The study by researchers at North Carolina State University examined the interactions of warmer temperatures, crop yield risk and crop insurance participation by farmers. For the study, researchers developed models using historical county-level corn and soybean production data in the United States, with an eye toward understanding the production impacts of rising temperatures.

The researchers found that variation in crop yields due to higher temperatures rose when more farmers had crop insurance. Interestingly, the results showed greater variability effects for corn yields than for soybean yields.

“This could be an unintended consequence of providing subsidies for crop insurance,” said Rod M. Rejesus, professor of agricultural and resource economics at NC State and the corresponding author of the research study. “The concept of moral hazard could be present here. If insurance will cover crop losses due to various effects like drought or severe weather, a farmer may not want to pay the extra expense for climate change adaptation efforts such as using cover crops to improve soil health, for example.”

Climate change — including warmer temperatures — increases the variability of crop yields; farming becomes a riskier proposition as this variability rises.

The study models indicate that an increase of daily minimum and maximum temperatures of 1 degree Celsius would increase county-level corn yield variability by 8.6 bushels per acre if 80% of farmers in a county have crop insurance. The same temperature rise in a county with 10% crop insurance participation would increase corn yield variability by just 6.2 bushels per acre.

The researchers pose possible solutions to this quandary for policymakers. They include providing more subsidies to encourage farmers’ use of climate change mitigation efforts — like soil health practices — and starting high-level policy conversations about how to possibly tweak rules and guidelines that govern crop insurance contracts in order to reduce the disincentive effects.

Rejesus will continue to study the effects of climate change, crop yields and crop insurance, including the role of certain climate mitigation efforts by farmers.

The paper appears in the European Review of Agricultural Economics. Former NC State Ph.D. student Ruixue Wang is the paper’s first author. NC State postdoctoral researcher Serkan Aglassan also co-authored paper. Support for the work was provided in part by the U.S. Department of Agriculture’s NIFA Hatch Project No. NC02696.

Story Source:

Materials provided by North Carolina State University. Original written by Mick Kulikowski. Note: Content may be edited for style and length.

Until now, quantum computer engineers and scientists have worked with a proof-of-concept model of quantum processors by demonstrating the control of only a handful of qubits.

But with their latest research, published today in Science Advances, the team have found what they consider ‘the missing jigsaw piece’ in the quantum computer architecture that should enable the control of the millions of qubits needed for extraordinarily complex calculations.

Dr Jarryd Pla, a faculty member in UNSW’s School of Electrical Engineering and Telecommunications says his research team wanted to crack the problem that had stumped quantum computer scientists for decades: how to control not just a few, but millions of qubits without taking up valuable space with more wiring, using more electricity, and generating more heat.

“Up until this point, controlling electron spin qubits relied on us delivering microwave magnetic fields by putting a current through a wire right beside the qubit,” Dr Pla says.

“This poses some real challenges if we want to scale up to the millions of qubits that a quantum computer will need to solve globally significant problems, such as the design of new vaccines.

“First off, the magnetic fields drop off really quickly with distance, so we can only control those qubits closest to the wire. That means we would need to add more and more wires as we brought in more and more qubits, which would take up a lot of real estate on the chip.”

And since the chip must operate at freezing cold temperatures, below -270°C, Dr Pla says introducing more wires would generate way too much heat in the chip, interfering with the reliability of the qubits.

“So we come back to only being able to control a few qubits with this wire technique,” Dr Pla says.

Lightbulb moment

The solution to this problem involved a complete reimagining of the silicon chip structure.

Rather than having thousands of control wires on the same thumbnail-sized silicon chip that also needs to contain millions of qubits, the team looked at the feasibility of generating a magnetic field from above the chip that could manipulate all of the qubits simultaneously.

This idea of controlling all qubits simultaneously was first posited by quantum computing scientists back in the 1990s, but so far, nobody had worked out a practical way to do this — until now.

“First we removed the wire next to the qubits and then came up with a novel way to deliver microwave-frequency magnetic control fields across the entire system. So in principle, we could deliver control fields to up to four million qubits,” says Dr Pla.

