Culture

The COVID-19 pandemic and subsequent lockdowns have led to a record crash in emissions. But it will be emission levels during the recovery--in the months and years after the pandemic recedes--that matter most for how global warming plays out, according to a new Nature commentary from researchers at the University of California San Diego.

While the skies have been noticeably cleaner, countries like the U.S., Mexico, Brazil, South Africa and others have recently relaxed laws controlling pollution and vehicle energy efficiency standards.

"This trend is worrisome because policy decisions being made now about how to save economies will determine how much CO2 enters the atmosphere over the coming decade," said Ryan Hanna, lead author of the Nature piece and assistant research scientist at UC San Diego.

Some economies are already ticking upward, and so too emissions. Coal consumption in China, for example, has already returned to pre-pandemic levels.

History shows that recoveries can spur green or dirty industrial turning points

Key in determining post-pandemic emissions is how governments choose to spend stimulus monies--whether they use it to prop up fossil fuel incumbents or bolster clean energy transitions already underway, according to Hanna and co-authors David Victor, professor of international relations at UC San Diego's School of Global Policy and Strategy, and Yangyang Xu, assistant professor of atmospheric sciences at Texas A&M University.

Economic shocks, the authors note, can be critical industrial turning points. Past shocks have led to both increases and decreases in the growth of CO2 emissions. After the 1998 Asian financial crisis, emissions doubled largely due to growth of China's heavy manufacturing and exports, all fueled by coal. By contrast, after the global financial crash of 2008, emissions growth halved over the next decade, aided by stimulus for green technologies--up to $530 billion in 2020 USD, or 15 percent of the total global stimulus. That's promising as it shows that structural change and lower emissions are possible if governments provide support.

Whether the coming recovery is green or dirty will have an outsized effect on climate. According to the authors' analysis, this year's crash in emissions, by itself, would lead to levels of atmospheric CO2 in 2050 about 10 PPM lower than the trajectory the world was on before the pandemic. By comparison, whether the recovery is green or dirty amounts to a difference of 19 PPM in the atmosphere by 2050--nearly double the impact on the climate.

Ensuring a green recovery will require government action. Yet, government responses have so far been mixed. The European Union and South Korea remain largely committed to their respective "Green New Deals," while other governments are falling short.

The Trump Administration in March rolled back U.S. auto fuel economy rules, committing the nation to higher transport emissions--now the largest source of warming gases in the U.S. In the same month, China authorized more coal power plants than it did in all of 2019.

Indeed, many governments have signaled a narrow focus on immediate concerns of the pandemic, such as securing health, jobs and the economy, rather than protecting the planet.

That's bad news for planetary warming. As the authors note, meeting the goals of the Paris agreement--limiting warming to well below 2ºC above pre-industrial levels--would require cutting emissions by an amount similar to that delivered by the current economic catastrophe every year for the next decade.

Charting a course that protects both jobs and the climate

How do you align the public's urgent needs with the need to also limit warming? "Political leaders--and climate activists who want to help them succeed--should filter policy actions for the climate by what's politically viable," said Hanna. "In short, that means coming up with projects that deliver jobs and revenues quickly."

Investing in sectors like renewables, energy efficiency and preserving the existing feat of zero emission nuclear plants can set the economy on track and deepen cuts to future emissions. Bolstering these sectors can deliver and save hundreds of thousands of jobs.

At the start of this year, more than 250,000 people worked in solar energy in the U.S. The pandemic has since wiped out five years of job growth in that sector -- jobs that could return quickly if credible investment incentives were in place.

Investing in energy efficiency and infrastructure construction, such as erecting power lines and conducting energy retrofits for buildings and public transportation, is another large potential employer.

"The trillions devoted to stimulus, so far, have been about stabilizing economies and workers," said Victor. "With a fresh focus that looks further into the future, the next waves of spending must also help to protect the climate."

The EU Green Deal as a model for stimulus

Hanna, Victor and Xu write, "The European Green Deal is a good model for stimulus packages. It is a massive, €1-trillion (U.S. $1.1-trillion) decade-long investment plan that combines industrial growth with deep decarbonization and efficiency and has maintained political support throughout the pandemic."

Existing firms will need to be involved in a green recovery because they are ready to restart, the authors recommend. And a savvy political strategy would isolate only those companies whose actions egregiously undermine climate goals, such as conventional coal, and would ensure their workers are treated justly and retrained in new areas of employment.

The authors also recommend a sector by sector approach to decarbonizing the economy, as the policies needed to rein in the largest emitters in each sector differ.

"On our current path, emissions are likely to tick upwards, as they have after each recession since the first oil shock of the early 1970s," said Victor. "The historic drop in recent months was too hard won to be so easily lost."

In the June 11 issue of the New England Journal of Medicine, a team of UCLA physicians and scientists describes the first case of immune modulation being used to cure a severe and often fatal fungal infection. The team "retuned" a 4-year-old's immune system so that it could fight off disseminated coccidioidomycosis.

The case, originally reported by UCLA in 2019, could pave the way for a new treatment for the infection, which affects hundreds of Americans each year, primarily in the Southwest, and kills approximately 40% of the people who contract it.

The technique described in the study could also suggest a new paradigm for treating other severe fungal infections, bacterial infections such as tuberculosis, and severe viral infections such as influenza and COVID-19.

"Immune modulation isn't currently part of the strategy with any of these severe infections," said Dr. Manish Butte, the report's senior author, who holds the E. Richard Stiehm Endowed Chair in Pediatric Allergy, Immunology and Rheumatology at the David Geffen School of Medicine at UCLA. "Our case suggests that rather than hoping to get the upper hand with more and more antibiotics or antifungals, we can have some success by combining these established approaches with the new idea of programming the patient's immune response to better fight the infection."

