Native to the southeastern United States, a weedy grass has spread northward to Canada and also made its way to Australia and Japan. Andropogon virginicus grows densely packed and up to seven feet tall, disrupting growth patterns of other plants and competing for resources. When burned, it grows back stronger. There is no way to effectively remove the weed once it has invaded. But there might be a way to use it to human advantage.
An international team of researchers has found that A. virginicus extracts appear to be effective against several human diseases, including diabetes and cancer. The results were published on Dec. 31, 2020, in a special issue of Plants, titled “Biological Activities of Plant Extracts.”
“A. virginicus is an invasive weed that seriously threatens agricultural production and economics worldwide,” said paper author Tran Dang Xuan, associate professor in the Transdisciplinary Science and Engineering Program in the Graduate School of Advanced Science and Engineering at Hiroshima University. “However, no solution efficiently utilizing and tackling this plant has been found yet. In this paper, we highlight the potential application of A. virginicus extracts in future medicinal production and therapeutics of chronic diseases such as type 2 diabetes and blood cancer, which can deal with both crop protection and human health concerns.”
Researchers found high levels of flavonoids in the samples they extracted from the weed. These plant chemicals have significant antioxidant and anti-inflammatory properties, according to Xuan. When tested against a variety of cell lines, the extracted plant chemicals bonded to free radicals, preventing damage to the cells. At skin level, this helps prevent age spots by inhibiting a protein called tyrosinase. Among other, deeper healthful actions, this bonding also helps prevent knock-on cellular actions that can lead to type 2 diabetes.
The team also specifically applied the extracted chemicals to a line of chronic myelogenous leukemia, a rare blood cancer. The extract appeared to kill off the cancer cells.
Xuan said the researchers plan to establish a comprehensive process to isolate and purify the compounds responsible for known biological properties, as well as work to identify new uses. They will further test the therapeutical effects of the compounds, with the eventual goal of preparing functional pharmaceuticals for human use.
“Although A. virginicus has been considered a harmful invasive species without economic value, its extracts are promising sources of antioxidant, anti-diabetic, anti-tyrosinase, and antitumor agents,” Xuan said.

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

New clues as to why night shift workers are at increased risk of developing certain types of cancer are presented in a new study conducted at Washington State University Health Sciences Spokane.
Published online in the Journal of Pineal Research, the study involved a controlled laboratory experiment that used healthy volunteers who were on simulated night shift or day shift schedules. Findings from the study suggest that night shifts disrupt natural 24-hour rhythms in the activity of certain cancer-related genes, making night shift workers more vulnerable to damage to their DNA while at the same time causing the body’s DNA repair mechanisms to be mistimed to deal with that damage.
Though more research still needs to be done, these discoveries could someday be used to help prevent and treat cancer in night shift workers.
“There has been mounting evidence that cancer is more prevalent in night shift workers, which led the World Health Organization’s International Agency for Research on Cancer to classify night shift work as a probable carcinogenic,” said co-corresponding author Shobhan Gaddameedhi, an associate professor formerly with the WSU College of Pharmacy and Pharmaceutical Sciences and now with North Carolina State University’s Biological Sciences Department and Center for Human Health and the Environment. “However, it has been unclear why night shift work elevates cancer risk, which our study sought to address.”
Studying the rhythms in cancer-related genes
As part of a partnership between the WSU Sleep and Performance Research Center and the U.S. Department of Energy’s Pacific Northwest National Laboratory (PNNL), Gaddameedhi and other WSU scientists worked with bioinformatics experts at PNNL to study the potential involvement of the biological clock, the body’s built-in mechanism that keeps us on a 24-hour night and day cycle. Though there is a central biological clock in the brain, nearly every cell in the body also has its own built-in clock. This cellular clock involves genes known as clock genes that are rhythmic in their expression, meaning their activity levels vary with the time of day or night. The researchers hypothesized that the expression of genes associated with cancer might be rhythmic, too, and that night shift work might disrupt the rhythmicity of these genes.

