, who co-authored the study with Patrick Reed, the Joseph C. Ford Professor of Civil and Environmental Engineering at Cornell. Tufts graduate student Flannery Dolan is lead author of the study, which suggests water scarcity dynamics are more complicated than traditionally acknowledged.

The study, “Evaluating the economic impact of water scarcity in a changing world,” was published March 26 in Nature Communications, and uniquely captures the interdependent effects of global trade consistently with differences in regional climate policies as well as river basin-specific capacity to address water scarcity risks.

The researchers coupled physical and economic models to simulate thousands of potential climate futures for 235 major river basins — a technique known as scenario discovery — to better understand how water scarcity is a globally-connected phenomenon, with local conditions having reverberations across the globe in industries such as agriculture, energy, transportation and manufacturing.

The research found that global trade dynamics and market adaptations to regional water scarcity result in positive and negative economic outcomes for every regional river basin considered in the study.

For instance, in the lower Colorado River basin, the worst economic outcomes arise from limited groundwater availability and high population growth, but that high population growth can also prove beneficial under some climatic scenarios. In contrast, the future economic outcomes in the Indus Basin depend largely on global land-use policies.

“What is happening elsewhere in the world through differences in regional choices related to energy transitions — how land is being managed as well as different regional water demands and adaptive choices — can shape relative advantages and disadvantages of water intensive economic activities,” said Reed.

Restrictions in water availability usually lead to a negative regional economic impact, but the research revealed that some regions can experience a positive economic impact if they hold an advantage over other water basins and can become a virtual exporter of water. The Orinoco basin in Venezuela, for example, usually has a reliable supply of water and is often in a relative position that can benefit when other regions are under stress, according to the researchers.

The study also found that small differences in projections for future climate conditions can yield very large differences in the economic outcomes for water scarcity.

“Human activities and market responses can strongly amplify the economic effects of water scarcity, but the conditions that lead to this amplification vary widely from one basin to the next,” said Lamontagne.

A river basin can be considered economically robust if it is able to adapt to drought with alternative sources of water or adjust economic activity to limit usage. If a basin is unable to adapt its supply options and if prolonged water scarcity leads to persistent economic decline, then the researchers describe the loss in water basin adaptive capacity as having reached an ‘economic tipping point.’

For example, in the Indus region in South Asia, the water supply is under stress due to heavy agricultural use and irrigation leading to unsustainable consumption of groundwater, which places it close to the tipping point.

The conditions that lead to these tipping points are highly variable from basin to basin, depending on a combination of local factors and global conditions. In the Arabian Peninsula, low groundwater availability and pricing of carbon emissions are key factors. In the lower Colorado River basin, a mixture of low groundwater availability, low agricultural productivity, and strong economic demands from the U.S. and Europe lead to tipping points.

“It is noteworthy that the lower Colorado River basin has some of the most uncertain and widely divergent economic outcomes of water scarcity of the basins analyzed in this study,” said Reed. “This implies that assumed differences in regional, national and global human system conditions as well as the intensity of climate change can dramatically amplify the uncertainty in the basin’s outcomes.”

As climate change makes the physical and economic effects of water scarcity more challenging for policy makers to understand, the researchers hope their work will provide the basis for similar analyses and draw attention to the importance of expanded data collection to improve modeling and decision making.

The study was co-authored by researchers from the Joint Global Change Research Institute at the Pacific Northwest National Laboratory, and was supported by the U.S. Department of Energy’s Office of Science.

Researchers discovered changes to 12 genetic regions in the DNA of people who have had a lacunar stroke — a type of stroke caused by weakening of the small blood vessels deep within the brain. Over time, damage to the blood vessels and subsequent interruption to blood flow can lead to long-term disability, causing difficulty with thinking, memory, walking and ultimately dementia.

There are few proven drugs to prevent or treat lacunar strokes. The blood vessels affected are less than a millimetre wide and a lacunar stroke can strike without the person knowing. It’s not usually until someone has had a number of these strokes and starts to see signs of dementia that they realise something is wrong.

To date, only one genetic fault has been associated with lacunar strokes. However, after over a decade of research, Professor Hugh Markus and his team at the University of Cambridge working with researchers from around the world now believe their genetic breakthrough holds the key to finding much-needed treatments for lacunar stroke and vascular dementia.

Researchers scanned and compared the genetic code of 7,338 patients who had a lacunar stroke with 254,798 people who had not. Participants were recruited from across Europe, United States, South America and Australia after they attended hospital and had an MRI or CT brain scan.

They discovered that many of the 12 genetic regions linked to lacunar strokes were involved in maintaining the neurovascular unit — the part of the brain that separates the blood vessels from the brain and ensures that nerves function normally. These genetic changes are thought to make the small blood vessels ‘leakier’, causing toxic substances to enter the brain, and meaning that messages travelling around the brain slow down or don’t arrive at all.

The team now plan to test whether new treatments can correct these abnormalities on brain cells in the lab. They hope to begin human clinical trials in the next ten years.

The study also highlighted that high blood pressure, type 2 diabetes and a history of smoking are causally associated with an increased risk of lacunar stroke, identifying things that we can immediately tackle.

Professor Hugh Markus, BHF-funded researcher, leader of the study and neurologist at the University of Cambridge, said:

“These small and often silent lacunar strokes have gone under the radar for a long time, and so we haven’t been able treat patients as well as we’d like to. Although small, their consequences for patients can be enormous. They cause a quarter of all strokes and they are the type of stroke which is most likely to lead to vascular dementia.