Dr Pla and the team introduced a new component directly above the silicon chip — a crystal prism called a dielectric resonator. When microwaves are directed into the resonator, it focuses the wavelength of the microwaves down to a much smaller size.

“The dielectric resonator shrinks the wavelength down below one millimetre, so we now have a very efficient conversion of microwave power into the magnetic field that controls the spins of all the qubits.

“There are two key innovations here. The first is that we don’t have to put in a lot of power to get a strong driving field for the qubits, which crucially means we don’t generate much heat. The second is that the field is very uniform across the chip, so that millions of qubits all experience the same level of control.”

Quantum team-up

Although Dr Pla and his team had developed the prototype resonator technology, they didn’t have the silicon qubits to test it on. So he spoke with his engineering colleague at UNSW, Scientia Professor Andrew Dzurak, whose team had over the past decade demonstrated the first and the most accurate quantum logic using the same silicon manufacturing technology used to make conventional computer chips.

“I was completely blown away when Jarryd came to me with his new idea,” Prof. Dzurak says, “and we immediately got down to work to see how we could integrate it with the qubit chips that my team has developed.

“We put two of our best PhD students on the project, Ensar Vahapoglu from my team, and James Slack-Smith from Jarryd’s.

“We were overjoyed when the experiment proved successful. This problem of how to control millions of qubits had been worrying me for a long time, since it was a major roadblock to building a full-scale quantum computer.”

Once only dreamt about in the 1980s, quantum computers using thousands of qubits to solve problems of commercial significance may now be less than a decade away. Beyond that, they are expected to bring new firepower to solving global challenges and developing new technologies because of their ability to model extraordinarily complex systems.

Climate change, drug and vaccine design, code decryption and artificial intelligence all stand to benefit from quantum computing technology.

Looking ahead

Next up, the team plans to use this new technology to simplify the design of near-term silicon quantum processors.

“Removing the on-chip control wire frees up space for additional qubits and all of the other electronics required to build a quantum processor. It makes the task of going to the next step of producing devices with some tens of qubits much simpler,” says Prof. Dzurak.

“While there are engineering challenges to resolve before processors with a million qubits can be made, we are excited by the fact that we now have a way to control them,” says Dr Pla.

The study, published today in the journal Cancer by researchers at Virginia Commonwealth University Massey Cancer Center, analyzed data from nearly 20,000 people over a span of four years and found that reports of marijuana use peaked at 9% for cancer patients, compared to 14% among people with no cancer history.

“Even when we looked at whether someone used cannabis over the four years of observation and we control for things like age and race, cancer patients are still not increasing their use over time like the general population,” said study lead author Bernard Fuemmeler, Ph.D., M.P.H., associate director for population science and interim co-leader of the Cancer Prevention and Control research program at VCU Massey Cancer Center. “I would have expected them to have at least mirrored what was happening in the general population.”

This paper drew on data collected between 2013 and 2018 from the Population Assessment of Tobacco and Health (PATH), which tracks a representative sample of Americans to survey smoking behaviors, including both tobacco and marijuana.

For people who never had cancer, rates of marijuana use rose during the four-year PATH study period. This same period saw a wave of recreational marijuana legalization sweep across the nation.

“Because of law enforcement changing, we expect to see changes in attitudes and perceived benefits and harms,” said study co-author Sunny Jung Kim, Ph.D., Harrison Scholar at VCU Massey Cancer Center and assistant professor of health behavior and policy at the VCU School of Medicine. “This work gives us perspective on prevalence of cannabis use among cancer patients and how it has changed over time.”

But why aren’t cancer patients following the same trend as the rest of the population? The odds of a cancer patient using marijuana in the past year were essentially flat between 2013 and 2018.

“There is that element of a life-changing moment when you have cancer,” said Fuemmeler, who is also a professor of health behavior and policy in the VCU School of Medicine and holds the Gordon D. Ginder, M.D., Chair in Cancer Research at Massey. “You have to be mindful of your health and contemplate whether something like cannabis is helpful or hurtful.”

Regardless of cancer history, this latest analysis revealed that people who reported higher levels of pain were more likely to use marijuana, whereas lower rates of marijuana use were seen among women, older people and those with higher incomes, medical insurance or better mental health.

