Wednesday, September 20, 2023

Analyzing ways to help golden eagle populations weather wind-energy growth

"We are taking basic information about golden eagle ecology in the Anthropocene and developing it into predictive frameworks for how to protect them," says Eric Lonsdorf, Emory assistant professor of environmental sciences.

By Carol Clark

Wind energy is a major component of the U.S. clean-energy goals. Already one of the fastest growing and lowest-cost sources of electricity in the country, it is poised for even more rapid growth, according to the U.S. Department of Energy. 

Wind power, however, does not come without tradeoffs, including some negative impacts on wildlife. Throughout the United States, for example, it’s been estimated that as many as three golden eagles per wind farm are killed each year by wind turbines. 

“Renewable energy sources, including wind energy, are critical for us to achieve a net-zero emissions future,” says Eric Lonsdorf, assistant professor of environmental sciences at Emory University. “We need to address conflicts between renewable energy and wildlife conservation so that we can combat climate change while also limiting damage to biodiversity.” 

Lonsdorf and colleagues are developing data-driven methods to determine how much effort is needed to save golden eagles in order to offset the impact of wind turbines on their populations. 

The Journal of Wildlife Management recently published their latest model for calculating the benefit of one mitigation strategy — removal of large, road-killed animals that can lead to golden eagles getting hit by cars. 

Quantifying the benefits of natural capital

Lonsdorf is an expert in natural capital, or the quantifiable benefits that nature provides humans. He translates ecological principles and data into computer models that enable industry leaders and policymakers to better manage natural resources. 

Co-authors of the current study include James Gerber and Deepak Ray, from the University of Minnesota; Steven Slater, from HawkWatch International; and Taber Allison, from the Renewable Energy Wildlife Institute. 

The U.S. Fish and Wildlife Service (FWS) monitors golden eagle populations, which are protected through the Bald and Golden Eagle Protection Act and the Migratory Bird Treaty Act. Threats to golden eagles include loss of habitat and prey. 

Additional threats that are directly linked to human activities include illegal shootings, electrocution at power poles, lead poisoning from consuming parts of bullets in the entrails of deer carcasses discarded at the site of hunters’ kills, collisions with cars at sites where the birds are scavenging roadkill and collisions with the blades of a wind turbine. 

Across the western United States, hundreds of wind turbines have gone up in sage-brush flats that are part of golden eagles’ core habitat, and many more turbines are planned. In order to meet the permit requirements of the FWS, wind-energy companies must agree to mitigate their impact on the animals by offsetting the predicted number of golden eagles that will fly into their turbines each year. 

Currently, the only offset strategy approved by the FWS for wind-energy companies is to retrofit power poles to prevent golden eagles from becoming electrocuted. 

Adding empirical data

For the past five years, Lonsdorf and his colleagues have combined their expertise to develop a range of potential offset strategies for golden eagle fatalities. 

Their current paper — an updated model for golden eagle mortality due to vehicle collisions based on data from Wyoming — considered myriad factors such as the population density for golden eagles in the region, the number and size of deer roadkill carcasses expected and the traffic volume on the roads. The model also incorporated observational evidence of eagle-carcass roadside interactions obtained by motion-triggered cameras, data that was lacking in a previous model the researchers created. 

The addition of this empirical data allowed the researchers to make estimates for how long a golden eagle typically spends at a carcass, how the decay rate of the carcass affects the number of visits from eagles and the effects of seasonality on the scavenging behavior of the eagles. 

The model results suggest that carcass relocation is a viable golden eagle mitigation strategy that could save up to seven golden eagles annually in some Wyoming counties. On average, the model indicates that the prompt removal of four roadside carcasses would save at least one golden eagle. 

The researchers can make a user-friendly version of the prediction framework available to the FWS and wind-energy companies if the FWS decides to approve carcass removal as an eagle mortality offset strategy. 

“We’re taking basic information about golden eagle ecology in the Anthropocene and developing it into predictive frameworks for how to protect them,” Lonsdorf says. “As wind energy continues to grow, more mitigation strategies will likely be needed. Our goal is to provide scientific evidence for a portfolio of methods to help accomplish a zero-net loss of golden eagles from wind-energy facilities.” 


