Hawaiian-Emperor undersea mystery revealed with supercomputers

The Hawaiian-Emperor seamount chain spans almost four thousand miles from the Hawaiian Islands to the Detroit Seamount in the north Pacific, an L- shaped chain that goes west then abruptly north. The 60-degree bend in the line of mostly undersea mountains and volcanic islands has puzzled scientists since it was first identified in the 1940s from the data of numerous echo sounding ships.

A team of scientists have now used supercomputers allocated by the Extreme Science and Engineering Discovery Environment (XSEDE) to model and reconstruct the dynamics of Pacific tectonic plate motion that might explain the mysterious mountain chain bend.

Major Findings

"We've shown with computer models for the first time how the Pacific plate can abruptly change direction from the north to the west," said Michael Gurnis, professor of Geophysics at the California Institute of Technology.

"It's been a holy grail to figure out why this change happened," he said. Gurnis co-authored the study on the origins of the seamount chain that was published in Nature Geoscience in January 2022.

Besides Gurnis, the team consisted of geoscientists Jiashun Hu, a post-doctoral scholar at Caltech, and Dietmar Mu?ller of Sydney University in Australia and computational scientists Johann Rudi of Argonne National Laboratory and Georg Stadler of New York University.

Plate Motion Clues

The plate motion provides a key to understanding how the seamount chain reflects plate motions. Gigantic tectonic plates in Earth's crust basically move over the hot, weak rock of the mantle.

The Pacific Plate is one of the largest. The plate spans about 40 million square miles undersea, outlined by the mountains and volcanos of the 'Ring of Fire' that are created by the return of the plates to the mantle.

But the volcanos of Hawaii and the Hawaiian-Emperor seamount chain weren't caused by this process. Instead, scientists theorize that plumes of Earth's hottest rock, from its core, travel upward through the mantle to generate a volcanic hotspot. And it's theorized that the seamount chain was created by the plate moving over the hot plume, something like a trail of burn marks on a paper moved over a candle.

About 80 million years ago, the Pacific plate traveled mostly north for about 30 million years, as evidenced by the line of Emperor seamounts. But about 50 million years ago, something odd happened. The Pacific plate apparently changed direction, and the mantle plume also shifted.

"Maybe there's an underlying physical reason why they would happen simultaneously," Gurnis said.

Prior Gordon Bell Prize

He pointed to previous work using techniques such as adaptive mesh refinement on the dynamics of mantle convection, computational work that scales well to a large number of CPUs and used the Stampede1 system of TACC and earned the team spearheaded by Johann Rudi the Gordon Bell Prize in 2015.

"Moreover, earlier work with Mu?ller, Gurnis and others showed how the physics of plumes could work inside the mantle such that the you could have a plume which rapidly migrated to the south and then stopped at 50 million years ago," Gurnis said.

"These two studies are complementary because going into the present study, we actually had a model which could explain the motion of the plume to the south and then stop abruptly, but we didn't have a model that could explain how the plate could change its direction," he added.

The team's computations of the physics of tectonic plates had to account for the faults at their boundaries but yet allow the movement of plates.

Computational Challenges

The challenge of getting both of those pieces of physics computed simultaneously meant that they needed computational methods that can handle vast changes in the mechanical properties from one plate to another plate as well as their faults.

Yet, the traditional ideas of plate motion failed to add up to enough force in the models to pull the Pacific Plate to the west and explain the bend.

"We discovered that there was another idea that had existed in the literature, but it wasn't getting much attention," Gurnis said.

New Factor

The new factor accounted for in the study was a subduction zone in the Russian Far East, a Kronotsky arc that terminated at about 50 million years ago. They built new plate tectonic reconstructions with these subduction zones.

When they put the zones in the models, they discovered that they could make the Pacific plate go to the north. And when that subduction terminated, the Pacific plate started to move to the west, slowly building up other subduction zones that over time provided more force to pull the Pacific plate.

"It's a new hypothesis that's much firmer in terms of the physics which it's based upon," Gurnis concluded. "It will allow other scientists to see if it will hold up to further scrutiny and if there are other ideas that can be tested on its assumptions."