Each year, more than 100,000 people are infected with Coccidioides fungi, which reside in the soils of California, Arizona and West Texas. Most people who are infected are asymptomatic, and about 20,000 experience the minor respiratory illness commonly known as Valley fever. The vast majority of people with Valley fever respond well to antifungal medications, but approximately 1% of the infections progress to disseminated coccidioidomycosis, in which the infection spreads rapidly throughout the body, leading to bone and tissue damage, and in many cases death.

"Historically, severe infections have been seen as 'bad luck,'" Butte said. "Doctors haven't looked at how we can harness the immune systems of these patients to fight the infection."

According to a 2019 study in the International Journal of Environmental Research and Public Health, California spends between $700 million and $900 million a year in direct and indirect costs related to the care of people infected by the cocci fungus, including more than $300 million to care for the approximately 200 people with disseminated coccidioidomycosis.

The boy who was treated by Butte and his team had previously been treated with high doses of multiple antifungal medicines, but by the time he arrived at UCLA, he could barely walk or talk and required a feeding tube to eat. When UCLA physicians homed in on the patient's immune system, they concluded that his T cells -- the white blood cells that play a key role in the body's immune response -- were failing to properly recognize the invading fungus. The T cells were responding as though the infection was a parasitic infection rather than a fungal one.

That prompted the team to supplement the boy's antifungal medications with an immune stimulator called interferon-gamma. And Dr. Maria Garcia-Lloret, a pediatric allergist and immunologist, suggested adding yet another medication, dupilumab, which was developed as a medication for allergic diseases and had never before been used to treat infections. Dupilumab is a prescription drug that has not been approved by the FDA as a treatment for disseminated coccidioidomycosis.

The combination of immune modulators restored the proper programming to the patient's T cells -- and the boy's infection went away in a month.

Chemical engineers from UNSW Sydney have developed new technology that helps convert harmful carbon dioxide emissions into chemical building blocks to make useful industrial products like fuel and plastics.

And if validated in an industrial setting and adopted on a large scale, the process could give the world breathing space as it transitions towards a green economy.

In a paper published today in the journal Advanced Energy Materials, Dr Rahman Daiyan and Dr Emma Lovell from UNSW's School of Chemical Engineering detail a way of creating nanoparticles that promote conversion of waste carbon dioxide into useful industrial components.

OPEN FLAME

The researchers, who carried out their work in the Particles and Catalysis Research Laboratory led by Scientia Professor Rose Amal, show that by making zinc oxide at very high temperatures using a technique called flame spray pyrolysis (FSP), they can create nanoparticles which act as the catalyst for turning carbon dioxide into 'syngas' - a mix of hydrogen and carbon monoxide used in the manufacture of industrial products. The researchers say this method is cheaper and more scalable to the requirements of heavy industry than what is available today.

"We used an open flame, which burns at 2000 degrees, to create nanoparticles of zinc oxide that can then be used to convert CO2, using electricity, into syngas," says Dr Lovell.

"Syngas is often considered the chemical equivalent of Lego because the two building blocks - hydrogen and carbon monoxide - can be used in different ratios to make things like synthetic diesel, methanol, alcohol or plastics, which are very important industrial precursors.

"So essentially what we're doing is converting CO2 into these precursors that can be used to make all these vital industrial chemicals."

CLOSING THE LOOP

In an industrial setting, an electrolyser containing the FSP-produced zinc oxide particles could be used to convert the waste CO2 into useful permutations of syngas, says Dr Daiyan.

"Waste CO2 from say, a power plant or cement factory, can be passed through this electrolyser, and inside we have our flame-sprayed zinc oxide material in the form of an electrode. When we pass the waste CO2 in, it is processed using electricity and is released from an outlet as syngas in a mix of CO and hydrogen," he says.

The researchers say in effect, they are closing the carbon loop in industrial processes that create harmful greenhouse gases. And by making small adjustments to the way the nanoparticles are burned by the FSP technique, they can determine the eventual mix of the syngas building blocks produced by the carbon dioxide conversion.

"At the moment you generate syngas by using natural gas - so from fossil fuels," Dr Daiyan says. "But we're using waste carbon dioxide and then converting it to syngas in a ratio depending on which industry you want to use it in."

For example, a one to one ratio between the carbon monoxide and hydrogen lends itself to syngas that can be used as fuel. But a ratio of four parts carbon monoxide and one part hydrogen is suitable for the creation of plastics, Dr Daiyan says.

CHEAP AND ACCESSIBLE

In choosing zinc oxide as their catalyst, the researchers have ensured that their solution has remained a cheaper alternative to what has been previously attempted in this space.

"Past attempts have used expensive materials such as palladium, but this is the first instance where a very cheap and abundant material, mined locally in Australia, has been successfully applied to the problem of waste carbon dioxide conversion," Dr Daiyan says.

Dr Lovell adds that what also makes this method appealing is using the FSP flame system to create and control these valuable materials.

"It means it can be used industrially, it can be scaled, it's super quick to make the materials and very effective," she says.

"We don't need to worry about complicated synthesis techniques that use really expensive metals and precursors - we can burn it and in 10 minutes have these particles ready to go. And by controlling how we burn it, we can control those ratios of desired syngas building blocks."

SCALING UP

While the duo have already built an electrolyser that has been tested with waste CO2 gas that contains contaminants, scaling the technology up to the point where it could convert all of the waste carbon dioxide emitted by a power plant is still a way down the track.

"The idea is that we can take a point source of CO2, such as a coal fired power plant, a gas power plant, or even a natural gas mine where you liberate a huge amount of pure CO2 and we can essentially retrofit this technology at the back end of these plants. Then you could capture that produced CO2 and convert it into something that is hugely valuable to industry," says Dr Lovell.

The group's next project will be to test their nanomaterials in a flue gas setting to ensure they are tolerant to the harsh conditions and other chemicals found in industrial waste gas.

