Culture

Plants have to interpret temperature fluctuations over timescales ranging from hours to months to align their growth and development with the seasons.

Much is known about how plants respond to temperature but the mechanisms that allow them to measure the temperature signal are less well understood.

In this study which appears in Nature, researchers Yusheng Zhao and Rea Antoniou-Kourounioti in the groups of Professor Dame Caroline Dean and Professor Martin Howard at John Innes Centre show that slow growth is used as a signal to sense long-term changes in temperature.

"We have found a new temperature sensing mechanism that holds a long-term memory of the cold, integrating over fluctuating temperatures to measure cold duration. This is a new type of physical mechanism for temperature-sensing and can guide further studies in this area" explains first author Dr Yusheng Zhao.

Using a forward genetic screen - looking at the genetics of plants showing a particular trait - they found a dysfunctional response. These plants showed high levels of a protein called VIN3 in warm temperatures. This protein is well known as being upregulated during periods of cold and interacts with the epigenetic molecular memory system that allows plants to remember cold.

Dr Yusheng Zhao found these plants had one of two versions of mutated NTL8, a transcription factor or regulator protein that activated VIN3 even without cold.

To understand the role of NTL8 they tagged it with a fluorescent protein (GFP) and looked with help from the Bioimaging platform at the John Innes Centre to show where this protein is present compared to VIN3. This showed that the mutated version was found everywhere in the plant and the wild type protein was mostly observed in the growing tips of roots. It also showed that it accumulates slowly over time in the cold.

Using a theoretical approach to explore the problem further, the team reasoned that understanding how fast the NTL8 protein degrades may offer insight into how the slow dynamics of NTL8 and VIN3 operate. They discovered the NTL8 protein is long-lasting, as predicted by the theory.

Mathematical modelling showed that the main factor determining the amount of NTL8 protein is growth dependent dilution. If the weather gets warmer, the plants grow quicker and as cells multiply, the amount of NTL8 becomes diluted. In contrast, in cooler temperatures plants grow more slowly and NTL8 is more concentrated, being able to accumulate over time. The mathematical model can reproduce the observations of NTL8 protein levels seen in the warm and cold.

To further test the model, they added chemicals and hormones to change plant growth to see if this changed the levels of NTL8 as predicted by the model, which it did. In the roots they added the plant growth hormone Gibberellin, which causes plants to grow faster and NTL8 levels were lower, as expected. When they added an inhibitor of growth, NTL8 protein levels were higher in the whole plant. The team did similar experiments on the roots, and these predictions were confirmed too.

Dr Rea Antoniou-Kourounioti joint first author adds: "We were surprised by the simplicity of the new temperature mechanism we discovered, which recycles temperature information from one process [growth] to create a completely new temperature sensing mechanism for another [vernalization - the acceleration of flowering by cold]. We could reproduce most of the temperature-dependent changes in our experimental observations with our model by just changing the growth rate between warm and cold."

"This study revolutionises our understanding of how temperature is sensed by plants, and particularly how fluctuating long-term environmental conditions are integrated," says Professor Martin Howard.

"This study shows the fantastic synergy when experimental approaches are combined with computational modelling. We would never have figured out this mechanism by doing either separately," says Caroline Dean.

The findings will be useful for understanding how plants as well as other organisms sense the long-term fluctuating environmental signals and could apply to crops.

Washington, DC - July 15, 2020 - Metabolic syndrome increases the risk of severe disease from viral infection, according to a review of the literature performed by a team of researchers from St. Jude Graduate School of Biomedical Sciences and the University of Tennessee Health Science Center, both in Memphis. The research appears this week in the Journal of Virology, a publication of the American Society for Microbiology.

Metabolic syndrome is a cluster of at least 3 co-occurring conditions that raise the risk of heart disease, stroke and type 2 diabetes mellitus (T2DM). These conditions include excess abdominal fat, high blood pressure, excess blood sugar, abnormalities of lipids (including excess triglycerides and cholesterol), insulin resistance and a proinflammatory state.

Multiple studies have shown that obesity is associated with increased severity of influenza A, higher viral titers in exhaled breath and prolonged transmission of the virus, according to the report. Changes in the viral population may abet the emergence of more pathogenic influenza variants, according to the report. Despite the fact that influenza vaccines generate robust antibody titers in obese subjects, obesity doubles the likelihood of developing influenza.

As with influenza virus, the Centers for Disease Control and Prevention recently recognized obesity as a risk factor for severe illness caused by SARS-CoV-2. "This is not surprising because excess body weight and fat deposition apply pressure to the diaphragm, which further increases the difficulty of breathing during a viral infection," the researchers write.

But the risk goes beyond the burden of excess weight. A recent study highlighted in the literature review looked at 174 diabetes patients with confirmed cases of COVID-19. The study found that these patients were at significantly higher risk for severe pneumonia compared to non-diabetic COVID-19 patients. CT scans revealed a greater severity of lung abnormalities in these patients.

There was also a profound increase in serum IL-6 levels, a predictive biomarker for disease severity, the investigators write. These data imply that SARS-CoV-2 causes severe disease in obese patients and in those with T2DM by inducing bilateral pneumonia and a cytokine storm that damages the lung epithelial-endothelial barrier. (The epithelium lines surfaces exposed to the outer environment, such as the respiratory tract, the endothelium lines inner pathways such as those of the vasculature.)

However, one hypothetical risk for patients with T2DM who have hypertension or heart disease appears not to be a problem, after all, according to the report. These patients are commonly treated with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). These increase expression of ACE2, the receptor that SARS-CoV-2 uses to gain entry into cells.

Clinicians and researchers were initially concerned that ACE inhibitors and ARBs could promote adhesion and entry of SARS-CoV-2 into host cells, thereby increasing the risk of severe COVID-19. Contrary to concerns, multiple studies now suggest that ACE inhibitors and ARBs do not lead to poorer outcomes in COVID-19 infection.

"Future research should seek to [determine] how metabolic abnormalities increase viral pathogenesis, as this information will play an essential role in global preparedness against emerging seasonal and pandemic virus strains," the investigators conclude.

ASM is keeping the pulse on the SARS-CoV-2 pandemic with the COVID-19 Research Registry of top-ranked research articles curated by experts. In the eye of a pandemic, this curated database will ensure that scientists, journalists and the public have an efficient way to find the timeliest and most valuable SARS-CoV-2/COVID-19 research from the latest journal articles and preprints.

The American Society for Microbiology is one of the largest professional societies dedicated to the life sciences and is composed of 30,000 scientists and health practitioners. ASM's mission is to promote and advance the microbial sciences.