Computational Resources

For the study, Gurnis was awarded access to the Stampede2 supercomputer at TACC through XSEDE funded by the National Science Foundation (NSF). He was also awarded access to the NSF-funded Frontera system also at TACC, the most powerful supercomputer in academia and the first phase of the NSF "Towards a Leadership Class Computing Facility" program.

"Both XSEDE and Frontera are absolutely vital for our research," Gurnis said.

"This capability computing is essential," he added. "We're spinning up projects with this collaboration that will be substantially larger than this, that are going to require something even beyond Frontera to compute."

This basic research aims to investigate mysteries about the dynamics of the past and present Earth.

"When you deal with some of the most fundamental processes in the earth, it's important to correctly figure out how they work," Gurnis said.

New Directions

He also highlighted the interplay between domain science and the applied work with computational scientists.

"The algorithms we've developed for adaptive mesh refinement can be applied to many pure and applied problems," Gurnis added. "That was a huge breakthrough."

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Agricultural expansion a major cause to doubling of annual tropical carbon loss over past two decades

Using multiple high-resolution satellite datasets, researchers from the Department of Civil Engineering at the University of Hong Kong (HKU) and Southern University of Science and Technology (SUSTech) found that tropical carbon loss has doubled over the past two decades due to excessive forest removal in the tropics.

The tropics are an important ecosystem as they store massive amounts of carbon in their woody vegetation and soil -- but they have suffered from extensive forest clearance since 2001. The researchers analysed the gross forest carbon loss associated with forest removal in the tropics (between 23.5° N and 23.5 S but excluding northern Australia) during the 21st century. They revealed a two-fold increase in gross tropical forest carbon loss worldwide from 0.97 gigatons of carbon per year in 2001-2005 to 1.99 gigatons of carbon per year in 2015-2019 due to rapid forest loss.

The study has been published in the academic journal Nature Sustainability in an article entitled "Doubling of annual forest carbon loss over the tropics during the early twenty-first century."

Given the key role of the tropics in the carbon cycle, the study poses serious implications. "The findings are critical because they suggest that existing strategies to reduce forest loss are questionable; this failure underscores the importance of monitoring deforestation trends following one of the new pledges made -- to halt and reverse deforestation -- by UN climate summit-the twenty-sixth Conference of the Parties (COP26) in Glasgow in November 2021," said Professor Ji CHEN from HKU's Department of Civil Engineering.

Tropical forests are the largest terrestrial component of the global carbon cycle, storing about 250 gigatons of biomass carbon in its woody vegetation and absorbing about 70 gigatons of atmospheric carbon per year through photosynthesis. The rapid and steady loss of forests could be devastating because it leads to the loss of stored carbon in biomass and soil. Deforestation also obstructs carbon sequestration or the process of capturing and retaining carbon dioxide.

"The doubling and acceleration in the loss of forest carbon, including biomass and soil organic carbon, is primarily driven by agricultural expansion which differs from current estimates of land-use change emissions in the assessments of the global carbon budget that shows a flat or decreasing trend. In addition to carbon, conversion of forests to agricultural lands also induces other environmental consequences, like biodiversity extinction and land degradation," said Yu FENG, a PhD candidate of the HKU and SUSTech joint programme.

Most of the tropical forest carbon loss (82%) was set off by agricultural expansion, for example shifting cultivation, particularly in Africa.

"While some agricultural lands may reappear as forested due to abandonment or policies, we still observed about 70% of former forest lands converted to agriculture in 2001-2019 remained so in 2020, confirming a dominant role of agriculture in long-term pan-tropical carbon reductions on formerly forested landscapes," said research team member Dr Zhenzhong Zeng, Associate Professor at SUSTech.

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Blowing bubbles in dough to bake perfect yeast-free pizza

In typical breads, yeast produces bubbles via a biochemical process, causing dough to rise and develop into light, airy, and tasty treats. Without that yeast, it is difficult to make morsels with the same characteristic taste and texture. The perfect, yeast-free pizza, as such a food, presents an important challenge for bakers and yeast-intolerant crust enthusiasts across the globe.

In Physics of Fluids, by AIP Publishing, researchers from the University of Naples Federico II developed a method to leaven pizza dough without yeast.