The authors note the need for greater research into the health effects of marijuana use for cancer patients and survivors so that doctors and patients can have more informed conversations about whether the potential benefits might outweigh the risks.

“As with all health decisions, it’s best to talk to your doctor before making any big changes,” said study co-author Egidio Del Fabbro, M.D., the Thomas Palliative Care Endowed Chair and director of palliative care at VCU Massey Cancer Center and professor of internal medicine at VCU. “Now that marijuana is becoming legal in more parts of the country, we’re expecting more questions, and although we may not have all the answers, we’re here to listen and provide our patients with the best available evidence.”

Additional authors on the study include Elizabeth Do, Ph.D., and Albert Ksinan, Ph.D., both of the VCU Department of Health Behavior & Policy.

This research was funded by Massey’s NCI Cancer Center Support Grant P30 CA016059.

Story Source:

Materials provided by Virginia Commonwealth University. Original written by Erin Hare, VCU Massey Cancer Center. Note: Content may be edited for style and length.

The biology of trees makes them resilient to even the most severe stressors. “Oak trees are planners, in a way,” says Meghan Blumstein, NSF Post-doctoral Research Fellow at MIT and a co-author of the study. “Some of the food they make during the growing season is used immediately for energy and some is stored in the stems and roots for a rainy day. With stored carbs, they are able to immediately create a new flush of leaves after an insect outbreak.”

But trees are not invincible, and the new study reveals the specific threshold of reserves necessary for them to survive: 1.5 percent carbohydrates in their dried wood- or about 20-25% of their normal storage capacity. The repeated emergence of Lymantria dispar (an insect formerly known as “gypsy moth”) from 2016 to 2018 challenged trees’ resilience by defoliating them year after year.

“The trees that died were the trees that were out of reserves,” says lead author Audrey Barker Plotkin, a Senior Scientist at the Harvard Forest. But the location of the trees mattered, too. The research team found that trees growing along forest edges tended to have more reserves, even at the same level of defoliation, making them more resilient than interior forest trees. The research team posits that forest edge trees may have simply experienced less severe defoliation in the years before 2018. And, because edge trees get lots of light, they may also be able to rebound without drawing down their reserves as much as their interior forest counterparts.

The new study provides direct evidence, that had until now been lacking, that trees can indeed starve to death when insects invade. This more nuanced understanding will help improve forest resilience models as new pests and a shifting climate continue to drive change in the region.

The Harvard Forest, founded in 1907 and located in Petersham, Mass., is Harvard University’s outdoor laboratory and classroom for ecology and conservation, and a Long-Term Ecological Research (LTER) site funded by the National Science Foundation. Its 4,000-acre property is one of the oldest and most intensively studied research forests in the U.S. More information can be found at: http://harvardforest.fas.harvard.edu/

More information

Read a blog post about the study, written by lead author Audrey Barker Plotkin, at: https://functionalecologists.com/2021/08/13/audrey-barker-plotkin-trees-can-starve-to-death-from-insect-defoliation/

Story Source:

Materials provided by Harvard University. Note: Content may be edited for style and length.

However, not all plastics — or their polymers — are created equal. The longer and stronger the polymer, the more durable the material.

Cornell researchers took a middling monomer and, by using a special catalyst, they created a tougher polymer that can form long chains. The polymer can then be easily depolymerized back to the monomer state with an acid catalyst, resulting in a chemically recyclable thermoplastic that competes with the most popular plastics, polyethylene and polypropylene.

The team’s paper, “Chemically Recyclable Thermoplastics from Reversible-Deactivation Polymerization of Cyclic Acetals,” published Aug. 13 in Science.

The co-lead authors are former postdoctoral researcher Brooks Abel and Rachel Snyder, Ph.D. ’21.

“Ideally, the perfect polymer is one that has really high initial stresses and then it undergoes really good elongation,” said Geoffrey Coates, the Tisch University Professor in the College of Arts and Sciences, and the paper’s senior author. “The polymers you’ve probably heard of, polyethylene and polypropylene, they just have great properties. A lot of new polymers don’t compare well with these tried-and-true ones. Our polymer is right in the middle of the pack. It has been around for 60 or 70 years, but no one’s been able to make really long chains of it and get really good properties.”