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To test this, they conducted a simulated shift work experiment that had 14 participants spend seven days inside the sleep laboratory at WSU Health Sciences Spokane. Half of them completed a three-day simulated night shift schedule, while the other half were on a three-day simulated day shift schedule. After completing their simulated shifts, all participants were kept in a constant routine protocol that is used to study humans’ internally generated biological rhythms independent of any external influences. As part of the protocol, they were kept awake for 24 hours in a semi-reclined posture under constant light exposure and room temperature and were given identical snacks every hour. Every three hours a blood sample was drawn.
Analyses of white blood cells taken from the blood samples showed that the rhythms of many of the cancer-related genes were different in the night shift condition compared to the day shift condition. Notably, genes related to DNA repair that showed distinct rhythms in the day shift condition lost their rhythmicity in the night shift condition.
The researchers then looked at what the consequences of the changes in the expression of cancer-related genes might be. They found that white blood cells isolated from the blood of night shift participants showed more evidence of DNA damage than those of day shift participants. What’s more, after the researchers exposed isolated white blood cells to ionizing radiation at two different times of day, cells that were radiated in the evening showed increased DNA damage in the night shift condition as compared to the day shift condition. This meant that white blood cells from night shift participants were more vulnerable to external damage from radiation, a known risk factor for DNA damage and cancer.
“Taken together, these findings suggest that night shift schedules throw off the timing of expression of cancer-related genes in a way that reduces the effectiveness of the body’s DNA repair processes when they are most needed,” said co-corresponding author Jason McDermott, a computational scientist with the Pacific Northwest National Laboratory’s Biological Sciences Division.
Potential for improved prevention, treatment
The researchers’ next step is to conduct the same experiment with real-world shift workers who have been consistently on day or night shifts for many years to determine whether in night workers the unrepaired DNA damage builds up over time, which could ultimately increase the risk of cancer. If what happens in real-world shift workers is consistent with the current findings, this work could eventually be used to develop prevention strategies and drugs that could address the mistiming of DNA repair processes. It could also be the basis for strategies to optimize the timing of cancer therapy so that treatment is administered when effectiveness is greatest and side effects are minimal, a procedure called chronotherapy that would need to be fine-tuned to the internal rhythms of night workers.
“Night shift workers face considerable health disparities, ranging from increased risks of metabolic and cardiovascular disease to mental health disorders and cancer,” said co-senior author Hans Van Dongen, a professor in the WSU Elson S. Floyd College of Medicine and director of the WSU Sleep and Performance Research Center. “It is high time that we find diagnosis and treatment solutions for this underserved group of essential workers so that the medical community can address their unique health challenges.”
In addition to Van Dongen, Gaddameedhi, and McDermott, study authors included Bala Koritala, Kenneth Porter, Osama Arshad, Rajendra Gajula, Hugh Mitchell, Tarana Arman, Mugimane Manjanatha, and Justin Teeguarden.
Funding: National Institutes of Health, Congressionally Directed Medical Research Programs, BRAVE Investment at the Pacific Northwest National Laboratory

Virtual reality avatar-based coaching shows promise to increase access to and extend the reach of nutrition education programs to children at risk for obesity, according to a new study in the Journal of Nutrition Education and Behavior, published by Elsevier.
Researchers introduced 15 adult-child dyads to a virtual avatar-based coaching program that incorporated age-specific information on growth; physical, social, and emotional development; healthy lifestyles; common nutrition concerns; and interview questions around eating behaviors and food resources and counseling.
“We developed a virtual reality avatar computer program as a way to get kids engaged in learning about nutrition education. The goal was to make this a program that could work to prevent childhood obesity,” said lead investigator Jared T. McGuirt, PhD, MPH, Department of Nutrition, University of North Carolina Greensboro, Greensboro, NC, USA. “We were primarily interested in how kids and parents reacted to this program — particularly lower income kids and parents who may not have been able to access this kind of experience in the past.”
A key finding in the study was the avatar’s ability to spark dialogue between the children and adults around dietary habits and behavior. All children and adults reported liking the program and planned to use it in the future, as they found it fun, informational, and motivating. The personalized social aspect of the avatar experience was appealing, as participants thought the avatar would reinforce guidance and provide support while acting as a cue to change health behaviors.
Looking to future implementation of this program in the public health field, Dr. McGuirt noted: “We feel we have a good start. The program was designed so others can build on it, and hopefully advance this technique into community nutrition education programs.