Researchers at the University of Maryland School of Medicine (UMSOM) have identified how certain gene mutations cause amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. The pathway identified by the researchers may also be responsible for a certain form of dementia related to ALS. The finding could offer potential new approaches for treating this devastating condition, which causes progressive, fatal paralysis and sometimes mental deterioration similar to Alzheimer's disease. Their discovery was published this week in the Proceedings of the National Academy of Sciences (PNAS) and included collaborators from Harvard University, University of Auckland, King's College London, and Northwestern University.

More than 5,000 Americans are diagnosed with ALS every year, a condition that is usually fatal and has no cure. Patients with ALS slowly lose the ability to move their muscles, leading to problems with basic functions such as breathing and swallowing. About half of ALS patients also develop dementia. Genetic studies of families with a predisposition to develop ALS have shown that the condition can be associated with certain gene mutations. Some of these mutations involve the gene UBQLN2 which regulates the disposal of misfolded "garbage" from the body's cells. Until now, researchers did not fully understand how UBQLN2 mutations interfere with this pathway and cause ALS.

"We mapped out the process by which ubiquilin-2 (UBQLN2) gene mutations disrupt an important recycling pathway that cells use to get rid of their trash," said Mervyn Monteiro, PhD, Professor of Anatomy and Neurobiology, who is affiliated with the UMSOM's Center for Biomedical Engineering and Technology (BioMET) at UMSOM. "Without this recycling, misfolded proteins build up in the nerve cell and become toxic, eventually destroying the cell. This destruction could lead to neurodegenerative disorders like ALS."

To investigate how UBQLN2 mutations cause ALS, Dr. Monteiro's group used both human cells and UBQLN2-mutant mouse models for their investigations. The mouse models, which they described in a 2016 PNAS publication, mimic the progression of the disease in people who inherit these gene mutations.

Dr. Monteiro's group first removed the UBQLN2 gene from human cells and found it completely stalled the recycling pathway. They then reintroduced either the normal gene or one of five gene mutations into the cells. They found that reintroduction of normal UBQLN2 restored the recycling pathway while all five of the gene mutations failed to restart the pathway.

Using the mouse model, Dr. Monteiro and his colleagues outlined the reason for the pathway disruption in the presence of gene mutations. They found that the mice with the gene mutations had reduced levels of a certain protein called ATP6v1g1, which is an essential part of a pump that acidifies the cell's trash container in order to initiate the breakdown and recycling process.

"Our new findings are exciting because similar acidification defects have been found in Alzheimer's, Parkinson's and Down syndrome," Dr. Monteiro said. "This suggests that restoration of the defect could have broad implications for not only treating ALS, but possibly other neurodegenerative diseases as well."

The research study was supported by grants from the Packard Center for ALS Research at Johns Hopkins, the ALS Association, and the National Institutes of Health (grant number: R01-NS100008).

"The BioMET research team led by Dr. Monteiro continues to make important advances in understanding the mechanisms that give rise to ALS," said Dean E. Albert Reece, MD, PhD, MBA, who is also Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor, University of Maryland School of Medicine. "Future treatments and preventive measures for this devastating disease would not be possible without this foundational work."

San Antonio, Texas (June 8, 2020) - Scientists at Texas Biomedical Research Institute's (Texas Biomed) Southwest National Primate Research Center (SNPRC) recently published findings indicating the baboon could prove to be a relevant model to test therapeutics and interventions for neurodegenerative diseases, such as early stage Alzheimer's and related dementias. The scientists observed a steep age-related cognitive decline in baboons about 20-years-old, which is the equivalent of a 60-year-old human. The team of scientists, led by Dr. Marcel Daadi, Associate Professor at Texas Biomed's SNPRC, published their findings in the May issue of Aging . These studies are a first step in developing the baboon as an appropriate animal model for early stage Alzheimer's disease.

According to the Alzheimer's Association, more than five million Americans are living with Alzheimer's, and one in three seniors die from the disease or related dementias. Dr. Daadi explained that early detection of age-associated cognitive dysfunction is crucial and may provide an understanding of the breakdown of brain systems, leading to better interventions.

"We don't know how Alzheimer's disease starts, and if you are trying to treat a patient already with advanced disease, it is nearly impossible to treat them because of the significant loss in brain cells" said Dr. Daadi. "If we detect early on pathology in the brain then we can target interventions to prevent it from progressing, and we are in a better position to help. This is the first time a naturally-occurring model for early-stage Alzheimer's has been reported. This model could be relevant to test promising drugs, to better understand how and why the disease develops and to study the areas of the brain affected in order to determine how can we impact these pathways."

Aging is currently irreversible and a significant reason for the gradual deterioration of general health and function. Neurodegenerative diseases, in particular, are related to the aging of brain cells and synaptic loss, which is a loss of the lines of communications inside the brain. As noted in the paper, humans and nonhuman primates (NHP) share many similarities, including age-dependent changes in gene expression and a decline in neural and immune functions. Previous studies have pinpointed the prefrontal cortex (PFC) of the brain as one of the regions most affected by age. The PFC plays an important role in working memory function, self-regulatory and goal-directed behaviors, which are all vulnerable to aging. To observe whether these PFC functions are impacted by aging in baboons and determine whether the baboons at varying ages could discern and learn new tasks, Dr. Daadi and his team separated the baboons into two groups based on age (adult group and aged group). Four cognitive tests were performed to observe novel learning, motor function and memory and shape association.

"What we found is that aged baboons lagged significantly in performance among all four tests for attention, learning and memory" Dr. Daadi said. "The delay or inability to collect rewards (response latency) also increased in older baboons, suggesting a decline in motivation and/or motor skills. The team then used a more complex task requiring integration of several cognitive processes and demonstrated that aged subjects actually have deficiencies in attention, learning and memory. Human studies have suggested a precipitous decline in brain systems function and cognition with 60 years as the potential breakpoint. These findings are consistent with our results."