The team, which included its very own professional pizza-maker/graduate student, prepared the dough by mixing water, flour, and salt and placing it in a hot autoclave, an industrial device designed to raise temperature and pressure.

From there, the process is like the one used to produce carbonation in soda. Gas is dissolved into the dough at high pressure, and bubbles form in the dough as pressure is released during baking. In comparison to other scientific experiments, the pressures involved were mild. They can be obtained by a typical at-home coffee maker.

However, the scientists-turned-bakers had to be cautious with the pressure release. Compared to soda, pizza dough does not respond as nicely to an abrupt change in pressure.

"The key to the process is to design the pressure release rate not to stress the dough, which likes to expand gently," said author Ernesto Di Maio.

The authors evaluated their dough with rheology, which measures the flow and deformation of a material. Fine-tuning the pressure release through rheological analysis made it possible to gently inflate bubbles to the desired extent.

"We mainly studied how dough behaves with and without yeast. How the softness changes with leavening, and how the dough responds to a temperature program during baking," said author Rossana Pasquino. "This was fundamental to designing the pressure protocol for the dough without yeast."

After many unofficial taste tests, the researchers are purchasing a larger, food-grade autoclave that will make full-sized pizzas in future experiments. They hope to see their idea used in pizza shops.

"We had a lot of fun applying things we know well to delicious polymers, instead of our typical and sometimes boring smelly plastics," said Pasquino. "The idea of approaching food samples with the same technologies and knowledge used for thermoplastic polymers was surprisingly successful!"

As a person with a yeast allergy, Di Maio is also excited about applications for other leavened products like bread, cakes, and snacks.

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Shining a light on protein aggregation in Parkinson's disease

A novel system to control protein aggregation in a model of Parkinson's disease may answer longstanding questions about how the disease begins and spreads, according to a new study published March 9 in the open-access journal PLOS Biology by Abid Oueslati of Laval University, Quebec, Canada, and colleagues. Initial results suggest that aggregation of the protein alpha-synuclein plays a critical role in disrupting neuronal homeostasis and triggering neurodegeneration.

Parkinson's disease is a neurodegenerative disorder, marked clinically by tremor, stiffness, and slowed movements, as well as a host of nonmotor symptoms. Within affected neurons, molecules of a protein called alpha-synuclein can be seen to clump together, forming characteristic aggregates called Lewy bodies. But it has been hard to answer whether alpha-synuclein aggregation contributes to disease development or progression, and when it may act in the toxic disease cascade, or whether instead the aggregates are innocent bystanders to some other malevolent process, or are even protective. These elements have been difficult to determine, in part because aggregation in cellular and animal models has not been controllable in either time or space.

To address that problem, the authors turned to optobiology, a technique in which a protein of interest is fused to another protein that changes its conformation in response to light, allowing the behavior of the target protein to be manipulated selectively and reversibly. Here, the authors fused alpha-synuclein to a protein known as cryptochrome protein 2, from a mustard plant. They found that when light of the correct wavelength fell on the mustard protein, its conformational change triggered aggregation of its alpha-synuclein partner.

The aggregates that formed were reminiscent of Lewy bodies in multiple important ways, including that they included several other key proteins besides alpha-synuclein found in Lewy bodies in people with Parkinson's disease, and that the alpha-synuclein in the aggregates adopted the characteristic beta-sheet conformation seen in many diseases of misfolded proteins. The aggregates induced dislocation of multiple cellular organelles, as Lewy bodies have been recently reported to do as well. They also induced misfolding in alpha-synuclein molecules not attached to the cryptochrome protein, mimicking the prion-like spread of aggregation seen with alpha-synuclein in the diseased brain and animal models.

Finally, the authors delivered the genes for the alpha-synuclein-cryptochrome fusion protein to mice, directly into the substantia nigra, the structure in the brain that is most prominently affected by Parkinson's disease, and surgically placed an optic fiber to deliver light to the targeted cells. Light treatment led to formation of alpha-synuclein aggregates, neurodegeneration, disruption of calcium activity in downstream neuronal targets, and Parkinson-like motor deficits.

"Our results demonstrate the potential of this optobiological system to reliably and controllably induce formation of Lewy body-like aggregations in model systems, in order to better understand the dynamics and timing of Lewy body formation and spread, and their contribution to the pathogenesis of Parkinson's disease," Oueslati said.

