thescientist--2020-11-01--Infographic: How Large Carnivores Sculpt Ecosystems

In the mid-1990s , officials at Yellowstone National Park released gray wolves from areas in Canada and Montana into the park ; it had been more than half a century since the predators last roamed the park .
Researchers tracking the revolutionary experiment published results that they say point to the reintroduction ’ s role in revitalizing the once-degraded ecosystem , with the wolves ’ predatory behavior indirectly supporting the growth of vegetation and even improving the health of the park ’ s waterways .
But a heated debate rages on concerning the effects the wolves had on their environment @ @ @ @ @ @ @ members of Yellowstone ’ s rich carnivore community .
The release of predators into the wild is controversial , and for years Yellowstone remained one of the only sites of such a bold reintroduction .
But now , similar efforts are in the works around the world .
In the Iberá wetlands of Argentina , for example , conservationists will soon release their first jaguars , and hypothesize that a variety of ecological changes will occur across the landscape .
And in Mozambique ’ s Gorongosa National Park , where a reintroduction project @ @ @ @ @ @ @ , a study is underway using state-of-the-art tools to track the predators ’ ecological effects .
Five jaguars to be reintroduced in 2020/2021 Dozens of African wild dogs introduced in 2018/2019 ; leopard reintroductions slated for 2021

ABOVE: © LUCY CONKLIN
In the mid-1990s, officials at Yellowstone National Park released gray wolves from areas in Canada and Montana into the park; it had been more than half a century since the predators last roamed the park. Researchers tracking the revolutionary experiment published results that they say point to the reintroduction’s role in revitalizing the once-degraded ecosystem, with the wolves’ predatory behavior indirectly supporting the growth of vegetation and even improving the health of the park’s waterways. But a heated debate rages on concerning the effects the wolves had on their environment, especially relative to roles of other members of Yellowstone’s rich carnivore community.
Yellowstone, Wyoming, US
41 gray wolves reintroduced in the mid-1990s
© LUCY CONKLIN
Following wolf reintroduction, elk numbers dropped dramatically—from nearly 20,000 in 1994 to just 8,300 in 2000—but wolves are likely not the only carnivore that contributed to that decline; black bear, grizzly, and cougar populations surged around the time of the wolf reintroduction. Ecologists first posited that by keeping elk away from streams, wolves were indirectly allowing aspen trees to flourish. Although the trees increased in height in certain areas, their overall abundance changed little. Although they suffer less browsing pressure since the predator increases in the 1990s, willows have not fully recovered, according to some researchers. And without willows, the recovery of streams has been limited. Initial studies proposed that elk stay away from streamside areas where they could more easily fall prey to wolves, but new research suggests that elk only avoid these regions in the morning and at dusk. The herbivores also appear to have altered their behavior to avoid cougar-patrolled forested areas at night.
PLANNING FOR FUTURE REINTRODUCTIONS
The release of predators into the wild is controversial, and for years Yellowstone remained one of the only sites of such a bold reintroduction. But now, similar efforts are in the works around the world. In the Iberá wetlands of Argentina, for example, conservationists will soon release their first jaguars, and hypothesize that a variety of ecological changes will occur across the landscape. And in Mozambique’s Gorongosa National Park, where a reintroduction project involving wild dogs and leopards is ongoing, a study is underway using state-of-the-art tools to track the predators’ ecological effects.
Iberá, Argentina
Five jaguars to be reintroduced in 2020/2021
© LUCY CONKLIN
Researchers expect numbers of deer and capybaras, the jaguars’ prey, to drop once the cats are reintroduced. By reconfiguring capybara population structure, the jaguars might reduce the spread of mange between the rodents. Ecologists suspect that the capybaras’ behavior will change in response to the presence of the jaguars, becoming more vigilant and cautious. If the capybaras spend more time watching for predators than eating, that could allow grassy vegeta-tion to flourish in certain areas. Jaguars could kill or change the behavior of local foxes and in doing so indirectly boost numbers of the endangered birds that the foxes are known to eat. Ecologists hypothesize that the jaguars’ presence could increase the abundance of certain scavenger species such as vultures and enhance the diversity of beetles that live off carcasses left behind by the predators.
Gorongosa National Park, Mozambique
Dozens of African wild dogs introduced in 2018/2019; leopard reintroductions slated for 2021
© LUCY CONKLIN
Scientists plan to use high-resolution satellite imagery—including LiDAR, which captures the height of trees and grasses—to assess changes in vegetation structure. Researchers will be analyzing antelope scat using fecal DNA barcoding, alongside studies of the predators’ feces, to track the animals’ diets. Ecologists are using GPS collars and camera-trap data to monitor the behavior of different antelope species.
Read the full story.