ASM advances the microbial sciences through conferences, publications, certifications and educational opportunities. It enhances laboratory capacity around the globe through training and resources. It provides a network for scientists in academia, industry and clinical settings. Additionally, ASM promotes a deeper understanding of the microbial sciences to diverse audiences.

Journal

Journal of Virology

Nuclear magnetic resonance (NMR) is employed in a wide range of applications. In chemistry, nuclear magnetic resonance spectroscopy is in standard use for the purposes of analysis, while in the medical field, magnetic resonance imaging (MRI) is used to see structures and metabolism in the body. Scientists at Johannes Gutenberg University Mainz (JGU) and the Helmholtz Institute Mainz (HIM), working in collaboration with visiting researchers from Novosibirsk in Russia, have developed a new method of observing chemical reactions. For this purpose they use NMR spectroscopy, but with an unusual twist: There is no magnetic field. "This technique has two advantages. For a start, we are able to analyze samples in metal containers and, at the same time, we can examine more complex substances made up of different types of components," said Professor Dmitry Budker, head of the Mainz-based group. "We think our concept could be extremely useful when it comes to practical applications."

As a chemical technique, NMR spectroscopy is used to analyze the composition of substances and to determine their structures. High-field NMR is frequently used, which allows the nondestructive examination of samples. However, this method cannot be used to observe chemical reactions in metal containers because the metal acts as a shield, preventing penetration of the relatively high frequencies. For this reason, NMR sample containers are typically made of glass, quartz, plastic, or ceramic. Furthermore, high-field NMR spectra of heterogeneous samples containing more than one component tend to be poor. There are more advanced concepts but these often have the drawback that they do not make in situ monitoring of reactions possible.

Use of zero- to ultralow-field magnetic resonance proposed as a solution

The team led by Professor Dmitry Budker has thus proposed the use of zero- to ultralow-field nuclear magnetic resonance, ZULF NMR for short, in order to circumvent the problems. In this case, due to the absence of a strong external magnetic field, a metal container will not have a screening effect. The research group used a titanium test tube and a conventional glass NMR test tube for comparison in their experiments. In each case, para-enriched hydrogen gas was bubbled into a liquid to initiate a reaction between its molecules and the hydrogen.

The results showed that the reaction in the titanium tube could be readily monitored using ZULF NMR. It was possible to observe the kinetics of the ongoing reaction with high spectroscopic resolution while continually bubbling parahydrogen gas. "We anticipate that ZULF NMR will find application in the field of catalysis for operando and in situ reaction monitoring as well as in the study of chemical reaction mechanisms under realistic conditions," write the researchers in their article published in the leading scientific journal Angewandte Chemie International Edition. Three researchers from the International Tomography Center in Novosibirsk were also involved in the project, namely Professor Igor V. Koptyug, a visiting scholar at HIM in Mainz, Dudari B. Burueva, a doctoral candidate of Koptyug who was also a visiting scholar and a joint first author of the now published study, and Dr. Kirill V. Kovtunov. "Sadly, our colleague Kirill Kovtunov passed away during the preparation of the manuscript for this publication. His contributions were very important to us," acknowledged Professor Dmitry Budker. Furthermore, a group of young scientists from HIM and JGU collaborated in the research project, namely joint first author Dr. James Eills, and Dr. John W. Blanchard, along with doctoral candidates Antoine Garcon and Román Picazo Frutos.

PHILADELPHIA -- Researchers from the Penn Institute of Immunology discovered three distinct immune responses to the SARS-CoV2 infection that could help predict the trajectory of disease in severe COVID-19 patients and may ultimately inform how to best treat them.

The findings were published in Science.

"For patients who are hospitalized with COVID-19, there isn't just one way for the immune system to respond. There's a lot of heterogeneity, which we've distilled down into what we're calling three "immunotypes," said senior author E. John Wherry, PhD, chair of the department of Systems Pharmacology and Translational Therapeutics and director of the Penn Institute of Immunology in the Perelman School of Medicine at the University of Pennsylvania. "We're hopeful we may actually be able to predict, or at least infer, the different immune patterns a patient has based on clinical data. This would allow us to start thinking about enrolling patients to different types of clinical trials investigating treatments."

The coronavirus triggers different immune responses and symptoms in critically ill patients, but how those two correspond has remained poorly understood, making treatment decisions more difficult.

While recent studies reveal details on the immune's response to the virus, most have been single-case reports or focused on a small group of individuals. This is the first study, to the author's knowledge, to offer up a comprehensive immune profile of a large number of hospitalized patients.

The researchers applied deep immune profiling to capture individual responses of 163 patients during the course of their infections. The study included 90 hospitalized patients treated at the Hospital of the University of Pennsylvania, 29 non-hospitalized patients, and 44 healthy donors with no COVID-19 infection. The immune responses varied among the group, but there were patterns that hold clinical promise.

The first immunotype had robust CD4+ T cell activity, with modest activation of CD8+ T cells and peripheral blood lymphocytes. CD4+ and CD8+ act as the main inflammatory immune cells that work to clear viruses. The second immunotype was characterized mainly by a subset of CD8+ T cells known as EM and EMRA and a modest activation of CD8+ T cells, memory B cells, and peripheral blood lymphocytes. The third immunotype showed little to no evidence of an immune response to the infection.

Next, researchers combined the profiling with clinical data to understand the relationships between immune responses and disease. The first immunotype was tied to more severe disease that included inflammation, organ failure, and acute kidney disease. The second correlated not with disease severity but instead pre-existing immunosuppression and mortality. The third type, which had no immune activation, was not associated with specific symptoms or clinical features, though they varied.

The immunotypes developed by Wherry and team represent adaptive immune responses. A second study from researchers at Penn, published in Science Immunology, uncovered new details about the innate, or initial, response to SARS-CoV2.

"T and B cell activity are informed by innate immune responses," said senior author Michael R. Betts, PhD, a professor of Microbiology and program leader in the Penn Institute of Immunology, who is also a co-author on the first study. "We believe what's happening with the innate response of the immune system might be what's leading to these three immune phenotypes Dr. Wherry's lab identified."

Profiling the blood samples of 42 infected patients (with moderate and severe disease) and 12 healthy donors, the researchers found a similar heterogeneity in immune adaptive responses: robust activation of CD4+ and CD8+ T cells, B cells, along with peripheral blood cells, like neutrophils, monocytes, and "natural killer," or NK, cells.

While the innate responses were also heterogenous, the researchers observed a decrease of CD15 and CD16 molecules on neutrophils and CD16 on NK cells, immature granulocytes, and monocytes, in patients with more severe disease. These two molecules are known players in the immune's response to viral infections that also represent a potential target for immunotherapy. How they are driving and exacerbating the adaptive responses in the three immunotypes is an important question the labs are working to better understand.