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Soil erosion and wildfire another nail in coffin for Triassic era

Curtin research has revealed that soil erosion and wildfires contributed to a mass extinction event 201 million years ago that ended the Triassic era and paved the way for the rise of dinosaurs in the Jurassic period.

Lead author Curtin PhD graduate Dr Calum Peter Fox, from the WA-Organic and Isotope Geochemistry Centre (WA-OIGC) in Curtin's School of Earth and Planetary Sciences, said the research identified the other factors that contributed to a combination of stresses that killed off Triassic life and allowed the ecological expansion of dinosaurs.

"This new study adds soil erosion and wildfire activity to the list of factors that drove this mass extinction to end the Triassic era, building on our previous research that found a rise in levels of acid and hydrogen sulfide in the ocean caused by rapid increases in carbon dioxide due to a surge in volcanic activity," Dr Fox said.

"Similar to modern large-scale fire events that are driven by climate change, periods of wildfire activity have significant impacts for land-dwelling fauna and flora and drive environmental and ecosystem stress that can lead to mass extinctions."

Dr Fox said the team investigated fire events 201 million years ago during the end-Triassic mass extinction event, which featured similar increases to carbon dioxide to those witnessed in the modern-day conditions due to greenhouse gas emissions.

"By studying polycyclic aromatic hydrocarbons, which can be formed during the incomplete combustion of organic matter, we found that soil erosion was a more prominent terrestrial ecological stress than intensive wildfire activity during the end-Triassic mass extinction event in the Bristol Channel of the south-west United Kingdom.

"This tells us land and marine ecosystem and environmental stresses occurred at the same time and were likely exacerbated by soil erosion, with fire activity likely to be more localised in other areas rather than widespread across Europe."

Co-author John Curtin Distinguished Professor Kliti Grice, also from WA-OIGC in Curtin's School of Earth and Planetary Sciences, said modern-day soil erosion was a major cause of land degradation as it removed fertilised soil and promoted the deoxygenation of water columns, much like the mass extinction events of the past.

"These processes certainly have implications in the modern day due to the introduction of pollutants and pesticides," Professor Grice said. "Observing that soil erosion had major impacts in our history and in comparing and contrasting a global record of the past, we can anticipate the scale and duration of currently-occurring and future soil erosion events."

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The secret to staying young: New research highlights power of life long exercise to keep muscles healthy

Lifelong physical activity could protect against age-related loss of muscle mass and function, according to research published in The Journal of Physiology. Individuals aged 68 and above who were physically active throughout their life have healthier ageing muscle that has superior function and is more resistant to fatigue compared to inactive individuals, both young and old.

This is the first study to investigate muscle, stem cell and nerve activity in humans. The researchers from University of Copenhagen, Denmark, found that elderly individuals who keep physically active throughout their adult life, whether by taking part in resistance exercise, ball games, racket sports, swimming, cycling, running and/or rowing had a greater number of muscle stem cells, otherwise known as satellite cells in their muscle. These cells are important for muscle regeneration and long-term growth and protect against nerve decay.

46 male participants took part in the study. They were divided into three groups: young sedentary (15), elderly lifelong exercise (16) and elderly sedentary (15). They performed a heavy resistance exercise, sitting in a mechanical chair performing a knee extension movement to evaluate muscle function. The amount of force produced was measured. Blood samples were taken, and muscle biopsies were analysed from both legs. The researchers found elderly lifelong exercisers outperformed both the elderly and young sedentary adults.

Lead author, Casper Soendenbroe, University of Copenhagen, Denmark said:

"This is the first study in humans to find that lifelong exercise at a recreational level could delay some detrimental effects of ageing. Using muscle tissue biopsies, we've found positive effects of exercise on the general ageing population. This has been missing from the literature as previous studies have mostly focused on master athletes, which is a minority group. Our study is more representative of the general population aged 60 and above, as the average person is more likely to take part in a mixture of activities at a moderate level. That's why we wanted to explore the relation between satellite cell content and muscle health in recreationally active individuals. We can now use this as a biomarker to further investigate the link between exercise, ageing and muscle health."