“We now plan to use this new genetic blueprint as a springboard to develop much needed treatments to prevent lacunar strokes from occurring in the first place and to help stave off dementia.”

Dr Matthew Traylor, first author of the study at Queen Mary University of London, said:

“Genetics offers one of the few ways we can discover completely new insights into what causes a disease such as lacunar stroke. It is only by better understanding of what causes the disease that we will be able to develop better treatments.”

Professor Sir Nilesh Samani, Medical Director at the British Heart Foundation and cardiologist, said:

“This is the most extensive genetic search to date which truly gets to grips with what cause lacunar strokes. These findings are a significant leap forward and we now have a much greater understanding of the genetics and biology behind what causes the small blood vessels deep in the brain to become diseased.

“Lacunar strokes affect around 35,000 people in the UK each year. This research provides real hope that we can prevent and treat this devastating type of stroke much better in the future.”

The BHF is funding £24 million of research to better understand, prevent, diagnose and treat strokes and vascular dementia.

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Materials provided by British Heart Foundation. Original written by Lisa Jones. Note: Content may be edited for style and length.

The study found the greater the activity in nerve cells in the amygdala region of the brain, the sooner the condition known as Takotsubo syndrome (TTS) can develop. The researchers suggest that interventions to lower this stress-related brain activity could help to reduce the risk of developing TTS; these could include drug treatments or techniques for lowering stress.

TTS, also known as “broken heart” syndrome, is characterised by a sudden temporary weakening of the heart muscles that causes the left ventricle of the heart to balloon out at the bottom while the neck remains narrow, creating a shape resembling a Japanese octopus trap, from which it gets its name. Since this relatively rare condition was first described in 1990, evidence has suggested that it is typically triggered by episodes of severe emotional distress, such as grief, anger or fear, or reactions to happy or joyful events. Patients develop chest pains and breathlessness, and it can lead to heart attacks and death. TTS is more common in women with only 10% of cases occurring in men.*

The amygdala is the part of the brain that controls emotions, motivation, learning and memory. It is also involved in the control of the autonomic nervous system and regulating heart function.

“The study suggests that the increased stress-associated neurobiological activity in the amygdala, which is present years before TTS occurs, may play an important role in its development and may predict the timing of the syndrome. It may prime an individual for a heightened acute stress response that culminates in TTS,” said Dr Ahmed Tawakol, co-director of the Cardiovascular Imaging Research Center at Massachusetts General Hospital and Harvard Medical School (Boston, USA), who led the study.

“We also identified a significant relationship between stress-associated brain activity and bone marrow activity in these individuals. Together, the findings provide insights into a potential mechanism that may contribute to the ‘heart-brain connection’.”

In the first study to look at brain scans using F-fluorodeoxyglucose positron emission tomography/computed tomography (PET-CT) to assess brain activity before TTS develops, Dr Tawakol and colleagues analysed data on 104 people with an average age of 68 years, 72% of whom were women.

The patients had undergone scans at Massachusetts General Hospital (Boston, USA) between 2005 and 2019. Most of them had the scans to see if they had cancer and the scans also assessed the activity of blood cells in bone marrow. The researchers matched 41 people who went on to develop TTS between six months and five years after the scan with 63 who did not. The interval between the scan, the onset of TTs, last follow-up or death was an average (median) of 2.5 years for the 104 patients.

Dr Tawakol said: “Areas of the brain that have higher metabolic activity tend to be in greater use. Hence, higher activity in the stress-associated tissues of the brain suggests that the individual has a more active response to stress. Similarly, higher activity in the bone marrow reflects greater bone marrow metabolism. The PET/CT scans produce images that reflect the distribution of glucose metabolism. The brain images thereby yield a map of brain metabolic activity: the higher the values, the greater the activity in those brain regions.”

The researchers found that people who went on to develop TTS had higher stress-related amygdalar activity on initial scanning (measured as a ratio of amygdalar activity to activity of brain regions that counter stress) compared to individuals who did not subsequently develop TTS. Further, the higher the amygdalar signal, the greater the risk of developing TTS. Among the 41 patients who developed TTS, the average interval between the scan and TTS was 0.9 months, whereas among the control group of 63 patients, the average interval between the scan and last follow-up or death was 2.9 years.

“It was notable that among the 41 patients who developed TTS, the top 15% with the very highest amygdalar activity developed TTS within a year of imaging, while those with less elevated activity developed TTS several years later,” said Dr Tawakol.

He said future studies should investigate whether reducing stress-related brain activity could decrease the chances of TTS recurring among patients who have experienced TTS previously.

“These findings add to evidence of the adverse effect of stress-related biology on the cardiovascular system. Findings such as these underscore the need for more study into the impact of stress reduction or drug interventions targeting these brain regions on heart health. In the meantime, when encountering a patient with high chronic stress, clinicians could reasonably consider the possibility that alleviation of stress might result in benefits to the cardiovascular system.”

The process by which stress induces TTS is not well understood but may involve a multi-organ mechanism starting with activation of the stress-sensitive tissues of the brain. This brain activity in turn triggers several further events, including release of stress hormones, activation of the sympathetic nervous system and release of inflammatory cells, each of which can contribute to the development of TTS.

Limitations of the study include that it was a single-centre, retrospective study that consisted mainly of patients with a diagnosis of cancer, a known TTS risk factor, which may limit the generalisability of the findings. The researchers were unable to measure instantaneous changes in brain activity in response to a stressful event that led to TTS and so cannot directly show a causal relationship. Nor were they able to measure changes in activity in other regions of the brain, which could also play a role.

* TTS affects less than 3% of people who suffer a heart attack and tends to occur between the ages of 60-75.