In an unexpected twist, the discovery didn’t emerge from conventional plastics research but rather from the Coates Group’s involvement with the Joint Center for Energy Storage Research, an interdisciplinary collaboration launched by the U.S. Department of Energy to realize next-generation batteries. Coates and his team had been working to develop sustainable polymers that can be used in energy storage and conversion materials when they realized their polymer — poly(1,3-dioxolane) or PDXL — was well-suited for creating a thermoplastic — a material with properties that allow it to be melted, recycled and remolded.

The researchers built their polymer from a cyclic acetal monomer called dioxolane, which is synthesized from potentially biorenewable formaldehyde and ethylene glycol feedstocks. Polyacetals are strong candidates for creating recyclable thermoplastics because they are stable upward of 300 degrees Celsius, but depolymerize at relatively low temperatures — usually below 150 degrees Celsius — in the presence of an acid catalyst. They are also inexpensive and can be biologically sourced. However, polyacetals have not seen prior use because the polymer chains are generally too short to achieve the mechanical strength necessary for commercial applications.

“We wanted to develop a new way to make polyacetals that would give us control over the length of the polymer chains,” Abel said. “Ultimately, we were able to make really high molecular weight polyacetals that were surprisingly ductile and strong as compared to their more brittle, low molecular weight counterparts.”

“If you want to make a cup that doesn’t crack when you flex it, you need to get really high molecular weight,” Coates said.

Using a process called reversible-deactivation cationic ring-opening polymerization, the researchers were able to connect the monomers into long chains of PDXL that have high molecular weight and high tensile strength.

The resulting thermoplastic is strong and flexible enough to be used for large-scale applications such as packaging products. The team demonstrated this potential by creating several prototype items, including protective pouches, molded packaging and inflatable air pillows of the sort Amazon uses to pad their boxes.

“Right now, nearly 40% of plastic is produced for packaging products that are used briefly and then disposed,” Snyder said. “PDXL has the necessary strength for packaging, but instead of throwing it away, we can collect and repurpose it using a very efficient chemical recycling process. This makes it a perfect candidate for a circular polymer economy.”

The recycling process is so efficient that PDXL can even be depolymerized from complex mixtures of plastic waste. The team mixed PDXL with other commodity plastics like polyethylene terephthalate, polyethylene and polystyrene. After applying a reusable acid catalyst and heat, they were able to recover 96% of the pure dioxolane monomer, demonstrating that it can be easily isolated from common contaminants like dyes and plasticizers. The recovered monomer was then repolymerized to PDXL, illustrating the circularity of polyacetal chemical recycling.

This points to the polymer’s most significant attribute: its sustainability.

“It takes a lot of fossil fuels to make these plastics, and the carbon footprint of common polyethylene or polypropylene is really bad. So we’ve got to be better at how we make them,” Coates said. “If you can have a way that you can chemically recycle the polymer, it’s not going to go in the ocean, right? And then instead of using all this energy to take oil out of the ground and break it up in little pieces and spend all this energy, all we have to do is just heat up the polymer and boom, we have a monomer again.”

The research was supported by the U.S. Department of Energy through the Joint Center for Energy Storage Research.

Story Source:

Materials provided by Cornell University. Original written by David Nutt, courtesy of the Cornell Chronicle. Note: Content may be edited for style and length.

The carbon footprint to create blue hydrogen is more than 20% greater than using either natural gas or coal directly for heat, or about 60% greater than using diesel oil for heat, according to new research published in Energy Science & Engineering.

Robert Howarth, professor of ecology and environmental biology at Cornell, together with Mark Z. Jacobson, professor of civil and environmental engineering at Stanford, authored the report.

Blue hydrogen starts with converting methane to hydrogen and carbon dioxide by using heat, steam and pressure, or gray hydrogen, but goes further to capture some of the carbon dioxide. Once the byproduct carbon dioxide and the other impurities are sequestered, it becomes blue hydrogen, according to the U.S. Department of Energy.