"The single most important message from this study, is that even a little exercise seems to go a long way, when it comes to protecting against the age-related decline in muscle function. This is an encouraging finding which can hopefully spur more people to engage in an activity that they enjoy. We still have much to learn about the mechanisms and interactions between nerves and muscles and how these change as we age. Our research takes us one step closer."

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Taste, temperature and pain sensations are neurologically linked

If you have eaten a chili pepper, you have likely felt how your body reacts to the spicy hot sensation. New research published by biologists at the University of Oklahoma shows that the brain categorizes taste, temperature and pain-related sensations in a common region of the brain. The researchers suggest the brain also groups these sensations together as either pleasant or aversive, potentially offering new insights into how scientists might better understand the body's response to and treatment of pain.

"The spicy hot sensation you get from a chili pepper is actually a pain sensation…this follows activation of pain-related fibers that innervate the tongue and are heat sensitive," said Christian H. Lemon, Ph.D., an associate professor in the Department of Biology in the Dodge Family College of Arts and Sciences at OU. "What happens is a chemical in chili peppers, called capsaicin, causes activation of pain fibers and 'tricks' the neurons to react like there is a heat stimulus in your mouth, so you'll notice when you eat spicy foods, your body will react to try to remove the heat - your blood vessels can dilate and you can start to sweat because your body 'thinks' it's overheating."

Lemon, who is also a member of the OU Institute for Biomedical Engineering, Science and Technology, and researchers in his lab, Jinrong Li, Ph.D., and?Md Sams Sazzad Ali, Ph.D., published an article in The Journal of Neuroscience that examines how taste, temperature and pain-related sensations interact in the brain. Their article was also selected for the journal's Featured Research section.

"Neural messages associated with pain are partly carried by neural circuits involved with sensing temperature," Lemon said. "This would explain, for example, why when you touch a hot stove, it's a burning pain. There are intimate ties between temperature and pain, and there are intimate ties between temperature and taste…just about everything we eat is either warmed or cooled, and that's known to have a fairly robust effect on the way we perceive certain tastes."

The research team wanted to better understand how temperature and pain intersect with taste neurologically. Building on their previous research that had shown that temperature and taste signals come together in a particular section of the midbrain, Lemon's research group used mouse models under anesthesia to artificially stimulate temperature and pain-related fibers, combined with a physiological method to monitor the actions occurring in the brain to determine the connection between these senses.

"It's been known that temperature and taste can activate some of the same cells in the brain, but this was rarely systematically studied," he said. "We wanted to know if the temperature responses that we were seeing in this part of the brain were actually attributable to activation of thermal and pain-related fibers that innervate the head, face and mouth. To do this we used a modern genetic technology where we could insert a protein into these 'temperature/pain' cells that allowed us to control these cells with blue light -- we could turn the cells on with a light, like a light switch."

"What we found is that these neurons that scientists have studied for a long time as taste neurons actually respond to artificial stimulation of these temperature/pain cells," he added. "This is significant because most scientists that have looked at taste, they're usually only studying neural circuits from the perspective of taste. Pain scientists are usually only looking at pain-related responses, but they actually come together in this part of the midbrain, and not only do they come together, they do so in a very systematic way where preferred tastes and preferred temperatures are separated from adverse taste and temperatures in terms of the way that the responses are happening in this part of the brain."

The researchers categorize preferred or pleasurable tastes as something sweet, like sugar, whereas adverse tastes are bitter -- which can signify that something may be toxic or harmful. Similarly, people, and mice, have preferred temperatures, like a comfortably warmed or cooled environment as compared to an extreme cold or extreme heat stimulus.

Through this artificial stimulation of temperature/pain cells and the corresponding taste neurons, they discovered the brain segregated preferable tastes and temperatures from adverse tastes and temperatures. This finding offers new insights into how these senses interact, which could have implications for how scientists understand the brain's responses to stimuli that cause pain.

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Scientists determine structure of a DNA damage 'first responder'

DNA is often likened to a blueprint. The particular sequence of As, Cs, Gs, and Ts in DNA provides information for building an organism.

What's not captured by this analogy is the fact that our DNA requires constant upkeep to maintain its integrity. Were it not for dedicated DNA repair machinery that routinely fixes mistakes, the information within DNA would be rapidly degraded.