Rodents have been the primary lab model to test therapeutic interventions for neurodegenerative diseases. However, mice do not always reflect human processes, so while this animal model has been integral to understanding neurodegenerative disease processes, it has not proven as effective in translating promising therapies to the clinic.

"The failure rate in clinical trials of Alzheimer's disease therapeutics is extremely high at about 99.6%, and we need to change that" said Dr. Daadi.

A nonhuman primate, or monkey, which is more similar to humans in terms of genetics, physiology, cognition, emotion and social behavior, could prove to be a more effective model to test therapeutic interventions.

Dr. Daadi and his team are moving forward and plan to submit a National Institutes of Health grant to allow for further research. This published study was funded by the Marmion Family Fund, the Worth Family Fund, The Perry and Ruby Stevens Charitable Foundation and The Robert J., Jr. and Helen C. Kleberg Foundation, The William and Ella Owens Medical Research Foundation, the NIH Primate Center Base grant (Office of Research Infrastructure Programs/OD P51 OD011133), the National Institute on Aging R56 AG059284.

"Our next step is to investigate the neuropathologies behind this cognitive decline and perform imaging to understand what happens to the neural connections and determine where defects may be," he said. "We will also look at biomarkers that can give us an idea of why this steep decline is happening. All this data will enable us to further characterize the baboon as a naturally-occurring model that may prove useful for testing early therapeutic interventions."

A new study shows that surface disturbance from energy development can hinder mule deer migrations when it exceeds 3 percent.

Researchers from the University of Wyoming and Western Ecosystems Technology used 15 years of movement data collected from GPS-collared mule deer in western Wyoming to evaluate how much disturbance mule deer could withstand during migration. The study was conducted in the Pinedale Anticline -- the sixth-largest natural gas field in the nation and home to one of the largest deer herds in West.

The findings were published in the Journal of Wildlife Management.

Researchers used 145 migrations from 56 individual deer to examine disturbance effects at various scales. Results consistently showed that mule deer use of migration corridors steeply declined when surface disturbance from roads and well pads surpassed 3 percent. Mule deer were able to migrate through areas where surface disturbance was lower.

"Better understanding the relationship between surface disturbance and migratory behavior can help managers identify trade-offs and potential mitigation measures associated with mineral leasing and energy development that overlap with the migratory routes of big game," research biologist and co-author Hall Sawyer says.

The authors note that similar disturbance thresholds likely vary across development types -- such as wind, solar and residential - as well as geographic regions and species.

"There is a growing need to understand and predict how our migratory animals respond to disturbed landscapes, so we hope to expand this type of work in the future," says Jerod Merkle, who is the Knobloch Professor of Migration and Conservation Ecology at UW.

Mallory Lambert, a UW graduate student and study co-author, says the next steps will be identifying disturbance thresholds for migrating pronghorn and wintering mule deer.

In breeding programs aimed at conserving animals from small or isolated populations, scientists must balance the competing needs of adding genetic diversity and avoiding the introduction of harmful genes. This makes for a delicate task of boosting diversity in the endangered Pacific pocket mouse, the focus of a long-running conservation breeding program undertaken by San Diego Zoo Global. There are just three remaining populations of this species in the wild, all of which are small and isolated from each other on the Southern California coast--preventing beneficial interbreeding and making inbreeding more likely.

Drawing on genetic data from six generations of Pacific pocket mice in this program, a new study has tracked reproductive success relative to a mouse's ancestral population. The findings, published this month in the journal Conservation Genetics, indicate that genetic diversity should be introduced from the larger, genetically healthier populations of Pacific pocket mice into a smaller, less healthy population--and not the reverse.

"These results reinforce the idea that, when there is a large difference in fitness of populations, gene flow should be unidirectional from the more fit to less fit population, in order to avoid the introduction of deleterious alleles into healthier populations," said Aryn Wilder, Ph.D., a senior researcher in Conservation Genetics at San Diego Zoo Global, who is the study's lead author.

The damaging effects of genetic load--the total of harmful mutations in the genome--are too rarely considered in management planning, said Wilder, but should be a central concern.

Using the number of offspring as a measure of fitness, the study examined the reproductive success of more than 300 Pacific pocket mice. Descendants of the smallest and least genetically diverse population had the lowest reproductive success, the researchers found. Interbreeding with the larger, more diverse populations increased the fitness of their offspring relative to this small population, but came at a cost to the larger population.

Weighing about the same as three pennies, Pacific pocket mice are the smallest mouse species in North America. They get their name from pouches in their cheeks, used to carry food and nesting materials. Endemic only to coastal scrublands, dunes and rivers within about 2 miles of the ocean, the Pacific pocket mouse's range once stretched from Los Angeles to the Tijuana River Valley. Because of human encroachment and habitat degradation, their numbers dropped sharply after 1932. In their native habitat, they disperse the seeds of native plants, and their underground burrows encourage plant growth.

Although the species was believed to be extinct for two decades, Pacific pocket mice were rediscovered in the early 1990s. By then, their range had been reduced to just three populations: one on the Dana Point headlands in Orange County, California and two on Marine Corps Base Camp Pendleton. Two of the populations rarely exceed 50 individuals.

In 2011, the Pocket Mouse Conservation Breeding Facility was created at the San Diego Zoo Safari Park to increase their numbers. In 2017, San Diego Zoo Global and partner organizations established a new population of Pacific pocket mice in Orange County's Laguna Coast Wilderness Park, where they began to breed without human assistance.

In addition to bolstering the species and maintaining high genetic diversity, the breeding program provides the added benefit of increasing the understanding of how to better manage genetic diversity of populations in the wild.