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

North Carolina State University engineers continue to improve the efficiency of a flexible device worn on the wrist that harvests heat energy from the human body to monitor health.
In a paper published in npj Flexible Electronics, the NC State researchers report significant enhancements in preventing heat leakage in the flexible body heat harvester they first reported in 2017 and updated in 2020. The harvesters use heat energy from the human body to power wearable technologies — think of smart watches that measure your heart rate, blood oxygen, glucose and other health parameters — that never need to have their batteries recharged. The technology relies on the same principles governing rigid thermoelectric harvesters that convert heat to electrical energy.
Flexible harvesters that conform to the human body are highly desired for use with wearable technologies. Mehmet Ozturk, an NC State professor of electrical and computer engineering and the corresponding author of the paper, mentioned superior skin contact with flexible devices, as well as the ergonomic and comfort considerations to the device wearer, as the core reasons behind building flexible thermoelectric generators, or TEGs.
The performance and efficiency of flexible harvesters, however, historically trail well behind rigid devices, which have been superior in their ability to convert body heat into usable energy.
The NC State proof-of-concept TEG originally reported in 2017 employed semiconductor elements that were connected electrically in series using liquid-metal interconnects made of EGaIn — a non-toxic alloy of gallium and indium. EGaIn provided both metal-like electrical conductivity and stretchability. The entire device was embedded in a stretchable silicone elastomer.
The upgraded device reported in 2020 employed the same architecture but significantly improved the thermal engineering of the previous version, while increasing the density of the semiconductor elements responsible for converting heat into electricity. One of the improvements was a high thermal conductivity silicone elastomer — essentially a type of rubber — that encapsulated the EGaIn interconnects.
The newest iteration adds aerogel flakes to the silicone elastomer to reduce the elastomer’s thermal conductivity. Experimental results showed that this innovation reduced the heat leakage through the elastomer by half.
“The addition of aerogel stops the heat from leaking between the device’s thermoelectric ‘legs,'” Ozturk said. “The higher the heat leakage, the lower the temperature that develops across the device, which translates to lower output power.
“The flexible device reported in this paper is performing an order of magnitude better than the device we reported in 2017 and continues to approach the performance of rigid devices,” Ozturk added.
Ozturk said that one of the strengths of the NC State-patented technology is that it employs the very same semiconductor elements used in rigid devices perfected after decades of research. The approach also provides a low-cost opportunity to existing rigid thermoelectric module manufacturers to enter the flexible thermoelectric market.
He added that his lab will continue to focus on improving the efficiency of these flexible devices.

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

Diphtheria — a relatively easily-preventable infection — is evolving to become resistant to a number of classes of antibiotics and in future could lead to vaccine escape, warn an international team of researchers from the UK and India.
The researchers, led by scientists at the University of Cambridge, say that the impact of COVID-19 on diphtheria vaccination schedules, coupled with a rise in the number of infections, risk the disease once more becoming a major global threat.
Diphtheria is a highly contagious infection that can affect the nose and throat, and sometimes the skin. If left untreated it can prove fatal. In the UK and other high-income countries, babies are vaccinated against infection. However, in low- and middle-income countries, the disease can still cause sporadic infections or outbreaks in unvaccinated and partially-vaccinated communities.
The number of diphtheria cases reported globally has being increasing gradually. In 2018, there were 16,651 reported cases, more than double the yearly average for 1996-2017 (8,105 cases).
Diphtheria is primarily caused by the bacterium Corynebacterium diphtheriae and is mainly spread by coughs and sneezes, or through close contact with someone who is infected. In most cases, the bacteria cause acute infections, driven by the diphtheria toxin — the key target of the vaccine. However, non-toxigenic C. diphtheria can also cause disease, often in the form of systemic infections.
In a study published today in Nature Communications, an international team of researchers from the UK and India used genomics to map infections, including a subset from India, where over half of the globally reported cases occurred in 2018.

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By analysing the genomes of 61 bacteria isolated from patients and combining these with 441 publicly available genomes, the researchers were able to build a phylogenetic tree — a genetic ‘family tree’ — to see how the infections are related and understand how they spread. They also used this information to assess the presence of antimicrobial resistance (AMR) genes and assess toxin variation.
The researchers found clusters to genetically-similar bacteria isolated from multiple continents, most commonly Asia and Europe. This indicates that C. diphtheriae has been established in the human population for at least over a century, spreading across the globe as populations migrated.
The main disease-causing component of C. diphtheriae is the diphtheria toxin, which is encoded by the tox gene. It is this component that is targeted by vaccines. In total, the researchers found 18 different variants of the tox gene, of which several had the potential to change the structure of the toxin.
Professor Gordon Dougan from the Cambridge Institute of Therapeutic Immunology and Infectious Disease (CITIID) said: “”The diphtheria vaccine is designed to neutralise the toxin, so any genetic variants that change the toxin’s structure could have an impact on how effective the vaccine is. While our data doesn’t suggest the currently used vaccine will be ineffective, the fact that we are seeing an ever-increasing diversity of tox variants suggests that the vaccine, and treatments that target the toxin, need to be appraised on a regular basis.”
Diphtheria infections can usually be treated with a number of classes of antibiotic. While C. diphtheriae resistant to antibiotics have been reported, the extent of such resistance remains largely unknown.