This repair happens at cell cycle checkpoints that are activated in response to DNA damage. Like a quality assurance agent on an assembly line, proteins that participate in the DNA damage checkpoint assess the cell's DNA for mistakes and, if necessary, pause cell division and make repairs. When this checkpoint breaks down -- which can happen as a result of genetic mutations -- DNA damage builds up, and the result is often cancer.

Though scientists have learned much about DNA damage and repair over the past 50 years, important outstanding questions remain. One particularly bedeviling puzzle is how a repair protein called the 9-1-1 clamp -- a DNA damage "first responder" -- attaches itself to the site of a broken DNA strand to activate of the DNA damage checkpoint.

"We know that this attachment is a pivotal step necessary for initiating an effective repair program," says Dirk Remus, a molecular biologist at the Sloan Kettering Institute (SKI) who studies the fundamentals of DNA replication and repair. "But the mechanisms involved are completely obscure."

Now, thanks to a collaboration between Dr. Remus' lab and that of SKI structural biologist Richard Hite, a clear picture of how the 9-1-1 clamp is recruited to sites of DNA damage has emerged. The results, which challenge conventional wisdom in the field, were published March 21, 2022, in the journal Nature Structural and Molecular Biology.

Complementary Expertise Yields Surprising Results

The startling discoveries grew out of a collaboration between two labs with complementary expertise. Dr. Remus' lab uses biochemical methods to study the process of DNA replication and repair. A primary goal of his research over the past several years has been to reconstitute the entire DNA replication-and-repair process in a test tube, apart from a surrounding cell.

As a result of this effort, his lab has purified several components of the repair machinery, including 9-1-1 proteins and proteins that facilitate the binding of 9-1-1 to DNA.

Dr. Remus realized that if these complexes could be viewed at atomic resolution, they would provide a set of freeze-frame images of the individual steps in the repair process. That's when he turned to Dr. Hite's lab for help.

"I said, 'We have this complex; can you help us determine its molecular structure to figure out how it works?' And that's what he did."

Dr. Hite is a structural biologist with expertise in using a technique called cryo-electron microscopy (cryo-EM), which enables the study of proteins and protein assemblies by visualizing their fine-grain movements at resolutions that can reveal the positions of individual amino acids within the proteins. Much like the gears and levers of a machine, it's these movements of amino acids that allow proteins to serve as the workhorses of the cell, including those that repair DNA.

"When Dirk came to us, we realized that many of the tools that our lab has developed over the past few years were perfectly suited to answering this question," Dr. Hite says. "Using cryo-EM, we're able to not only determine one structure but an ensemble of structures. By putting these structures together in a logical pattern, based on the new data and previous biochemical data, we can come up with a proposal for how this clamp works."

They did, and the results were surprising.

"The model we developed had interesting features that contradicted what had been previously thought to be the way these types of clamps are being loaded onto DNA," Dr. Hite says.

"When Rich first produced the structure, I thought he got it wrong because it was against all the expectations," Dr. Remus adds. "Now, in hindsight, it all makes perfect sense."

A New Model for Opening and Closing a DNA Clamp Around DNA

The 9-1-1 clamp is shaped like a ring. To carry out its function, it needs to surround the broken DNA at the junction between an exposed end of one strand of a double-stranded piece of DNA abutting a single-stranded one. Consequently, the ring structure of the 9-1-1 clamp must open to allow the single-stranded DNA to swing into the center of the clamp and then reclose around it. This does not occur spontaneously but is facilitated by another protein complex, called the clamp loader complex.

"It had been thought from all studies prior to this that clamps would open in the manner of lock washer, where basically the two open ends of the clamp would rotate out of plane to create a narrow gap," Dr. Remus says. "But what Rich observed is that the 9-1-1 clamp opens much more widely than anticipated, and it opens completely in plane -- there's no twisting like in the lock-washer scenario."

The scientists point out that the lock-washer model has been around for two decades and has been the guiding paradigm in the field for how a clamp gets loaded around DNA. But in this case, it's wrong.

Another surprise was that the 9-1-1 clamp loader complex was observed to bind DNA in the opposite orientation from other clamp loader complexes that act on undamaged DNA during normal DNA replication. This observation explained how 9-1-1 is specifically recruited to sites of DNA damage.