COVID-19 studies have been moving at an unprecedented speed as researchers band together to find answers. Among its many efforts, Penn formed lab and clinical research teams from diverse backgrounds to strengthen its focus on the immune system, along with the COVID Processing Unit to manage specimens to profile.

"Understanding the power of the immune system to regulate responses to disease is one of the major advances in medicine in the last decade, and Penn has been at the center leading that discovery. We are now applying the broad expertise and experience of our more than 200-person immunology community toward the research and treatment of COVID-19," said Jonathan A. Epstein, MD, executive vice dean, chief scientific officer, and a professor of Cardiovascular Research at Penn. "The deep immuno-profiling work the investigators applied here is likely to be useful not only now, for this disease, but into the future for many others."

An analysis of immune responses in 42 COVID-19 patients, both infected and recovered, identified immune signatures that distinguish severe COVID-19 cases. Notably, the analysis features insights not only into adaptive immune cell responses, but also those of innate immune cells responding to the virus. The findings will inform development of COVID-19 therapeutics. As the global COVID-19 pandemic continues, knowledge of the immunological signatures of severe COVID-19 is continually evolving. Whether there is a common profile of immune dysfunction in critically ill COVID-19 patients remains a question. To date, studies investigating this are limited, reporting on single patients or small cohorts. Seeking to expand upon them, Leticia Kuri-Cervantes and colleagues - a group overlapping in part with authors of the study by Mathew et al. published in Science today (15 July, 2020) - performed a high dimensional flow cytometry analysis on immune cells in blood from 42 COVID-19 patients with varying levels of disease state (moderate, severe, and recovered). Consistent with previous reports, they identified (and further defined) a characteristic immune phenotype in severe COVID-19 patients - distinct from the response in both healthy donors and also in COVID-19 patients with moderate or recovered disease. They also uncovered changes in the innate immune system - circulating neutrophils, monocytes and natural killer cells - in severe COVID-19 patients, though whether these are a "consequence or contributing factor towards COVID-19 severity remains to be defined," they say. The authors suggest the immune dysregulation they observed in severe COVID-19 patients "may necessitate targeted strategies to effectively manage clinical care" for this group. Longitudinal studies will be needed, they say, to determine whether early detection of these immunological perturbations predict severe disease trajectory in patients who are asymptomatic or have mild disease.

Expanding on observations made in smaller patient cohorts, researchers studying immune responses of 125 hospitalized COVID-19 patients identified distinct immune profiles -- "Immunotypes" -- and showed how these signatures correlated with disease severity. "By localizing patients on an immune topology map," Divij Mathew and colleagues say, "we can begin to infer which types of therapeutic interventions may be most useful in specific patients." As the global COVID-19 pandemic continues, researchers continue to investigate the characteristics of the human immune response in fighting it. Whether there is a common profile of immune dysfunction in critically ill COVID-19 patients remains a question. To date, studies investigating this are limited, reporting on single patients or small cohorts. Seeking to expand upon them, and also to better connect immune features in COVID-19 patients with clinical features of disease, Mathew and colleagues performed a high dimensional flow cytometry analysis on immune cells in blood from 125 COVID-19 patients at two points during their first week of hospitalization. Mathew and colleagues also collected clinical data on their patient cohort. Combining the flow cytometric and clinical data, they report several key findings, including that a defining feature of COVID-19 disease in this group is variability in immune response. At the same time, they found certain stable immune response signatures in subsets of their patients, which changed over time in consistent ways. Some of these patterns, like impaired CD8 T cell activation, were associated with worse disease outcomes. Mathew et al. ultimately defined three immune response signatures, or Immunotypes, in this cohort, associated with poor clinical trajectories versus improving health. "These Immunotypes may reflect fundamental differences in the ways patients respond to SARS-CoV2 infection," they say. They note that their "findings provoke the idea of the tailoring clinical treatments or future immune-based clinical trials to patients whose immunotype suggests greater potential benefit."

DALLAS, July 15, 2020 -- People who are homeless may experience 60-70% higher rates of cardiovascular events, such as heart attacks, strokes and heart failure, compared to the general population, according to a study cited in "The Importance of Housing and Cardiovascular Health and Well-Being," a new Scientific Statement from the American Heart Association published today in the Association's journal Circulation: Cardiovascular Quality and Outcomes.

The statement reviews and summarizes current research about how housing stability, safety, affordability, lack of access to high-quality housing and neighborhood environment affect cardiovascular disease risk. Homelessness is defined by the U.S. Department of Housing and Urban Development as the inability to obtain permanent housing. This includes serial renters who move often, people who temporarily live in a hotel, homeless shelter or with friends, and those living on the street.

Housing is one of several social determinants that impact cardiovascular health. Additional social determinants of health include socioeconomic factors, such as lack of education, unemployment or under-employment, and access to health care, among others.

"The disparities in cardiovascular health among people who are homeless and marginally housed are largely due to psychosocial stressors, unhealthy behaviors used as coping mechanisms and barriers to health care, including lack of insurance and stigmatization among this population," said Mario Sims, Ph.D., M.S., FAHA, chair of the writing group for the scientific statement, chief science officer of the Jackson Heart Study and professor in the department of medicine at the University of Mississippi Medical Center in Jackson, Mississippi.

"Chronic housing insecurity may impact a person's ability to eat properly, get quality sleep, schedule regular medical care or fill prescriptions due to cost. These factors all contribute to inadequate treatment to reduce cardiovascular risk factors such as high blood pressure, high cholesterol and tobacco use, and to the greater likelihood of having a cardiovascular event such as a heart attack or stroke," said Sims.

Among adults who were homeless and housing insecure:

70-80% smoke cigarettes, and smoking is attributed to 60% of CVD deaths in this population;

25% report recent cocaine use, which increases risk of heart attack; and

25% have mental illness, which may contribute to delayed diagnosis and fragmented medical care.

Poor housing quality - including structural deterioration, insufficient heating/cooling and exposure to cardiotoxic pollutants such as mold, lead or secondhand smoke - impacts cardiovascular disease risk factors. Studies have found that adults who live in older, public or low-income housing are more likely to have cardiovascular disease. Substandard living conditions affect mental health, which is also associated with heart and blood vessel health in both children and adults. Improving air quality, reducing dampness and living in a comfortable temperature have been shown to lower blood pressure.

Residential segregation by race and ethnicity as well as gentrification have further affected cardiovascular health by making it harder for more individuals to find affordable, high-quality housing. Gentrification is the process of revitalizing a deteriorating neighborhood, with affluent people displacing lower-income residents.