The process to make blue hydrogen takes a large amount of energy, according to the researchers, which is generally provided by burning more natural gas.

“In the past, no effort was made to capture the carbon dioxide byproduct of gray hydrogen, and the greenhouse gas emissions have been huge,” Howarth said. “Now the industry promotes blue hydrogen as a solution, an approach that still uses the methane from natural gas, while attempting to capture the byproduct carbon dioxide. Unfortunately, emissions remain very large.”

Methane is a powerful greenhouse gas, Howarth said. It is more than 100 times stronger as an atmospheric warming agent than carbon dioxide when first emitted. The United Nations’ Intergovernmental Panel on Climate Change report released on Aug. 9 shows that cumulatively to date over the past century, methane has contributed about two-thirds as much to global warming as carbon dioxide has, he said.

Emissions of blue hydrogen are less than for gray hydrogen, but only by about 9% to 12%.

“Blue hydrogen is hardly emissions free,” wrote the researchers. “Blue hydrogen as a strategy only works to the extent it is possible to store carbon dioxide long-term indefinitely into the future without leakage back to the atmosphere.”

On Aug. 10, the U.S. Senate passed its version of the $1 trillion Infrastructure Investment and Jobs Act, which includes several billion dollars to develop, subsidize and strengthen hydrogen technology and its industry.

“Political forces may not have caught up with the science yet,” Howarth said. “Even progressive politicians may not understand for what they’re voting. Blue hydrogen sounds good, sounds modern and sounds like a path to our energy future. It is not.”

An ecologically friendly “green” hydrogen does exist, but it remains a small sector and it has not been commercially realized. Green hydrogen is achieved when water goes through electrolysis (with electricity supplied by solar, wind or hydroelectric power) and the water is separated into hydrogen and oxygen.

“The best hydrogen, the green hydrogen derived from electrolysis — if used wisely and efficiently — can be that path to a sustainable future,” Howarth said. “Blue hydrogen is totally different.”

This research was supported by a grant from the Park Foundation. Howarth is a fellow at the Cornell Atkinson Center for Sustainability.

Story Source:

Materials provided by Cornell University. Original written by Blaine Friedlander, courtesy of the Cornell Chronicle. Note: Content may be edited for style and length.

A paper published in the Proceedings of the National Academy of Sciences (PNAS) and co-authored by Beth Pruitt, a UC Santa Barbara professor of mechanical engineering and the director of the campus’s Institute for BioEngineering, describes the results of a complex long-term collaboration that included researchers at Stanford University, the University of Washington, and the University of Kentucky. The study has led to new understanding of how genetic mutations play out at the cellular level to cause HCM, and new perspectives on how to prevent it.

In their paper, the authors explain that more than one thousand genetic mutations that cause HCM have been identified. The majority of them are found in genes that encode sarcomeric proteins, the structural building blocks of heart muscle responsible for generating and regulating contraction and relaxation. Roughly a third of the mutations are located in beta cardiac myosin, the primary protein that drives contraction of the heart cells. Contraction of the heart muscle, and every other muscle in our bodies, results from a process in which the motor protein myosin “walks” along a chain of actin molecules, a process known as the cross-bridge cycle. During this process, chemical energy in the form of ATP is converted to mechanical energy, ultimately leading to cardiac contraction.

Prior to a contraction, the head of one strand of an intertwined two-strand myosin molecule is tucked up against an actin molecule. Muscle contraction is initiated when a molecule of ATP, known as the “energy currency” of biological systems, binds to the myosin head. The myosin head, and the attached ATP, then detaches from the actin, initiating hydrolysis of the ATP, which is transformed into ADP plus a phosphate group. That process releases energy that “cocks” the myosin protein into a high-energy state and changes the shape of the myosin so that it is ready to crawl along the actin. At that point, the phosphate is released from the myosin, causing the myosin to push on the actin and release the phosphate, which leads the myosin to walk to the next chain of actin and contract the muscle. All of this, involving millions of heads of myosin walking across actin in steps that take microseconds to complete, must occur at the proper rate in order to maintain heart health.