From Basic to Translational Research

Aside from providing a satisfying answer to a fundamental biological puzzle, Dr. Remus thinks the research may eventually lead to better cancer drugs.

Many existing chemotherapy drugs work by interfering with DNA replication of cancer cells and generating the type of DNA damage that is normally fixed by repair processes elicited by the 9-1-1 clamp. Because cancer cells already have a reduced ability to repair DNA damage, the addition of DNA-damaging chemotherapy drugs can overwhelm the cells' ability to fix their DNA, and so they die. (This is how drugs called PARP inhibitors work, for example.)

With this new knowledge about how 9-1-1 interacts with other repair proteins and with DNA, scientists could potentially design drugs that interfere specifically with this step of the repair process, making chemotherapy drugs even more effective.

"One of the great things about working here at SKI is that a basic scientist's research can be the starting point for translational studies that ultimately lead to better treatments," Dr. Hite says.

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Comet 67P’s abundant oxygen more of an illusion, new study suggests

When the European Space Agency's Rosetta spacecraft discovered abundant molecular oxygen bursting from comet 67P/Churyumov-Gerasimenko (67P) in 2015, it puzzled scientists. They had never seen a comet emit oxygen, let alone in such abundance. But most alarming were the deeper implications: that researchers had to account for so much oxygen, which meant reconsidering everything they thought they already knew about the chemistry of the early solar system and how it formed.

A new analysis, however, led by planetary scientist Adrienn Luspay-Kuti at the Johns Hopkins Applied Physics Laboratory (APL) in Laurel, Maryland, shows Rosetta's discovery may not be as strange as scientists first imagined. Instead, it suggests the comet has two internal reservoirs that make it seem like there's more oxygen than is actually there.

"It's kind of an illusion," Luspay-Kuti said. "In reality, the comet doesn't have this high oxygen abundance, at least not as far as its formation goes, but it has accumulated oxygen that gets trapped in the upper layers of the comet, which then gets released all at once."

While common on Earth, molecular oxygen (two oxygen atoms doubly linked to each other) is markedly uncommon throughout the universe. It quickly binds to other atoms and molecules, especially the universally abundant atoms hydrogen and carbon, so oxygen appears only in small amounts in just a few molecular clouds. That fact led many researchers to conclude any oxygen in the protosolar nebula that formed our solar system likely had been similarly scooped up.

When Rosetta found oxygen pouring out of comet 67P, however, everything turned on its head. Nobody had seen oxygen in a comet before, and as the fourth most abundant molecule in the comet's bright coma (after water, carbon dioxide and carbon monoxide), it needed some explanation. The oxygen seemed to come off the comet with water, causing many researchers to suspect the oxygen was either primordial -- meaning it got tied up with water at the birth of the solar system and amassed in the comet when it later formed -- or formed from water after the comet had formed.

But Luspay-Kuti and her team were skeptical. As the comet's dumbbell shape gradually rotates, each "bell" (or hemisphere) faces the Sun at various points, meaning the comet has seasons so the oxygen-water connection might not be present all the time. On short time frames, volatiles could potentially turn on and off as they thaw and refreeze with the seasons.

Now You See It, Now You Don't

Taking advantage of these seasons, the team examined the molecular data on short- and long-time periods just before the comet's southern hemisphere entered summer and then again just as its summer ended. As reported in their study, published March 10 in Nature Astronomy, the team found that as the southern hemisphere turned away and was sufficiently far from the Sun, the link between oxygen and water disappeared. The amount of water coming off the comet dropped precipitously, so instead the oxygen seemed strongly linked to carbon dioxide and carbon monoxide, which the comet was still emitting.

"There's no way that should be possible under the previous explanations suggested," Luspay-Kuti said. "If oxygen were primordial and tied to water in its formation, there shouldn't be any time that oxygen strongly correlates with carbon monoxide and carbon dioxide but not water."

The team instead proposed the comet's oxygen doesn't come from water but from two reservoirs: one made of oxygen, carbon monoxide and carbon dioxide deep inside the comet's rocky nucleus, and a shallower pocket closer to the surface where oxygen chemically combines with water ice molecules.