"This study provides direct data to help us understand how populations will respond to assisted migration," said Wilder. "Boosting genetic diversity by introducing genes from outside populations may help prevent inbreeding and increase fitness, to better enable wild populations to be self-sustaining."

Scientists in the Department of Biomedical Engineering at Texas A&M University are developing new ways to advance the field of regenerative medicine and cancer treatment. They are developing a 2D nanosheet that is 1,000 times smaller than a strand of hair.

Dr. Akhilesh Gaharwar, associate professor, has developed a new class of 2D nanosheets called molybdenum disulfide that can adsorb near infrared (NIR) light and modify cell behavior. These nanosheets are an emerging class of materials that have shown distinct physical and chemical properties due to their unique shape and size. Recently, some nanosheets have been explored for biomedical applications due to their light-responsive ability. Despite strong potential, Gaharwar's research is entering new territory, as few studies have investigated their cellular compatibility and none have explored their ability to modulate cellular functions using light.

To explore the possibility of controlling the cell response via light, Gaharwar's research group has synthesized an atomically thin nanosheet that can adsorb NIR light and convert it into heat. NIR light can penetrate deep inside the tissue compared to other types of light, including ultraviolet and visible light, and can be used to stimulate natural biological repair mechanisms in deep tissue.

Due to the high-surface area of nanosheets, they can stick to the outer membrane of cells and transmit a cellular signal to the nucleus, thereby controlling their behavior. Some of the nanosheets are also eaten by the cells and can influence cellular functions from inside.

"Light-responsive biomaterials have a strong potential for developing the next generation of noninvasive, precise and controllable medical devices for a range of biomedical applications, including drug delivery, cancer therapy, regenerative medicine and 3D printing," Gaharwar said.

His research was recently featured in the journal Proceedings of the National Academy of Sciences.

In collaboration with Dr. Irtisha Singh, assistant professor in the Department of Molecular and Cellular Medicine of the Texas A&M Health Science Center, Gaharwar's team used a next-generation sequencing technique to decipher the effect of light and/or nanosheets on the gene regulation of cells. Picture a cell as a blank canvas, and gene regulation as the paint that turns the canvas into something unique or interesting. For stem cells, that would mean determining what kind of cell they will be, such as muscle, bone, etc. Slight agitations in gene expression, either from light or these nanosheets, can significantly affect the functions of these cells such as movement, reproduction and expression.

Global gene expression profiles of cells reveal that light stimulation of the nanosheet can have a significant influence on cellular migration and wound healing. They demonstrated that cancer cells treated with a nanosheet and light are not able to move freely, which is good news. This is important as cancer spreads in the body by moving from one tissue to another. The combination of the nanosheet and light may provide new approaches to control and regulate cellular migration and functions.

The team found that the nanosheets bind to a cell surface receptor known as an integrin, a simple protein with a sugar attached. These integrin proteins are important in normal cell functioning by providing information to cells about its surroundings. If these proteins are covered by nanosheets, they cannot tell the cells to move around, effectively stopping the cells for an indefinite time.

Researchers in the USA have developed a graphene-based electrochemical sensor capable of detecting histamines (allergens) and toxins in food much faster than standard laboratory tests.

The team used aerosol-jet printing to create the sensor. The ability to change the pattern geometry on demand through software control allowed rapid prototyping and efficient optimization of the sensor layout.

Commenting on the findings, which are published today in the IOP Publishing journal 2D Materials, senior author Professor Mark Hersam, from Northwestern University, said: "We developed an aerosol-jet printable graphene ink to enable efficient exploration of different device designs, which was critical to optimizing the sensor response."

As an additive manufacturing method that only deposits material where it is needed and therefore minimizes waste, aerosol-jet-printed sensors are low-cost, straightforward to make, and portable. This could potentially enable their use in places where continuous on-site monitoring of food samples is needed to determine and maintain the quality of products, as well as other applications.

Senior author Professor Carmen Gomes, from Iowa State University, said: "Aerosol-jet printing was fundamental to the development of this sensor. Carbon nanomaterials like graphene have unique material properties such as high electrical conductivity, surface area, and biocompatibility that can significantly improve the performance of electrochemical sensors.

"But, since in-field electrochemical sensors are typically disposable, they need materials that are amenable to low-cost, high-throughput, and scalable manufacturing. Aerosol-jet printing gave us this."

The team created high-resolution interdigitated electrodes (IDEs) on flexible substrates, which they converted into histamine sensors by covalently linking monoclonal antibodies to oxygen moieties created on the graphene surface by a CO2 thermal annealing process.

They then tested the sensors in both a buffering solution (PBS) and fish broth, to see how effective they were at detecting histamines.

Co-author Kshama Parate, from Iowa State University, said: "We found the graphene biosensor could detect histamine in PBS and fish broth over toxicologically-relevant ranges of 6.25 to 100 parts per million (ppm) and 6.25 to 200 ppm, respectively, with similar detection limits of 2.52 ppm and 3.41 ppm, respectively. These sensor results are significant, as histamine levels over 50 ppm in fish can cause adverse health effects including severe allergic reactions - for example, scombroid food poisoning.

"Notably, the sensors also showed a quick response time of 33 minutes, without the need for pre-labelling and pre-treatment of the fish sample. This is a good deal faster than the equivalent laboratory tests."

The researchers also found the biosensor's sensitivity was not significantly affected by the non-specific adsorption of large protein molecules commonly found in food samples and used as blocking agents.

Senior author Dr Jonathan Claussen, from Iowa State University, said: "This type of biosensor could be used in food processing facilities, import and export ports, and supermarkets where continuous on-site monitoring of food samples is needed. This on-site testing will eliminate the need to send food samples for laboratory testing, which requires additional handling steps, increases time and cost to histamine analysis, and consequently increases the risk of foodborne illnesses and food wastage.