The 2007-2010 foreclosure crisis also had a substantial effect on housing accessibility. Multiple studies found an association between foreclosures and poorer cardiovascular health, with significant differences among races. Hispanics in residential areas at risk for foreclosure had higher rates of high blood pressure and high cholesterol. Foreclosures were also associated with higher rates of heart attacks and strokes among middle-aged Black residents.

"Neighborhood environments are strong predictors of cardiovascular health and well-being," said Sims. "Studies have consistently shown that individuals residing in economically distressed neighborhoods with high poverty and unemployment rates have a higher incidence of cardiovascular risk factors, including obesity, diabetes, hypertension and heart disease, and higher risk of stroke and death from a cardiovascular disease such as heart attacks, strokes, heart failure and others."

Urban design features, such as an area's walkability and accessibility to healthy food options, are associated with body mass index (a way to measure body weight), blood pressure, type 2 diabetes and metabolic syndrome (a cluster of risk factors that include high blood pressure, high blood sugar, excess body fat around the waist and abnormal cholesterol or triglyceride levels). Research suggests that neighborhood greenness, or vegetation, may also be beneficial for cardiovascular health. Higher levels of greenness are also associated with lower rates of type 2 diabetes, heart attack, coronary artery disease and heart failure.

Providing equitable housing opportunities may improve cardiovascular health, and efforts to reduce health disparities should consider multi-level housing interventions, particularly for under-resourced communities, according to the writing group.

If you've ever held a trilobite fossil, seen one in a classroom, or walked by one in a store, chances are it was Elrathia kingii, one of the most common and well-recognized trilobites, and collected by the hundreds of thousands in western Utah. But despite the popularity of this species, scientists had not determined how it grew--from hatchling to juvenile to adult--until now. New work from the American Museum of Natural History published today in the journal Papers in Palaeontology describes the development and growth rate of Elrathia kingii--only the second such dataset to be compiled for a trilobite--allowing for the first comparison among trilobite species.

"There's quite a big size range among trilobites. Some never got bigger than about a centimeter, while the largest on record is 72 centimeters (28 inches)," said Melanie Hopkins, an associate curator in the Museum's Division of Paleontology and the study's author. "Growth-rate studies like this one can help us tackle some of the big-picture questions: How did some trilobites get so big? What was the environmental context for that? And how did body size evolve over the evolutionary history of the clade?"

Trilobites are a group of extinct marine arthropods--distantly related to the horseshoe crab--that lived for almost 300 million years. They were incredibly diverse, with more than 20,000 described species. Their fossilized exoskeletons are preserved in sites all over the world, from the United States to China. Like insects, they molted throughout their lifetimes, leaving clues to how they changed during development. But to calculate the species' growth rate, scientists need fossils representing all stages of the animal's life--and lots of them.

"There are tons of specimens of Elrathia kingii out there but most of them are adults, and data from exactly where they were collected is inconsistent," Hopkins said. "I needed material that I could collect from as small a section as possible that included a lot of juveniles."

So in May 2018, Hopkins spent five days in Utah with a crew consisting of Museum staff and volunteers at a new fossil site said to preserve bucketloads of Elrathia kingii. By the end of the trip, they had collected about 500 specimens--many of them juveniles, which can be as small as half a millimeter long--from a section of outcrop just 1.5 meters (about 5 feet) long.

Hopkins estimated the growth rate and compared it to previously published data on a different trilobite, Aulacopleura konincki--the first time two trilobite species have been compared in this way. The two species look very similar and Hopkins found that they also grow in similar ways: for example, the growth of the trunk--the area immediately below the trilobite's head made up of segments that increase with age--was controlled by a growth gradient, with those that were younger and closer to the back of the body undergoing faster growth. But while Elrathia kingii was smaller in early development and went through fewer molts before adulthood, it had faster growth rates, ultimately reaching sizes on par with Aulacopleura konincki, the largest of which are about 4 centimeters long.

In future studies, Hopkins is planning to add growth-rate data on different, more diverse-looking trilobite species to her models.

The most powerful and advanced computing is still primitive compared to the power of the human brain, says Chinedu E. Ekuma, Assistant Professor in Lehigh University's Department of Physics.

Ekuma's lab, which aims to gain an understanding of the physical properties of materials, develops models at the interface of computation, theory, and experiment. One area of focus: 2-Dimensional (2D) materials. Also dubbed low-dimensional, these are crystalline nanomaterials that consist of a single layer of atoms. Their novel properties make them especially useful for the next-generation of AI-powered electronics, known as neuromorphic, or brain-like devices.

Neuromorphic devices attempt to better mimic how the human brain processes information than current computing methods. A key challenge in neuromorphic research is matching the human brain's flexibility, and its ability to learn from unstructured inputs with energy efficiency. According to Ekuma, early successes in neuromorphic computing relied mainly on conventional silicon-based materials that are energy inefficient.

"Neuromorphic materials have a combination of computing memory capabilities and energy efficiency for brain-like applications," he says.

Now Ekuma and his colleagues at the Sensor and Electrons Devices Directorate at the U.S. Army Research Laboratory have developed a new complex material design strategy for potential use in neuromorphic computing, using metallocene intercalation in hafnium disulfide (HfS2). The work is the first to demonstrate the effectiveness of a design strategy that functionalizes a 2D material with an organic molecule. It has been published in an article called "Dynamically reconfigurable electronic and phononic properties in intercalated HfS2" in Materials Today. Additional authors: Sina Najmaei, Adam A.Wilson Asher C. Leff and Madan Dubey of the United States Army Research Laboratory.

"We knew that low-dimensional materials showed novel properties, but we did not expect such high tunability of the HfS2-based system," says Ekuma. "The strategy was a concerted effort and synergy between experiment and computation. It started with an afternoon coffee chat where my colleagues and I discussed exploring the possibility of introducing organic molecules into a gap, known as van der Waals gap, in 2D materials. This was followed by the material design and rigorous computations to test the feasibility. Based on the encouraging computational data, we proceeded to make the sample, characterize the properties, and then made a prototype device with the designed material."

Scholars in search of energy-efficient materials may be particularly interested in this research, as well as industry, especially semiconductor industries designing logic gates and other electronic devices.

"The key takeaway here is that complex materials design based on 2D materials is a promising route to achieving high performing and energy-efficient materials," says Ekuma.

COLUMBUS, Ohio - Whether you use a taxi or a rideshare app like Uber, you're still going to get a driver who will take you to your destination.

But consumers view an employee of a taxi company differently from an independent driver picking up riders via an app, a new Ohio State University study suggests.

Consumers see themselves as helping independent providers like those on rideshare apps. When they use traditional firms, like a taxi company, they don't view themselves as helping the employees - they're just purchasing a service.

The peer-to-peer business model of firms like Uber or Airbnb is changing how consumers view some service providers, said John Costello, lead author of the study and a doctoral candidate in marketing at Ohio State's Fisher College of Business.