Valuing 'natural capital' vital to avoid next pandemic, global experts warn

International trade bans on endangered species tend to help mammals but hurt reptiles

Wednesday, September 13, 2023

Natural compound found in plants inhibits deadly fungi

A 3D illustration of the newly emerged species of fungus Candida auris, which is often drug-resistant and has a high mortality rate. (Dr_Microbe, Getty Images)

By Carol Clark

A new study finds that a natural compound found in many plants inhibits the growth of drug-resistant Candida fungi — including its most virulent species, Candida auris, an emerging global health threat. The journal ACS Infectious Diseases published the discovery led by scientists at Emory University. 

Laboratory-dish experiments showed that the natural compound, a water-soluble tannin known as PGG, blocks 90% of the growth in four different species of Candida fungi. The researchers also discovered how PGG inhibits the growth: It grabs up iron molecules, essentially starving the fungi of an essential nutrient. By starving the fungi rather than attacking it, the PGG mechanism does not promote the development of further drug resistance, unlike existing antifungal medications. 

Laboratory-dish experiments also showed minimal toxicity of PGG to human cells. 

“Drug-resistant fungal infections are a growing healthcare problem but there are few new antifungals in the drug-development pipeline,” says Cassandra Quave, senior author of the study and associate professor in Emory School of Medicine’s Department of Dermatology and the Center for the Study of Human Health. “Our findings open a new potential approach to deal with these infections, including those caused by deadly Candida auris.” 

C. auris is often multidrug-resistant and has a high mortality rate, leading the Centers for Disease Control and Prevention (CDC) to label it a serious global health threat. 

“It’s a really bad bug,” says Lewis Marquez, first author of the study and a graduate student in Emory’s molecular systems and pharmacology program. “Between 30 to 60% of the people who get infected with C. auris end up dying.” 

An emerging threat 

Candida is a yeast often found on the skin and in the digestive tract of healthy people. Some species, such as Candida albicans, occasionally grow out of control and cause mild infections in people. In more serious cases, Candida can invade deep into the body and cause infections in the bloodstream or organs such as the kidney, heart or brain. 

Immunocompromised people, including many hospital patients, are most at risk for invasive Candida infections, which are rapidly evolving drug resistance. 

In 2007, the new Candida species, C. auris, emerged in a hospital patient in Japan. Since then, C. auris has caused health care-associated outbreaks in more than a dozen countries around the world with more than 3,000 clinical cases reported in the United States alone. 

A ‘natural’ approach to drug discovery 

Quave is an ethnobotanist, studying how traditional people have used plants for medicine to search for promising new candidates for modern-day drugs. Her lab curates the Quave Natural Product Library, which contains 2,500 botanical and fungal natural products extracted from 750 species collected at sites around the world. 

“We’re not taking a random approach to identify potential new antimicrobials,” Quave says. “Focusing on plants used in traditional medicines allows us to hone in quickly on bioactive molecules.” 

Previously, the Quave lab had found that the berries of the Brazilian peppertree, a plant used by traditional healers in the Amazon for centuries to treat skin infections and some other ailments, contains a flavone-rich compound that disarms drug-resistant staph bacteria. Screens by the Quave lab had also found that the leaves of the Brazilian peppertree contain PGG, a compound that has shown antibacterial, anticancer and antiviral activities in previous research. 

A 2020 study by the Quave lab, for instance, found that PGG inhibited growth of Carbapenem-resistant Acinetobacter baumannii, a bacterium that infects humans and is categorized as one of five urgent threats by the CDC. 

The Brazilian peppertree, an invasive weed in Florida, is a member of the poison ivy family. “PGG has popped up repeatedly in our laboratory screens of plant compounds from members of this plant family,” Quave says. “It makes sense that these plants, which thrive in really wet environments, would contain molecules to fight a range of pathogens.” 

Experimental results 

The Quave lab decided to test whether PGG would show antifungal activity against Candida. Laboratory-dish experiments demonstrated that PGG blocked around 90% of the growth in 12 strains from four species of Candida: C. albicans, multidrug-resistant C. auris and two other multidrug-resistant non-albicans Candida species. 

PGG is a large molecule known for its iron-binding properties. The researchers tested the role of this characteristic in the antifungal activity. 