Because HCM is often observed in patients having mutations in the beta cardiac myosin protein, it had been hypothesized that HCM mutations cause a cascade of events that manifest, ultimately, in damage to the heart itself. This study put that idea to the test, focusing on a single mutation, P710R, which dramatically decreased in vitro motility velocity — the rate at which the myosin motor walks on actin — in contrast to other MYH7 mutations, which led to increased motility velocity.

The overarching research question of this project was to learn how a mutation linked to heart disease in patients changes heart function at a cellular level.

The team used CRISPR technology to edit human induced pluripotent derived stem cell cardiomyocytes (cells responsible for heart contraction) by inserting the P710R mutation into them. Pruitt leads the stem cell bank at UCSB, where “clean” cell lines, having no genetic abnormalities, are maintained and reproduced for university researchers. Such clean, mutation-free lines provide a perfect benchmark for comparison with cells to see very precisely the effects of the P710R mutation. For example, the research team is now testing the effects of different mutations linked to heart disease in the same genetic background.

“You can have ten people with the same gene mutation in this protein, and they can have varying degrees of clinical significance, because the rest of their genome is different; that’s what makes us individuals,” Pruitt said. “These lines let us examine what is a result of the genetic mutation. By comparing the effect of different mutations, we can begin to tease apart how these changes lead to HCM. It allows us to look closely at how and why the cells adapt to the mutation in that way, and to get data and relate it to the thickness of the heart wall and all the other things that happen downstream.”

This research began nearly 15 years ago, while Pruitt was still at Stanford, and led to this collaborative paper. Now CRISPR technology enables researchers to design cells expressing specific mutations that are linked to cardiac diseases, and then assess molecular and functional changes to determine the cellular impact of individual mutations that have been identified in patients with HCM. These studies will provide a mechanistic understanding of how individual mutations at the molecular level translate to HCM in patients.

In this project, once the mutation was introduced, the cells were assayed in a collaboration between the Pruitt lab (UCSB) and the Bernstein lab (Stanford University), using traction force microscopy, an assay that allows simultaneous observation of a beating cell and the force it generates. The Spudich lab (Stanford), led separate studies of the same mutated protein at the molecular level using an optical trap, in which light pressure is applied to control precisely the location and force of an actin “dumbbell” held between beads as myosin heads walk along the actin, to measure myosin’s power cycle. The assay revealed that the P710R mutation reduced the step size of the myosin motor (i.e. the length of each step) and the rate at which the myosin detaches from actin.

In a collaboration with University of Kentucky researcher Kenneth Campbell, these observations were then compared to a computational model of how the myosin motors interact in the cell to generate force. The results confirmed a key role for regulation of what is called myosin’s “super-relaxed state.” As Pruitt explained, “Myosin heads spend a lot of time in a super-relaxed state, referring to when it is unbound from actin. Any mutation or drug that shifts how long or how strongly myosin motors are bound to actin will change the cell force production and change downstream signaling events that drive remodeling and growth or hypertrophy.”

The P710R mutation in this study was found to destabilize the super-relaxed state. As a result, more myosin heads are bound to actin in cells that harbor the mutation, which explains the increase in force that was observed in those cells.

For Pruitt, a key takeaway from the work, beyond the important scientific findings, is the value of sustained collaboration. “The scales that the paper covers are not typically the subject of research in any one lab or even any two labs,” she said. “That’s why the paper has so many authors, including several students and postdocs working with me, James Spudich and Daniel Bernstein.

“It’s significant scientifically but also satisfying in that this level of integration makes it possible to test this idea across multiple scales. It’s been fun to work across these labs and these skills on such an extensive, multidisciplinary collaboration, and to see that the power of molecular measurements and computation, and the cell-derived measurements that allow us to genetically engineer and dissect out a single mutation,” said Pruitt. “This is really phenomenal, to test directly how a particular mutation introduces changes that lead to HCM.”

As a result of this collaboration, Pruitt added, “We can understand what goes on at the cell level. Then we can start to develop models and identify next-generation drug therapies. Instead of just identifying the symptoms, we can look at the mechanisms that underlie the dysfunctions and then address those at the cell level before it turns into a disease.”