"Previous work has shown that consumers view employees as being an extension of the company they work for," Costello said.

"But we found that consumers see providers for these peer-to-peer companies as separate from the company - as people just like themselves."

The study was published online recently in the Journal of Marketing.

These different views of service providers have important implications for how firms like Uber and Airbnb market themselves to consumers, the study found. It may also have consequences for issues like how consumers tip independent providers and their support for regulations in the sharing economy.

Results showed that peer-to-peer companies had better success marketing themselves to consumers when they focused on the people that provide their service, and less success when they focused on their companies or apps.

"When peer-to-peer companies focus their marketing on the people who provide their services, we found it made consumers think about how their purchases benefit the individual providers," said study co-author Rebecca Reczek, professor of marketing at Ohio State's Fisher College.

"But when peer-to-peer firms focused on their apps instead, it makes people think that they're just purchasing from a company rather than thinking about how their purchase helps an individual."

In one real-life field study, the researchers partnered with a peer-to-peer company whose app allowed college students to buy or rent textbooks from each other.

The company set up a table on a college campus for several days to promote their service. On half the days, the banner on the table and the promotional cards they had available focused on using the company's app to buy or rent books. On the other half of the days, the banner and cards focused on how you could buy or rent books directly from your classmates.

Results showed that more of the promotional cards were taken when the focus was on the student providers (379) than when the focus was on the app itself (281).

In a second study, 259 students were shown ads for one of two fictitious firms, either "Reliable Rideshare" or "Reliable Cab." Some of the ads focused on the companies themselves (the cab or the rideshare company) and some focused on people (employees of the cab company or drivers for the rideshare company).

Participants were also asked if they thought their purchases from either the rideshare or cab company would help someone.

Findings showed that consumers were more likely to say they would purchase from the rideshare company when the ad focused on the providers rather than the company itself. But for the cab company, the ads' focus made no difference in purchase intention.

The reason was that participants were more likely to say their purchases were helping people when they used the rideshare drivers than when they used the cab company employees, the study found.

"When people are buying from an employee, like those who work for a taxi company, they don't really think of themselves as helping these workers. They're just making a transaction," Costello said.

Overall, the results show that peer-to-peer companies should focus on people who provide their services in their ads and marketing materials, Reczek said.

But the findings may also have wider implications. For example, if people think they are already helping rideshare drivers simply by hiring them, they may be less likely to tip them or tip them less. They may also be less likely to support regulations that financially protect these workers.

But some research suggests that rideshare drivers often make less than minimum wage, she noted.

"This perception of consumers that they're helping simply through their purchases may have negative consequences for providers," Reczek said.

"Their beliefs may not match the economic reality of what it is like to be a provider for a peer-to-peer firm."

From mRNA vaccines entering clinical trials, to peptide-based vaccines and using molecular farming to scale vaccine production, the COVID-19 pandemic is pushing new and emerging nanotechnologies into the frontlines and the headlines.

Nanoengineers at UC San Diego detail the current approaches to COVID-19 vaccine development, and highlight how nanotechnology has enabled these advances, in a review article in Nature Nanotechnology published July 15.

"Nanotechnology plays a major role in vaccine design," the researchers, led by UC San Diego Nanoengineering Professor Nicole Steinmetz, wrote. Steinmetz is also the founding director of UC San Diego's Center for Nano ImmunoEngineering. "Nanomaterials are ideal for delivery of antigens, serving as adjuvant platforms, and mimicking viral structures. The first candidates launched into clinical trials are based on novel nanotechnologies and are poised to make an impact."

Steinmetz is leading a National Science Foundation-funded effort to develop--using a plant virus-- a stable, easy to manufacture COVID-19 vaccine patch that can be shipped around the world and painlessly self-administered by patients. Both the vaccine itself and the microneedle patch delivery platform rely on nanotechnology. This vaccine falls into the peptide-based approach described below.

"From a vaccine technology development point of view, this is an exciting time and novel technologies and approaches are poised to make a clinical impact for the first time. For example, to date, no mRNA vaccine has been clinically approved, yet Moderna's mRNA vaccine technology for COVID-19 is making headways and was the first vaccine to enter clinical testing in the US."

As of June 1, there are 157 COVID-19 vaccine candidates in development, with 12 in clinical trials.

"There are many nanotechnology platform technologies put toward applications against SARS-CoV-2; while highly promising, many of these however may be several years away from deployment and therefore may not make an impact on the SARS-CoV-2 pandemic," Steinmetz wrote. "Nevertheless, as devastating as COVID-19 is, it may serve as an impetus for the scientific community, funding bodies, and stakeholders to put more focused efforts toward development of platform technologies to prepare nations for readiness for future pandemics," Steinmetz wrote.

To mitigate some of the downsides of contemporary vaccines--namely live-attenuated or inactivated strains of the virus itself-- advances in nanotechnology have enabled several types of next-generation vaccines, including:

Peptide-based vaccines: Using a combination of informatics and immunological investigation of antibodies and patient sera, various B- and T-cell epitopes of the SARS-CoV-2 S protein have been identified. As time passes and serum from convalescent COVID-19 patients are screened for neutralizing antibodies, experimentally-derived peptide epitopes will confirm useful epitope regions and lead to more optimal antigens in second-generation SARS-CoV-2 peptide-vaccines. The National Institutes of Health recently funded La Jolla Institute for Immunology in this endeavor.

Peptide-based approaches represent the simplest form of vaccines that are easily designed, readily validated and rapidly manufactured. Peptide-based vaccines can be formulated as peptides plus adjuvant mixtures or peptides can be delivered by an appropriate nanocarrier or be encoded by nucleic acid vaccine formulations. Several peptide-based vaccines as well as peptide-nanoparticle conjugates are in clinical testing and development targeting chronic diseases and cancer, and OncoGen and University of Cambridge/DIOSynVax are using immunoinformatics-derived peptide sequences of S protein in their COVID-19 vaccine formulations.

An intriguing class of nanotechnology for peptide vaccines is virus like particles (VLPs) from bacteriophages and plant viruses. While non-infectious toward mammals, these VLPs mimic the molecular patterns associated with pathogens, making them highly visible to the immune system. This allows the VLPs to serve not only as the delivery platform but also as adjuvant. VLPs enhance the uptake of viral antigens by antigen-presenting cells, and they provide the additional immune-stimulus leading to activation and amplification of the ensuing immune response. Steinmetz and Professor Jon Pokorski received an NSF Rapid Research Response grant to develop a peptide-based COVID-19 vaccine from a plant virus: https://jacobsschool.ucsd.edu/news/news_releases/release.sfe?id=3005. Their approach uses the Cowpea mosaic virus that infects legumes, engineering it to look like SARS-CoV-2, and weaving antigen peptides onto its surface, which will stimulate an immune response.