"It could also likely be used in other biosensing applications where rapid monitoring of target molecules is needed, as the sample pre-treatment is eliminated using the developed immunosensing protocol. Apart from sensing small allergen molecules such as histamine, it could be used to detect various targets such as cells and protein biomarkers. By switching the antibody immobilized on the sensor platform to one that is specific towards the detection of suitable biological target species, the sensor can further cater to specific applications. Examples include food pathogens (Salmonella spp.), fatal human diseases (cancer, HIV) or animal or plant diseases (avian influenza, Citrus tristeza)."

Experts from the University of Nottingham have discovered that some chimpanzees have a bone in their heart, which could be vital in managing their health and conservation.

Very few species of animals have this bone - called an os cordis - therefore this is a particularly rare find.

The exciting research, which was carried out by experts from the University's School of Veterinary Medicine and Science, is published today in Scientific Reports.

Wild chimpanzees are endangered and cardiovascular disease is very common in this species. Understanding their hearts is vital in making medical advances and managing their health and conservation.

The tiny 'os cordis' heart bones, measuring a few millimetres in size, were more likely to be present in chimps with idiopathic myocardial fibrosis - a type of heart disease found in chimps and people. Myocardial fibrosis is the most common type of heart disease in chimpanzees and has been linked to the occurrence of cardiac arrhythmias and sudden death.

"The discovery of a new bone in a new species is a rare event, especially in chimps which have such similar anatomy to people. It raises the question as to whether some people could have an os cordis too,' said lead author Dr Catrin Rutland from the University.

This astonishing new find was made possible using several techniques including an advanced imaging method called micro-computed tomography. This enabled the hearts to be scanned at much higher magnifications than standard hospital or veterinary CT scans.

"Looking for ways to help chimps with heart disease is essential. Understanding what is happening to their hearts helps us manage their health" Said Dr Sophie Moittié, from the University.

The heart bone is present in many bovines (cattle, ox and buffalo), and is often quite large, butchers even remove it some that meat can be used for soups. Sheep, otters, dogs and camels sometimes have the heart bone too. Sometimes the os cordis is present in most animals of a species but in other cases it is associated with heart disease.

The function of an os cordis is still being researched, but this work shows that cartilage was present in addition to bone, which gives insight into the mechanisms via which bone growth started. The scientists also showed that the heart bone was present in male and female chimps of differing ages.

Many suggestions have been given for the reasons behind an os cordis developing. The bone may support the essential heart valves, develop due to heart disease or even alter the electrical system which controls the heart.

"This research has brought together researchers and veterinary professionals, working on a common aim to advance chimpanzee health and conservation," adds Dr Rutland.

African Americans who smoke are nearly 2.5 times more likely to have a stroke than those who never smoked, while former smokers show a similarly lower risk as never smokers, according to a new study funded by the National Institutes of Health.

The findings from the Jackson Heart Study suggests that even after years of smoking, African Americans--who as a group are twice as likely as whites to have a stroke and die from it--could significantly reduce their risk if they kicked the habit. The study's findings, funded by the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute for Minority Health and Health Disparities (NIMHD), both part of NIH, will appear online in the Journal of the American Heart Association.

Numerous studies have shown the link between smoking and stroke, but few have directly assessed the relationship solely in African Americans. This new study did that and also analyzed traditional risk factors for cardiovascular diseases and inflammation.

"This study provides further strong evidence of the link between cigarette smoking and stroke in African Americans," said David Goff, M.D., Ph.D., director of the Division of Cardiovascular Sciences at NHLBI. "We know that quitting smoking is one way to lower the risk for stroke, which is particularly important for the most vulnerable populations during this pandemic."

The study included 4,410 black men and women without a history of stroke and who were enrolled in the Jackson Heart Study, the largest study of cardiovascular disease in African Americans. Researchers classified the participants, who were 54 on average, into three groups based on their self-reported smoking history: current smokers, past smokers who smoked at least 400 cigarettes in their lifetimes, and never smokers.

The researchers further classified current smokers based on smoking intensity. One group included participants who smoked up to 19 cigarettes a day; another included those who smoked 20 or more cigarettes a day. Researchers followed participants from their initial evaluations beginning in 2000 through 2015.

At its start, the study included 781 past smokers, 546 current smokers, and 3,083 never smokers. By 2015, 5.2% of past smokers, 6.6% of those were smoking up to 19 cigarettes a day, and 7.2% of those smokers smoking more than 20 cigarettes a day had experienced a stroke, compared to 3.4% of never smokers.

After accounting for multiple risk factors for stroke, such as high blood pressure, diabetes, high "bad" cholesterol levels, and older age, researchers calculated that current smokers carried a risk for stroke that was more than double the risk for never smokers. And, the risk nearly tripled for those smoking 20 or more cigarettes each day. But past smokers showed an almost identical risk as never smokers.

"The bottom line is the more a person smokes, the greater their chance is of having a stroke," said Adebamike A. Oshunbade, M.D., M.P.H., the lead study author and postdoctoral research fellow at the University of Mississippi Medical Center. "It's important to communicate this risk to vulnerable populations, especially with the growing popularity of new tobacco products."

Michael E. Hall, M.D., associate professor of medicine at the University of Mississippi Medical Center, Jackson, and corresponding study author, agreed. He noted that while smoking has been shown in major studies to raise the risk of stroke 1.5 times for the general population, "these adverse health effects seem to be magnified in African Americans."
1In their analysis, the researchers also looked more closely at the already-established link between inflammation and atherosclerosis and smoking. They measured for C-reactive protein (CRP), a marker of inflammation, and carotid intima-media thickness, or CIMT, to assess the buildup of fatty plaques in the carotid arteries that supply blood to the brain.
1The researchers found that African American smokers who smoked 20 or more cigarettes a day had higher CIMT compared to never smokers. Researchers said this suggests that the buildup of plaque in the major blood vessels of the brains of African American smokers could play a role in the development of stroke.

