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.

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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/

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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.

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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.

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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.”

The Norwegian mountains can be pretty darn inhospitable during the colder months. Nevertheless, there are plants that cope splendidly with the biting temperatures. They include the dwarf birch Betula nana and the black crowberry Empetrum hermaphroditum. Both thrive in arctic-alpine conditions; this makes them typical representatives of tundra vegetation.

Up until now, it has been unclear how the growth of dwarf birch and crowberry is influenced by specific environmental conditions. In the alpine regions of Norway, a project has been underway for 30 years that aims to change that. “We wired up some of the plants here and fitted them with so-called data loggers that record the measurements,” explains Prof. Dr. Jörg Löffler from the Department of Geography at the University of Bonn. A pin-like sensor records the diameter of the trunk — minute by minute, 365 days a year, to an accuracy of less than a thousandth of a millimeter. At the same time, the researchers measure solar radiation, temperature in the root zone and just above the soil surface, and soil moisture.

Shrinkage against frost damage

In the current study, researchers analyzed nearly 500 million measurements from 40 plants between 2015 and 2019. “We mainly studied how the microclimate, that is, the conditions encountered by the individual plant, affects its growth,” says Svenja Dobbert, who is doing her doctorate in Prof. Löffler’s research group. This revealed a striking rhythm in both dwarf birch and crowberry: During the colder months, their trunk diameter shrank significantly in each case — a process that was reversed in the spring. However, it was not until late summer that the deficits were made up to such an extent that actual growth began.

“Due to low temperatures in the colder months, there is hardly any liquid water available for the plants,” Dobbert says, explaining the finding. “They also reduce their trunk diameter by even actively reducing the water content of their cells to avoid frost damage.” Just how important this strategy is for both species to thrive is demonstrated by another observation: Plants that shrank very little during the winter often showed little or no growth the following summer.

A second important finding: The deciduous dwarf birches usually grew better after a mild winter. They therefore seem to generally benefit from warmer winters. With the evergreen crowberries it was the other way around. “In cold winters, there is usually less snowfall,” Löffler says. “This could be an advantage for evergreen species because they can then keep up photosynthetic activity for longer and hence enter the growth phase earlier in the spring.” It is therefore possible that climate change is causing an increasing spread of deciduous species and a concomitant displacement of evergreen species. Since the leaves of deciduous plants have a comparatively large surface area (in contrast, those of evergreen species are usually needle-like), this effect could contribute to the further greening of arctic-alpine regions.

The microclimate is crucial

“However, our results also show that microclimatic conditions can be extremely different depending on the location,” explains Löffler. For instance, at exposed, windy locations, snow cover tends to be very thin. The deciduous dwarf birch however requires a sufficiently thick insulating layer of snow in winter. It then has to use fewer resources to protect itself from frost. Without this warming blanket, the dwarf birch has a difficult time. The evergreen crowberry, in contrast, benefits from the extra sunlight during such snow-free periods. “Overall, our measurements prove that global climate data provide little valid evidence for local vegetation effects,” emphasizes the geographer. “Studies like ours can potentially help us better model such complex effects and in turn better predict the effects of climate change on plant life.”

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