Their approach, as well as other plant-based expression systems, can be easily scaled up using molecular farming. In molecular farming, each plant is a bioreactor. The more plants are grown, the more vaccine is made. The speed and scalability of the platform was recently demonstrated by Medicago manufacturing 10 million doses of influenza vaccine within one month. In the 2014 Ebola epidemic, patients were treated with ZMapp, an antibody cocktail manufactured through molecular farming. Molecular farming has low manufacturing costs, and is safer since human pathogens cannot replicate in plant cells.

Nucleic-acid based vaccines: For fast emerging viral infections and pandemics such as COVID-19, rapid development and large scale deployment of vaccines is a critical need that may not be fulfilled by subunit vaccines. Delivering the genetic code for in situ production of viral proteins is a promising alternative to conventional vaccine approaches. Both DNA vaccines and mRNA vaccines fall under this category and are being pursued in the context of the COVID-19 pandemic.

* DNA vaccines are made up of small, circular pieces of bacterial plasmids which are engineered to target nuclear machinery and produce S protein of SARS-CoV-2 downstream.

* mRNA vaccines on the other hand, are based on designer-mRNA delivered into the cytoplasm where the host cell machinery then translates the gene into a protein - in this case the full-length S protein of SARS-CoV-2. mRNA vaccines can be produced through in vitro transcription, which precludes the need for cells and their associated regulatory hurdles

While DNA vaccines offer higher stability over mRNA vaccines, the mRNA is non-integrating and therefore poses no risk of insertional mutagenesis. Additionally, the half-life, stability and immunogenicity of mRNA can be tuned through established modifications.

Several COVID-19 vaccines using DNA or RNA are undergoing development: Inovio Pharmaceuticals has a Phase I clinical trial underway, and Entos Pharmeuticals is on track for a Phase I clinical trial using DNA. Moderna's mRNA-based technology was the fastest to Phase I clinical trial in the US, which began on March 16th, and BioNTech-Pfizer recently announced regulatory approval in Germany for Phase 1/2 clinical trials to test four lead mRNA candidates.

Subunit vaccines: Subunit vaccines use only minimal structural elements of the pathogenic virus that prime protective immunity-- either proteins of the virus itself or assembled VLPs. Subunit vaccines can also use non-infectious VLPs derived from the pathogen itself as the antigen. These VLPs are devoid of genetic material and retain some or all of the structural proteins of the pathogen, thus mimicking the immunogenic topological features of the infectious virus, and can be produced via recombinant expression and scalable through fermentation or molecular farming. The frontrunners among developers are Novavax who initiated a Phase I/II trial on May 25, 2020. Also Sanofi Pasteur/GSK, Vaxine, Johnson & Johnson and the University of Pittsburgh have announced that they expect to begin Phase I clinical trials within the next few months. Others including Clover Biopharmaceuticals and the University of Queensland, Australia are independently developing subunit vaccines engineered to present the prefusion trimer confirmation of S protein using the molecular clamp technology and the Trimer-tag technology, respectively.

Delivery device development

Lastly, the researchers note that nanotechnology's impact on COVID-19 vaccine development does not end with the vaccine itself, but extends through development of devices and platforms to administer the vaccine. This has historically been complicated by live attenuated and inactivated vaccines requiring constant refrigeration, as well as insufficient health care professionals where the vaccines are needed.
"Recently, modern alternatives to such distribution and access challenges have come to light, such as single-dose slow release implants and microneedle-based patches which could reduce reliance on the cold chain and ensure vaccination even in situations where qualified health care professionals are rare or in high demand," the researchers write. "Microneedle-based patches could even be self-administered which would dramatically hasten roll-out and dissemination of such vaccines as well as reducing the burden on the healthcare system."

Pokorski and Steinmetz are co-developing a microneedle delivery platform with their plant virus COVID-19 vaccine for both of these reasons.

This work is supported by a grant from the National Science Foundation (NSF CMMI-2027668)

"Advances in bio/nanotechnology and advanced nanomanufacturing coupled with open reporting and data sharing lay the foundation for rapid development of innovative vaccine technologies to make an impact during the COVID-19 pandemic," the researchers wrote. "Several of these platform technologies may serve as plug-and-play technologies that can be tailored to seasonal or new strains of coronaviruses. COVID-19 harbors the potential to become a seasonal disease, underscoring the need for continued investment in coronavirus vaccines."

A genomic error that causes Rett Syndrome, a serious lifelong neurological disorder, can be corrected in the brains of mice by rewriting the genetic instructions carried by the RNA.

The new research, published July 14 in the journal Cell Reports, shows that RNA editing may repair the underlying cause of Rett Syndrome in a mouse model. The technology recoded enough RNA to restore half of the normal protein in three different kinds of neurons in the Rett mouse.

The results represent a promising early step in using RNA editing to treat Rett Syndrome, a disorder that affects about 350,000 individuals worldwide. The authors in the neuroscience lab of Gail Mandel at the Vollum Institute at Oregon Health and Science University (OHSU) in Portland, caution, however, that much work lies ahead to advance the potential therapeutic to the clinic.

"This was a proof of principle" that the technique works in the brain, says lead author John Sinnamon.

People diagnosed with Rett Syndrome have mutations in a gene called MECP2. The gene makes a protein that is abundant in brain cells and controls the activity of many other genes.

Disease symptoms usually appear between 12 and 18 months of age and can include loss of speech and purposeful hand use, respiratory problems, motor deficits, seizures, and gastrointestinal and orthopedic issues. No cure exists, but studies in mice suggest restoring healthy MeCP2 protein function can dramatically reverse the condition.

Hundreds of different mutations in the MECP2 gene have been found in people with Rett Syndrome. The instructions for the protein it makes are coded in a unique combination of four genomic "letters" -- A, C, G and T. The cell transcribes the DNA code into RNA and then into protein.

The idea behind the strategy used in this new study is to produce a healthy MeCP2 protein by repairing or "editing" the genetic error in the RNA.

The team used a mouse model of a human MECP2 mutation in which a single letter is wrong, an A where a G should be. They adapted an RNA editing technique by designing a guide to recognize the mutated section and change the A back to the normal G.

In 2017, Sinnamon, Mandel, and their colleagues reported their first success with the RNA approach, efficiently repairing the Rett mouse mutant RNA in developing neurons in a lab dish. In the new study, the team expanded on these results. They asked three questions: Is it possible to edit MeCP2 RNA in several different types of neurons in adult mice in vivo? If so, what types of neurons can be edited? Does editing restore MeCP2 protein function?