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When the team looked for genes that might confer some degree of resistance to antimicrobials, they found that the average number of AMR genes per genome was increasing each decade. Genomes of bacteria isolated from infections from the most recent decade (2010-19) showed the highest average number of AMR genes per genome, almost four times as many on average than in the next highest decade, the 1990s.
Robert Will, a PhD student at CITIID and the study’s first author, said: “The C. diphtheriae genome is complex and incredibly diverse. It’s acquiring resistance to antibiotics that are not even clinically used in the treatment of diphtheria. There must be other factors at play, such as asymptomatic infection and exposure to a plethora of antibiotics meant for treating other diseases.”
Erythromycin and penicillin are the traditionally recommended antibiotics of choice for treating confirmed cases of early-stage diphtheria, though there are several different classes of antibiotics available to treat the infection. The team identified variants resistant to six of these classes in isolates from the 2010s, higher than in any other decades.
Dr Pankaj Bhatnagar from the World Health Organization country office for India said: “AMR has rarely been considered as a major problem in the treatment of diphtheria, but in some parts of the world, the bacterial genomes are acquiring resistance to numerous classes of antibiotics. There are likely to be a number of reasons to this, including exposure of the bacteria to antibiotics in their environment or in asymptomatic patients being treated against other infections.”
The researchers say that COVID-19 has had a negative impact on childhood vaccination schedules worldwide and comes at a time when reported case numbers are rising, with 2018 showing the highest incidence in 22 years.
Dr Ankur Mutreja from CITIID, who led the study, said: “It’s more important than ever that we understand how diphtheria is evolving and spreading. Genome sequencing gives us a powerful tool for observing this in real time, allowing public health agencies to take action before it’s too late.
“We mustn’t take our eye off the ball with diphtheria, otherwise we risk it becoming a major global threat again, potentially in a modified, better adapted, form.”
The research was funded primarily by the Medical Research Council, with additional support from the NIHR Cambridge Biomedical Research Centre.

Results from a study led by Joan Seoane, Director of Preclinical and Translational Research co-program at VHIO and ICREA Professor, show that immune cells accessing cerebrospinal fluid faithfully recapitulate the characteristics of cells identified in brain metastasis, and could therefore constitute novel biomarkers of response to immune-based therapies.
Immune checkpoint inhibitors including anti-PD1, anti-PD-L1, and anti-CTLA4, have shown significant clinical benefits in patients with progressive or metastatic solid tumors, including some brain metastasis. Notably, these immune-based therapies have improved outcomes for some of those suffering from lung cancer and melanoma. Together, these tumor types (represent between 30-40% of all cancers), along with breast cancer, are three common malignancies that lead to brain metastases.
“One of the major challenges in improving outcomes for patients suffering from brain metastases caused by these cancers is that new lesions can differ immensely from the primary tumor, and thus respond in a different way to immune-based therapies,” observes Joan Seoane, co-Corresponding Author of this present study that published today in Nature Communications.
Brain metastases are the most frequent tumor of the brain, with a dismal prognosis. While a fraction of patients benefit from treatment with immune checkpoint inhibitors, the majority do not. To predict response to these therapies necessitates the characterization of tumor specimens. Due to the anatomical location of brain tumors and the risk of surgical procedures, accessing samples from brain malignancies is challenging.
Results from previous studies led by Joan Seoane, as well as those of other groups, have evidenced that cerebrospinal fluid can provide vital insights into the genomic characteristics of brain tumors and therefore be used as a minimally invasive liquid biopsy. Spurred by these findings, the investigators conducted this present research to establish whether they could effectively characterize the immunological phenotype through the analysis of cerebrospinal fluid.
To test this hypothesis, Joan Seoane’s team analyzed samples from 48 patients with brain metastasis. These samples were obtained thanks to the generosity of patients receiving treatment at our Vall d’Hebron University Hospital (HUVH), as well as the Hospital Clínic in Barcelona, who gave their full consent to use their samples. The collection of samples was possible thanks to the dedication and expertise of these hospitals’ Neurosurgery Services.
The researchers assessed the immune cells present in the brain metastases, and in parallel, performed immune cell profiling of the cerebrospinal fluid. They sought to identify which cell types were present in the cerebrospinal fluid and compare them with those obtained from the metastatic lesions.
“By establishing similarities between the two, we have identified a novel and minimally invasive method that can allow us to predict response to immunotherapy in these patients. This pioneering approach could more precisely guide clinical decision making in treating these patients with immune-based therapeutic strategies,” adds Joan Seoane.
By analyzing cerebrospinal fluid, Joan Seoane’s team have been able to identify the T-cells that recognize the tumor, and those that are active in treatment. “Each immune T-cell has a unique sequence that recognizes a particular tumor antigen. When their tracing and targeting commence, these cells are activated and begin to proliferate. Through this study, we have been able to characterize the individual sequences of immune cells and, in this way, identify which immune cells are fighting the tumor and discern how they evolve over time,” continues Joan Seoane.
The study was also carried out in collaboration with colleagues at the National Centre for Genomic Analysis-Centre for Genomic Regulation (CNAG-CRG), Barcelona. Directed by Holger Heyn, Head of CNAG-CRG’s Single Cell Genomics Team, theu performed single cell transcriptome sequencing of around 6000 cells by scRNA-seq technology.
“Single cell transcriptome sequencing provides the highest resolution for the detection and monitoring of several different diseases. The identification of clonal T-cells in both metastasis and liquid biopsy is of particular interest. We have shown that the sequencing of T-cell receptors provides a cellular barcode that can be assessed outside of the tumor. Importantly, this approach opens up new avenues for the detection of systemic disease,” concludes Holger Heyn, co-Corresponding Author of this present study.