Even before soaring unemployment caused millions of Americans to lose their health insurance, 18.2 million individuals at increased risk of severe COVID-19 were either uninsured or underinsured, according to a new study published today (June 10) in the Journal of General Internal Medicine by researchers at Harvard Medical School and CUNY's Hunter College. Although most of those at high medical and financial risk were white, racial minorities were over-represented.

Researchers determined who was at risk of severe COVID-19 based on age and medical risk factors such as diabetes. They found that Blacks, Native Americans, lower-income individuals of all races/ethnicities, and those residing in rural areas or in states that had not expanded Medicaid were doubly disadvantaged: they were both more likely to be at high risk of severe COVID-19 and to lack adequate coverage. For instance, compared to non-Hispanic whites, Blacks were 42% and Native Americans 90% more likely to be at risk for severe COVID-19, and high-risk persons from those racial groups were 51% and 53% more likely to have inadequate coverage compared to high-risk whites. Persons in states that failed to expand Medicaid were 6% more likely to be high risk, and 52% more likely to have inadequate coverage compared to those in states that accepted the ACA's Medicaid expansion. Hispanics at high medical risk were more than twice as likely as non-Hispanic whites to have inadequate coverage.

"The pandemic is laying bare the lethal inequality of American society and American health care," said lead author Dr. Adam Gaffney, a pulmonary and critical care physician at the Cambridge Health Alliance and Harvard Medical School. "Our ICU has been flooded with poor and minority patients; having COVID-19 is scary enough without worrying that you'll be bankrupted by medical bills," he added.

Despite recent federal actions to help fund COVID-19 care, and some insurers' promises to upgrade coverage for the disease, many American still lack protection from COVID-19's costs. The Families First Coronavirus Response Act mandated full coverage for COVID-19 testing, but not for treatment, and the CARES Act provided some funding for hospitals treating uninsured patients, but the protection is far from adequate. While some private insurers have promised to waive copays and deductibles for treatment as well as testing, this promise doesn't apply to out-of-network care, or to the majority of privately-insured workers whose employers are self-insured. Moreover, most of these waivers will expire by July 1. A Gallup poll found that many remain fearful of treatment costs, with 14% of Americans saying they would avoid care because of costs even if they develop symptoms of COVID-19.

"These promises of new protections for patients with COVID-19 are full of holes," noted senior author Dr. Danny McCormick, a primary care physician and associate professor at Harvard Medical School. "COVID-19 threatens the health of people everywhere, but only in the U.S. will it also ruin patients financially. When people avoid testing and care because they fear the costs, it fuels the epidemic's spread," he added.

The investigators also noted that the new federal legislation and insurers' promises won't help patients with COVID-19-like symptoms who are found to have a different diagnosis. "It's not just COVID care that's unaffordable," said co-author Dr. Steffie Woolhandler, Distinguished Professor of Public Health at CUNY's Hunter College and a Lecturer in Medicine at Harvard Medical School. "Patients with heart disease, asthma, and diabetes need protection too. Medicare for All is the long-term answer. But in the meantime, passage of the stopgap Medicare expansion bills introduced by Sen. Bernie Sanders and Rep. Pramila Jayapal would ensure that patients can get the care they need during the crisis, regardless of their diagnosis."

In a new study, Johns Hopkins researchers found that testing people for SARS-CoV-2 -- the virus that causes COVID-19 -- too early in the course of infection is likely to result in a false negative test, even though they may eventually test positive for the virus.

A report on the findings was published in the May 13 issue of Annals of Internal Medicine.

"A negative test, whether or not a person has symptoms, doesn't guarantee that they aren't infected by the virus," says Lauren Kucirka, M.D., Ph.D., M.Sc., obstetrics and gynecology resident at Johns Hopkins Medicine. "How we respond to, and interpret, a negative test is very important because we place others at risk when we assume the test is perfect. However, those infected with the virus are still able to potentially spread the virus."

Kucirka says patients who have a high-risk exposure should be treated as if they are infected, particularly if they have symptoms consistent with COVID-19. This means communicating with patients about the tests' shortcomings. One of several ways to assess for the presence of SARS-CoV-2 infection is a method called reverse transcriptase polymerase chain reaction (RT-PCR). These tests rapidly make copies of and detect the virus's genetic material. However, as shown in tests for other viruses such as influenza, if a swab misses collecting cells infected with the virus, or if virus levels are very low early during the infection, some RT-PCR tests can produce negative results. Since the tests return relatively rapid results, they have been widely used among high-risk populations such as nursing home residents, hospitalized patients and health care workers. Previous studies have shown or suggested false negatives in these populations.

For the new analysis, Johns Hopkins Medicine researchers reviewed RT-PCR test data from seven prior studies, including two preprints and five peer-reviewed articles. The studies covered a combined total of 1,330 respiratory swab samples from a variety of subjects including hospitalized patients and those identified via contact tracing in an outpatient setting.

Using RT-PCR test results, along with reported time of exposure to the virus or time of onset of measurable symptoms such as fever, cough and breathing problems, the researchers calculated the probability that someone infected with SARS-CoV-2 would have a negative test result when they had the virus infection. In the published studies, health care providers collected nasal and throat samples -from patients and noted the time of virus exposure or symptom -onset and sample collection.

From this data, the Johns Hopkins researchers calculated daily false-negative rates, and have made their statistical code and data publicly available so results can be updated as more data are published.

The researchers estimated that those tested with SARS-CoV-2 in the four days after infection were 67% more likely to test negative, even if they had the virus. When the average patient began displaying symptoms of the virus, the false-negative rate was 38%. The test performed best eight days after infection (on average, three days after symptom onset), but even then had a false negative rate of 20%, meaning one in five people who had the virus had a negative test result.