“Each PGG molecule can bind up to five iron molecules,” Marquez explains. “When we added more iron to a dish, beyond the sequestering capacity of the PGG molecules, the fungi once again grew normally.” 

Dish experiments also showed that PGG was well-tolerated by human kidney, liver and epithelial cells. “Iron in human cells is generally not free iron,” Marquez says. “It is usually bound to a protein or is sequestered inside enzymes.” 

A potential topical treatment 

Previous animal studies on PGG have found that the molecule is metabolized quickly and removed from the body. Instead of an internal therapy, the researchers are investigating its potential efficacy as a topical antifungal. 

“If a Candida infection breaks out on the skin of a patient where a catheter or other medical instrument is implanted, a topical antifungal might prevent the infection from spreading and entering into the body,” Marquez says. 

As a next step, the researchers will test PGG as a topical treatment for fungal skin infections in mice. 

Meanwhile, Quave and Marquez have applied for a provisional patent for the use of PGG for the mitigation of fungal infections. 

“These are still early days in the research, but another idea that we’re interested in pursuing is the potential use of PGG as a broad-spectrum microbial,” Quave says. “Many infections from acute injuries, such as battlefield wounds, tend to be polymicrobial so PGG could perhaps make a useful topical treatment in these cases.” 

Scientists from the University of Toronto are co-authors of the paper, including Yunjin Lee, Dustin Duncan, Luke Whitesell and Leah Cowen. Whitesell and Cowen are co-founders and shareholders in Bright Angel Therapeutics, a platform company for development of antifungal therapeutics, and Cowen is a science advisor for Kapoose Creek, a company that harnesses the therapeutic potential of fungi. 

The work was supported by grants from the National Institutes of Health, National Center for Complementary and Integrative Health; the Jones Center at Ichauway, the CIHR Frederick Banting and Charles Best Canada Graduate Scholarship and the Canadian Institutes of Health Research Foundation. 


Extracts from two wild plants inhibit COVID virus, study finds

Scientists identify chemicals in noxious weed that 'disarm' deadly bacteria

Into the heart of brightness: An ethnobotanist's memoir

Friday, September 8, 2023

NIH funds Emory center to advance cellular mechanics

"We are catalyzing the process of spreading our technology so that studying biomechanics becomes common and routine in biology," says Khalid Salaita, Emory professor of chemistry and director of the new Center for Molecular Mechanobiology.

By Carol Clark

The National Institutes of Health (NIH) awarded Emory University $5.6 million to establish a national center to advance pioneering technology for cellular mechanics. The center is directed by Khalid Salaita, Emory professor of chemistry, whose lab developed the first sensors for detecting cell-receptor forces at the molecular level. 

“We’ve been working on our molecular-force probes for more than a decade,” Salaita says. “We’ve demonstrated that these probes can be used to visualize, measure and map cellular forces down to the level of piconewtons. The center allows us to get this technology into the hands of end users — researchers in the biomedical sciences.” 

The Center for Molecular Mechanobiology encompasses labs from seven leading research institutions including: Children’s Hospital of Philadelphia, Dana-Farber Cancer Institute, Emory, Georgia Tech, Memorial Sloan Kettering, University of Utah and Vanderbilt University. 

The center members will use the molecular-force probes to investigate the biomechanics of processes such as the clotting of blood cells, the response of immune cells to an infection and the migration of cancer cells. Better understanding these processes may lead to the development of new treatments and therapies for a range of diseases and disorders. 

In addition to supplying the technology, the center will train researchers to use the molecular-force probes and help adapt the technology to answer specific biomedical research questions. 

“Working directly with the research community will help us to further refine and optimize the technology,” Salaita says. “We envision that measuring cellular forces will soon become part of the standard repertoire of biochemical techniques that scientists use to study living systems.” 

The center’s associate directors are Yonggan Ke (associate professor in the Wallace H. Coulter Department of Biomedical Engineering at Emory and Georgia Tech) and Alexa Mattheyses (associate professor in the Department of Cell Developmental and Integrative Biology at the University of Alabama). 

The five-year award from the National Institute of General Medical Sciences is part of the NIH Biomedical Technology Optimization and Dissemination Centers program. The goal is to optimize and disseminate state-of-the-art, late-stage biomedical technologies. 