To address these questions, the researchers packaged a mouse Mecp2 RNA guide and human editing enzyme (the "editase") in a viral vector and introduced it directly into the hippocampus, a well-studied brain structure associated with learning and memory.

The injected editase repaired about half of the RNA produced by the mutant MeCP2 gene in each of three types of neurons located in different regions of the hippocampus and, importantly, MeCP2 protein function was equally repaired in the neurons.

"It is encouraging that this RNA editing approach seems to be efficacious in different types of neurons in the brain," says Mandel, the senior author whose lab has pioneered the concept of RNA editing in Rett Syndrome. A similar repair rate should be achievable throughout the brain, the researchers believe, if a vector can be delivered diffusely throughout the brain.

"In the next set of experiments," Mandel says "we will administer the virus by blood, so that the entire brain is subject to editing. This will allow us to monitor whether there is any amelioration of Rett symptoms in the mice."

As a strategy to restore the normal function of MECP2, the single-base RNA editing approach of swapping out A and G could address about 40% of all known mutations that cause Rett Syndrome, Sinnamon says.

The researchers reported that RNA of genes other than Mecp2 also were inadvertently edited, known as off-target effects. It is unknown what, if any, effect the off-target edits had in the mice. The experimental treatment appeared to cause no harm to the mice over the study time period.

As the RNA editing approach progresses through experimental steps, additional questions will need to be answered. "We need to know how much MECP2 RNA we need to repair in an individual cell and in how many cells in the nervous system," Mandel says.

Her research group and others in the editing field also want to learn more about how to increase editing efficiency while diminishing off-target effects. "There are many bright and determined investigators working on these problems," she says. "My hope is this paper will stimulate these creative minds even further. We are trying to take advantage of what's happening in the field in real time and apply the emerging optimizations to Rett and other neurological diseases.

"The study is the first example of RNA editing in a mouse model of a neurological disease, and therefore a considerable step forward in the potential of RNA editing becoming a therapeutic for Rett Syndrome," says Monica Coenraads, executive director of Rett Syndrome Research Trust, which helped fund the study. "Strategies that edit the mutation are an elegant way of addressing the problem. This exciting progress would not be possible without all of RSRT's supporters and the affected families that are so dedicated to raising funds for us."

RSRT funds six genetic approaches to restore a functioning MeCP2 protein in patients with disease causing mutations. Beyond RNA editing, other approaches are gene replacement, which is the closest to the clinic, gene editing, RNA trans-splicing, protein replacement and reactivation of the silent MeCP2 on the inactive X.

The study was funded by the Rett Syndrome Research Trust and the National Institutes of Health. Mandel is a scientific co-founder of Vico Therapeutics, a biotech company working on non-viral approaches to edit RNA in Rett syndrome and other neurological conditions.

In a world with a consistently growing population and a climate crisis, food shortage is a looming threat. To alleviate this threat, crop scientists, botanists, genetic engineers, and others, have been exploring ways of boosting crop productivity and resilience. One way to control plant growth and physiology is to regulate the levels of "phytohormones" or plant hormones.

However, much remains to be known about the mechanisms that underlie this hormonal regulation in plants, limiting advancement in this direction. Now, in a study led by Nagoya University Japan, a team of scientists has discovered, using rice plants as the study model, that a process called "allosteric regulation" is involved in maintaining the phytohormonal balance in plants. Their findings, published in Nature Communications, could hold the key to significantly advancing the research on plant growth and development, providing a potential solution for food security.

Plants survive by adapting their development and physiology to their surrounding environments by controlling the levels of enzymes driving the synthesis of two phytohormones, gibberellin and auxin. Enzymes are proteins that bind to one or more reactant chemicals and speed up a reaction process. The binding site is called the activation site. In 1961, it was discovered that in bacteria, enzyme activity is enhanced or inhibited via allosteric regulation, which essentially is the binding of a molecule called the "effector" at a site other than the active site of the enzyme. In allosteric regulation, the structure of the enzyme changes to either support or hinder the reaction that the enzyme enables.

Professor Miyako Ueguchi-Tanaka of Nagoya University, lead scientist in the team that has now observed allosteric regulation in plants for the first time, explains their research findings, ''We used a technique called X-ray crystallography and found that, as molecules of the enzymes (gibberellin 2-oxidase 3 [GA2ox3], and auxin dioxygenase [DAO]) bind to gibberellin and auxin (respectively), they interact among themselves and form 'multimeric' structures, comprising four and two units respectively. As the amounts of gibberellin and auxin increase, so does the rate of multimerization of the enzymes. And multimerization enhances the activity of the enzymes, enabling greater degradation of gibberellin and auxin. Synchronous structural changes and activity enhancement are typical of allosteric-regulation events."

The scientists further carried out "phylogenetic" analysis of GA2ox3 and DAO, which revealed that plants independently developed this hormone regulation mechanism at three separate time-points over the course of the evolutionary process.

Enthusiastic about the future prospects of these findings, Prof Ueguchi says, "The activity control system revealed here can be used to artificially regulate the activity of the growth inactivating hormones in plants. As a result, rice crop productivity can be improved and high-biomass plants can be produced in the event of food shortage or an environmental crisis."

Of course, this study is only a stepping stone for now, and much remains to be done to see how the findings of this study can be applied practically in agricultural lands. However, these findings certainly are encouraging, and they signal the coming of a new era of sustainable development fueled by biotechnological advancements.

DALLAS - July 14, 2020 - A team led by UT Southwestern researchers has identified brain circuitry that plays a key role in the dysfunctional social, repetitive, and inflexible behavioral differences that characterize autism spectrum disorders (ASD). The findings, published online this week in Nature Neuroscience, could lead to new therapies for these relatively prevalent disorders.

The Centers for Disease Control and Prevention estimate that about 1 in 54 children in the U.S. have ASD, a broad range of neurodevelopmental conditions thought to be caused by a combination of genetic and environmental factors. Although researchers have identified some key genes and pathways that contribute to ASD, the underlying biology of these disorders remains poorly understood, says Peter Tsai, M.D., Ph.D., assistant professor in the departments of neurology and neurotherapeutics, neuroscience, pediatrics, and psychiatry at UT Southwestern Medical Center and a member of the Peter O'Donnell Jr. Brain Institute.

However, Tsai explains, one key brain region that's been implicated in ASD dysfunction is the cerebellum, part of the hindbrain in vertebrates that holds about three-quarters of all the neurons in the body and has traditionally been linked with motor control. Recent studies by Tsai and his colleagues have demonstrated that inhibiting activity in a region of the cerebellum known as Rcrus1 can cause altered social and repetitive/inflexible behaviors reminiscent of ASD in mice. Their work also found that stimulation of this area could rescue social behaviors in an ASD-relevant model but was unable to improve repetitive or inflexible behaviors. Together, these studies suggested that additional regions of the cerebellum might also regulate repetitive and/or inflexible behaviors.