"We are using these tests to rule out COVID-19, and basing decisions about what steps we take to prevent onward transmission, such as selection of personal protective equipment for health care workers," says Kucirka. "As we develop strategies to reopen services, businesses and other venues that rely on testing and contact tracing, it is important to understand the limitations of these tests."

Ongoing efforts to improve tests and better understand their performance in a variety of contexts will be critical as more people are infected with the virus and more testing is required. The sooner people can be accurately tested and isolated from others, the better we can control the spread of the virus, the researchers say.

CORVALLIS, Ore. - An Oregon State University environmental engineering professor has solved a decades-old mystery regarding the behavior of fluids, a field of study with widespread medical, industrial and environmental applications.

The research by Brian D. Wood, published in the Journal of Fluid Mechanics, clears a roadblock that has been puzzling scientific minds for nearly 70 years and paves the way to a clearer picture of how chemicals mix in fluids.

A more complete grasp of that basic principle provides a foundation for advances in a range of areas - from how pollutants spread in the atmosphere to how drugs perfuse tissues within the human body.

Funded by the National Science Foundation, Wood's work with dispersion theory builds on research by one of the most accomplished scientists in Oregon State history, Octave Levenspiel. A 1952 chemical engineering Ph.D. graduate and later a longtime faculty member, Levenspiel in 1957 published an important paper on dispersion in chemical reactors on his way to becoming the college's first inductee to the National Academy of Engineering.

Even more importantly, the research by Wood bridges a longstanding gap in one of the fundamental tenets of fluid mechanics: Taylor dispersion theory. Named for British physicist and mathematician G.I. Taylor, author of a seminal 1953 paper, the theory concerns phenomena in which ?uctuations in a fluid's velocity ?elds cause chemicals to spread within it.

"The process of dispersive spreading tends to increase over time until it reaches a steady level," Wood said. "You can think of it as analogous to investment in a startup, in which the rates of return can initially be very large before settling in to a more sustainable level that is close to constant."

Taylor's theory was the first to allow researchers to predict that steady level of dispersion using what's known as the macroscopic dispersion equation. The equation can describe the net movement of a chemical species in a fluid -- provided enough time has elapsed from when the chemical entered the fluid.

"That was a signi?cant revelation at the time," Wood said. "It was on par with what researchers were doing theoretically in other disciplines, like quantum mechanics."

While Taylor's theory was successful and revolutionary, researchers still struggled with the problem of how dispersive spreading evolves from its dynamic, early behavior - what's termed as its initial condition - to when it attains the more constant value predicted by Taylor.

Scientists found some success by adding to the equation a time-dependent dispersion coe?cient, but the coefficient created problems of its own, the primary one being paradoxes.

"For example, if chemical solutes injected into a fluid at two di?erent times overlap, which time do you assign to the dispersion coe?cient?" Wood said. "Taylor himself understood that, where a time-dependent dispersion coe?cient was adopted, contemporary theories violated basic notions of causality in physics."

Wood and collaborators used another canon, the theory of partial di?erential equations, to show that problems with the time-dependent dispersion coefficient arose from neglecting the relaxation of the solute - the chemical injected into the fluid, or solution - from its initial condition.

"When chemical species are ?rst injected, their behavior is not necessarily consistent with a dispersion-type equation," Wood explained. "Rather, the initial condition first has to 'relax.' During this time, there is an additional term to account for that was missing in Taylor's macroscale dispersion equation."

In an equation, a term refers to a single number or a variable, or numbers and variables multiplied together.

The term Wood added corrects the dispersion equation to account for the initial con?guration of the chemical species moving around in the fluid. Somewhat surprisingly, Wood said, the theory also resolves paradoxes in other theories with time-dependent dispersion coe?cients.

"In the new theory, there is never a question about what dispersion coe?cient should be used when chemical solutes overlap," he said. "The adjustment to the spreading process is accounted for automatically by the presence of the additional term."

Metal-organic frameworks (MOFs) are unique micromaterial compounds consisting of a sponge-like network of metal ions or clusters linked together by organic linkers, and are able to store specific gas molecules in their pores. MOFs have such a high surface area due to their porosity that a single gram of the material has enough surface area to cover the size of a football field!

These super-sponges are used in research and industry to separate and store gases within tailor-made pockets, enabling their use in gas storage, separations, and sensing. Unlike traditional porous materials, MOFs can be modified as per need; in theory, their structure can be controlled through careful selection of the components of the synthesis process. But in practice, this process is challenged by the restricted synthetic conditions and high thermal and chemical sensitivity of MOFs. An attractive alternative is the post-synthetic modification (PSM) of MOFs.

Leading a team of scientists from Daegu Gyeongbuk Institute of Science and Technology (DGIST), Korea, Professor Jinhee Park approached this issue with the dual goals of giving desired functional groups to MOFs and introducing "mesoscopic" (bigger than microscopic) holes, which improve adsorption kinetics. Professor Park shares her convictions, stating, "We believe that this kind of study can facilitate the use of MOFs as a key material in environmental and energy related areas."

PSM through carbon-carbon bond formation has historically been difficult due to the lack of suitable reaction conditions that maintain the MOF structures. The scientists introduced stable carbon-carbon bonds by converting existing carbon-hydrogen bonds using elevated temperatures and adding "electrophilic organic halides or carbonyl compounds", allowing simultaneous introduction of the required functional groups as well as the mesoscopic holes.

Professor Park reports, "These results confirm the ability of the dual-PSM protocol to introduce desired alterations in MOFs while generating highly porous mesostructures." This technique could potentially improve the safety of workers in enclosed, gas-filled environments such as in the nuclear industry, and provide a more economically viable method of gas storage and purification.