Multinational companies headquartered in countries with tougher environmental policies tend to locate their polluting factories in countries with more lax regulations, a new study finds.
While countries may hope their regulations will reduce emissions of carbon dioxide and other greenhouse gases, these results show that these policies can lead to “carbon leakage” to other nations, said Itzhak Ben-David, co-author of the study and professor of finance at The Ohio State University’s Fisher College of Business.
“Firms decide strategically where to locate their production based on existing environmental policies, with the result being that they pollute more in countries with lenient regulations,” Ben David said.
“This highlights the importance of worldwide collective action to combat climate change, given the global scale of firms’ operations.”
The study was published online recently in the journal Economic Policy.
Researchers used a novel dataset covering 1,970 large public firms headquartered in 48 countries and their carbon dioxide emissions in 218 countries from 2008 to 2015. The database was provided by CDP, a nonprofit formerly known as the Carbon Disclosure Project.

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“What makes this dataset unique is that we can observe the carbon dioxide emissions of each multinational firm in each country in which it operates,” Ben-David said.
“This provides direct evidence of the effect of environmental policies and each firm’s actual carbon dioxide emissions at the country level.”
The researchers also used rankings from the World Economic Forum that rated the strength of each country’s environmental policies on a scale of 1 (worst) to 7 (best).
The results of the new study don’t mean that tougher environmental regulations have no effect at all on global emissions, Ben-David said. Findings suggest that stringent policies are still associated with a partial, but positive, impact on reducing overall global pollution.
For example, an increase in the environmental policy score from China (2.1, suggesting weak regulations) to Germany (5.5, stronger regulations) is associated with 44% lower global emissions.

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But it is also associated with a 299% increase in foreign emissions when compared to the companies’ home countries.
“If you make it more difficult to pollute in a company’s home country, firms will move some of that pollution activity to somewhere else,” Ben-David said.
The study examined whether stricter policies “pushed” firms to pollute elsewhere or lax regulations “pulled” firms to countries where it was easier to pollute.
“We found that the results were primarily driven by the environmental policies in the home country, rather than by opportunities to pollute elsewhere,” he said. “It was more of a ‘push’ effect than a ‘pull’ effect.”
Not surprisingly, firms in the most polluting industries were the ones most likely to respond to strict policies in their home countries by locating their pollution activities elsewhere.
Overall, most carbon dioxide is released in an average company’s home country, but the share of home emissions declined substantially over time from 72% in 2008 to 57% in 2015, the researchers found.
In addition, the number of countries in which the average firm polluted increased from six to nine during the period of the study.
“Environmental regulations in each country do work to somewhat reduce global emissions of carbon dioxide, but they also have this negative side effect of pushing pollution to other countries,” Ben-David said.
“Countries need to collaborate if they really want environmental policies to have the strongest impact.”

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Materials provided by Ohio State University. Original written by Jeff Grabmeier. Note: Content may be edited for style and length.