The first detailed view of mechanical forces

The Salaita lab works at the intersection of chemistry, biology and the physical sciences. It uses the building blocks of nature — nucleic acids — to create synthetic micro motors and probes for investigating fundamental questions of biology. 

The molecular-force probes, developed by the Salaita lab in 2011, provide the first detailed view of the mechanical forces on the surface of a cell. The technology can detect mechanical forces as fleeting as the blink of an eye and as faint as piconewtons — about one billionth the weight of a paperclip. 

The probes are made from strands of synthetic DNA tagged with fluorescence so that they function like molecular beacons, shining when they sense force. The technique is noninvasive, does not modify the cell and can be done with a standard fluorescence microscope. 

In 2014, the lab used the new method to demonstrate how adherent cells — the kind that form the architecture of all multicellular organisms — mechanically sense their environments, migrate and stick to things. 

In 2016, the molecular-force probes provided the first direct evidence for the mechanical forces of T cells, the security guards of the immune system. The lab’s experiments on T cells drawn from mice showed how they use a kind of mechanical “handshake” to test whether a cell they encounter is a friend or a foe. 

In 2017, the lab shined its molecular beacons on platelets, the cells in the blood whose job is to stop bleeding by sticking together to form clots and plug up a wound. That work revealed the key molecular forces on platelets that trigger the clotting process. 

In 2020, the lab and its collaborators combined advances in optical imaging with the molecular-force probes to capture forces at a resolution of 25 nanometers — far shorter than the length of a light wave. “That resolution is akin to being on the moon and seeing the ripples caused by raindrops hitting the surface of a lake on the Earth,” Salaita said at the time. 

Key technological goals 

The Center for Molecular Mechanobiology will build on this foundational work of the Salaita lab. It will focus on three key technological development goals:

• Optimizing the highest-resolution technique of the molecular-force probes so that it can be applied to a range of research questions. 

• Tagging cells based on their force level in order to use force as a marker to barcode cells and their receptors. The idea is to classify the mechanics of individual cells and then link these classifications to gene-expression levels to study the cause-and-effect relationships. 

• Amplifying the molecular-force signals to better understand the role of even the weakest forces involved in cellular mechanics, including those involved in the immune response. 

Researchers from throughout the country will come to the Center for Molecular Mechanobiology to receive hands-on training in the molecular-force probes and then return to their home labs to become ambassadors for the technology. 

“We’ll be adding a whole other layer of information for researchers working on everything from designing vaccines to cancer immunotherapy agents,” Salaita says. 

Decades ago, he points out, complicated techniques such as crystallography, PCR and mass spectrometry were not frequently used but have since become routine workhorses in the biomedical sciences. 

“We are catalyzing the process of spreading our technology so that studying biomechanics also becomes common and routine in biology,” Salaita says. “Molecular forces are a missing piece to understanding the way biology works.” 


‘Firefly’ imaging method makes cellular forces visible

Chemists reveal the force within you

T cells use ‘handshakes’ to sort friends from foes

New methods reveal the mechanics of blood clotting

@font-face {font-family:"Cambria Math"; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:roman; mso-font-pitch:variable; mso-font-signature:-536870145 1107305727 0 0 415 0;}@font-face {font-family:Calibri; panose-1:2 15 5 2 2 2 4 3 2 4; mso-font-charset:0; mso-generic-font-family:swiss; mso-font-pitch:variable; mso-font-signature:-536859905 -1073732485 9 0 511 0;}p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-unhide:no; mso-style-qformat:yes; mso-style-parent:""; margin:0in; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Calibri",sans-serif; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Calibri; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;}a:link, span.MsoHyperlink {mso-style-priority:99; color:#0563C1; mso-themecolor:hyperlink; text-decoration:underline; text-underline:single;}a:visited, span.MsoHyperlinkFollowed {mso-style-noshow:yes; mso-style-priority:99; color:#954F72; mso-themecolor:followedhyperlink; text-decoration:underline; text-underline:single;}.MsoChpDefault {mso-style-type:export-only; mso-default-props:yes; font-family:"Calibri",sans-serif; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:Calibri; mso-fareast-theme-font:minor-latin; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi; mso-font-kerning:0pt; mso-ligatures:none;}div.WordSection1 {page:WordSection1;}