In addition, how these cerebellar regions might regulate these ASD-relevant behaviors remained unknown. To learn more about the brain circuitry controlling these behaviors, Tsai and his colleagues worked with mice genetically engineered to reduce the activity of Purkinje cells, specialized cells that turn down the activity of other brain regions. When they examined the activity of the rest of the brain, they saw increased activity in the medial prefrontal cortex (mPFC), another region previously implicated in ASD. Behavioral tests showed that these animals displayed characteristic social and repetitive/inflexible behaviors reminiscent of ASD. When the researchers inhibited mPFC activity in these animals, both social impairments and repetitive/inflexible behaviors improved.

Because the cerebellum and the mPFC are on opposite ends of the brain, Tsai and his colleagues used microscopic imaging to trace how these regions are linked. They found connections specifically between Rcrus1 and the mPFC in these animals, with decreased Rcrus1 activity leading to increased mPFC activity. Further investigation showed that connectivity in this region wasn't just disrupted in these particular mice. It also existed in about a third of 94 different mouse lines carrying autism-related mutations and in two independent cohorts of people with ASD.

Looking further to better determine the anatomical connections between these regions, the researchers saw that signals from Rcrus1 appear to be routed to the mPFC through an area known as the lateral nucleus; however, modulation of this region was only sufficient to improve social behaviors in their genetic mouse model while repetitive/inflexible behaviors remained abnormal. Thus, Tsai and colleagues interrogated other cerebellar regions and found that modulation of another ASD-implicated cerebellar region, the posterior vermis, results in improvement in repetitive and inflexible behaviors. They then asked whether this cerebellar region also targets the mPFC and found that both posterior vermis and Rcrus1 converge on the mPFC through another intermediate region, the ventromedial thalamus.

Each of these regions could play a key role in potential future therapies for ASD, Tsai explains. And because their experiments could improve dysfunctional social and repetitive/inflexible behaviors even in adult animals, it raises the possibility that therapies that target this circuit in humans might be able to improve ASD-related dysfunction even into adulthood.

Just as an electrician can repair a home's wiring once he or she understands the wiring diagram, these findings give us potential hope for improving dysfunctional activity in the circuits involved in ASD," Tsai says.

The fear that people developed at the start of the COVID-19 outbreak has given way to anger over the course of the pandemic, a study of global sentiments led by Nanyang Technological University, Singapore (NTU Singapore) has found.

In an analysis of over 20 million tweets in English related to the coronavirus, an international team of communication researchers observed that tweets reflecting fear, while dominant at the start of the outbreak due to the uncertainty surrounding the coronavirus, have tapered off over the course of the pandemic.

Xenophobia was a common theme among anger-related tweets, which progressively increased, peaking on 12 March - a day after the World Health Organisation declared the COVID-19 outbreak a pandemic. The anger then evolved to reflect feelings arising from isolation and social seclusion.

Accompanying this later shift is the emergence of tweets that show joy, which the researchers say suggested a sense of pride, gratitude, hope, and happiness. Tweets that reflected sadness doubled, although they remain proportionally lower than the other emotions.

The rapid evolution of global COVID-19 sentiments within a short period of time points to a need to address increasingly volatile emotions through strategic communication by government and health authorities, as well as responsible behaviour by netizens before they give rise to "unintended outcomes", said Professor May O. Lwin of NTU's Wee Kim Wee School of Communication and Information.

Prof Lwin, who led the team representing four countries, said: "Worldwide, strong negative sentiments of fear were detected in the early phases of pandemic but by early April, these emotions have gradually been replaced by anger. Our findings suggest that collective issues driven by emotions, such as shared experiences of distress of the COVID-19 pandemic including large-scale social isolation and the loss of human lives, are developing.

"If such overbearing public emotions are not addressed through clear and decisive communication by authorities, citizen groups and social media stakeholders, there is potential for the emergence of issues such as breeding mistrust in the handling of the disease, and a belief in online falsehoods that could hinder the ongoing control of the disease."

The study was published in the scientific journal JMIR Public Health & Surveillance in May.

A glimmer of hope and gratitude amidst anger

To identify trends in the expression of the four basic emotions - fear, anger, sadness, and joy - and examine the narratives underlying those emotions, Prof Lwin and her team first collected 20,325,929 tweets in English containing the keywords 'Wuhan', 'corona', 'nCov', and 'covid'.

The tweets, collected from late January to early April at the Institute of High Performance Computing in Agency for Science, Technology and Research (A*STAR) using Twitter's standard search application interface programme, came from over 7 million unique users in more than 170 countries.

"Although the data looks at only public tweets surrounding the four selected keywords, the results are sufficient to start a conversation about possible issues arising from the pandemic at present," said Prof Lwin, whose collaborators also include Tianjin University, University of Lugano, and University of Melbourne.

The underlying emotions of tweets were then analysed using an algorithm developed by A*STAR, whose accuracy has been demonstrated in previous studies. Word clouds based on the top single words and two-word phrases were generated for each of the four emotions.

Upon analysing the results, the team found that words such as 'first case' and 'outbreak' were among the most-used words in tweets from late January, indicating fear that was possibly related to the emerging coronavirus and the unknown nature of it, causing uncertainty about containment and spread.

Xenophobia was also reflected at the start of the pandemic, when the disease was predominantly contained in China and Asia, as indicated by words such as 'racist' and 'Chinese people'.

As the pandemic escalated, fears around shortages of COVID-19 diagnostic tests and medical supplies emerged, as suggested by words such as 'test shortages' and 'uncounted'. Anger then shifted to discourses around the isolation fatigue that can occur from social seclusion, indicated by words such as "stay home" and several swear words.

Signs of sadness surrounding the topics of losing friends and family members also started to surface, with words relating to 'loved one' and 'passed away' highlighting potential social concerns arising from personal traumatic experiences of the pandemic.

But accompanying these negative emotions were parallel escalating sentiments of joy relating to national pride, gratitude, and community spirit, the NTU-led team found, with words such as 'thank', 'good news' and 'feel good'.

Tweets that were collected and analysed from early April to mid-June as an extension of the JMIR study also showed that these positive sentiments exceeded fear postings on social media.

Upcoming follow-up studies led by Prof Lwin will dive into country-specific trends in public emotions. Preliminary findings show that in Singapore, there is a moderate balance of positive sentiments relating to resilience, civic pride, and celebration of heroic acts and acts of kindness. This is in contrast to other countries where strong negative emotions overwhelmingly feature in the social media posts.