The idea goes like this: A deep reservoir of oxygen, carbon monoxide and carbon dioxide ice is constantly emitting gases because oxygen, carbon dioxide and carbon monoxide all vaporize at very low temperatures. As oxygen traverses from the comet's interior toward the surface, however, some chemically inserts into water ice (a major constituent of the comet's nucleus) to form a second, shallower oxygen reservoir. But water ice vaporizes at a much higher temperature than oxygen, so until the Sun sufficiently heats the surface and vaporizes the water ice, the oxygen is stuck.

The consequence is that oxygen can accumulate in this shallow reservoir for long periods until the comet surface is finally warmed enough for water ice to vaporize, releasing a plume far richer in oxygen than was actually present in the comet.

"Put another way, the oxygen abundances measured in the comet's coma aren't necessarily reflecting its abundances in the comet's nucleus," Luspay-Kuti explained.

The comet would consequently also vacillate with the seasons between strongly associating with water (when the Sun heats the surface) and strongly associating with carbon dioxide and carbon monoxide (when that surface faces away from the Sun and the comet is sufficiently far) -- exactly what Rosetta observed.

"This isn't just one explanation: It's the explanation because there is no other possibility," said Olivier Mousis, a planetary scientist from France's Aix-Marseille Université and a study co-author. "If oxygen were just coming from the surface, you wouldn't see these trends observed by Rosetta."

The major implication, he said, is that it means comet 67P's oxygen is, in fact, oxygen that accreted at the beginning of the solar system. It's just that it's only a fraction of what people had thought.

Luspay-Kuti said she wants to probe the topic more deeply by examining the comet's minor molecular species, such as methane and ethane, and their correlation with molecular oxygen and other major species. She suspects this will help researchers get a better idea of the type of ice that the oxygen was incorporated into.

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Those with facial scars rate their own appearance more critically than surgeons and strangers

Patients who undergo facial surgery think their surgical scars look worse than surgeons and independent observers do, according to a new study from the Perelman School of Medicine at the University of Pennsylvania. Surgeons and those not tied personally to the particular scarring felt similarly about how significant a scar appeared, but those who looked at their own faces had more negative feelings about the condition and appearance of the scar. Researchers say that surgeons should explain to their patients in detail how their scar will likely look post-surgery and explicitly say to their patients that they themselves will likely perceive their scars to be more significant than others will. The study is published in the journal Facial Plastic Surgery & Aesthetic Medicine.

Eighty-one patients who had facial skin cancer and then received Mohs micrographic surgery (a type of precise skin surgery where layers of skin are removed a little at a time) rated their scars a week after surgery and then three months after. While their feelings about their scar improved by roughly 40% from week one to the three-month mark, they still judged their scars more critically than Mohs surgeons and independent observers after three months.

"Our research seems to support the saying 'we are our own worst critics,'" said senior author Joseph F. Sobanko, MD, director of Dermatologic Surgery Education and an associate professor of Dermatology at Penn. "Patients are probably going to view scarring on their faces as more severe than their own surgeon will and even someone they walk by on the street."

Armed with that knowledge, surgeons should speak to their patients not just about the process of surgery but also what to expect during the healing process and what their face will look like after the incision is completely healed, Sobanko said.

"Our goal as surgeons should be to remove cancer effectively while minimizing scarring," Sobanko added. "Nevertheless, skin cancer surgery will produce highly visible changes early in the healing process and our job as surgeons is to prepare patients for how their skin will look during the healing process. We should also be direct with our patients and tell them that they are going to be the most critical of their appearance."

The Penn researchers made very specific choices when designing the study. The team decided to use facial scarring because of the obviously personal relationship people have with their faces. Previous research from Sobanko and colleagues showed that people are the most sensitive about scars on their faces compared to scars on other parts of their body. The researchers also chose to have participants assess scars at the one-week mark and at three months.

"At one week, incisions from surgery are quite visible, and that can be very jarring for patients," Sobanko said. "As weeks progress the incisions heal predictably and our prior research has shown that most patients return to their baseline quality of life approximately 3 months after surgery."

While the advice for providers is to be honest and clear with their patients about scarring, Sobanko and his team are planning to study specific ways that surgeons can help patients feel better about their surgical mark.

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