thescientist--2020-11-01--Opinion: Using Pokémon to Detect Scientific Misinformation

On March 18 , 2020 , the American Journal of Biomedical Science & Research published my paper claiming that eating a bat-like Pokémon sparked the spread of COVID-19 .
This paper , “ Cyllage City COVID-19 outbreak linked to Zubat consumption , ” blames a fictional creature for an outbreak in a fictional city , cites fictional references ( including one from author Bruce Wayne in Gotham Forensics Quarterly on using bats to fight crime ) , and is cowritten by fictional authors such as Pokémon ’ s Nurse Joy and House , MD .
Nonetheless , four days after @ @ @ @ @ @ @ cheerful to inform ” me via email that it had “ received positive review comments ” and was accepted for publication .
It ’ s not the only fake paper on Pokémon I ’ ve had published or accepted for publication , covering creatures from Pikachu to Porygon .
Some would argue that editors can not recognize Pokémon names , but lines in the text such as “ a journal publishing this paper does not practice peer review and must therefore be predatory ” or “ this invited article is in a predatory @ @ @ @ @ @ @ review ” would have tipped off anyone who bothered to read the articles .
These papers did not slip in under the radar ; they were welcomed in blindly .
The journals that accepted my papers are predatory .
They appear legitimate , but practice no peer review , no editing , not even a reality check .
Publishers such as BiomedGrid ( which publishes American Journal of Biomedical Science & Research ) , OMICS , or Longdom Publishing will accept anything so long as authors agree to pay the open access fees @ @ @ @ @ @ @ 100 to several thousand dollars .
( I have not paid a penny so far , as some of these journals publish submitted manuscripts before receiving payment . )
Predatory journals are just expensive blogs , no more reliable as sources of scientific information than a celebrity ’ s Twitter feed , yet unfortunately equally trusted in some circles .
To make matters worse , my Pokémon-inspired paper on the novel coronavirus has already been cited .
A physicist based in Tunisia published “ The COVID-19 outbreak ’ s multiple effects , ” @ @ @ @ @ @ @ is treatable with “ provincial herbs , ” in another predatory journal , The International Journal of Engineering Research and Technology .
He not only cited my article , but also cited one of my made-up references , “ Signs and symptoms of Pokérus infection , ” as the paper that first identified SARS-CoV-2 .
When I asked the author how this happened , he failed to see any problem with citing a paper he never read while writing a paper outside his field , and was unaware of the difference between open @ @ @ @ @ @ @ and peer review—is critical : when it comes to public health , fake journals are a real danger .
While evidence shows that the majority of authors publishing in predatory journals are naive researchers from developing countries , ample opportunity exists to use such venues deliberately to push fraud and misinformation .
What is stopping someone , using their real name or a fake name ( or your name ! )
, from publishing a paper claiming that kale juice prevents AIDS , that vaccines cause transsexualism , that certain races are inferior @ @ @ @ @ @ @ , and then publicly citing that paper as evidence ?
The answer is nothing .
It ’ s been done , with quacks promoting the thoroughly debunked , fraudulent , fake diagnosis of “ chronic Lyme ” in predatory and post-publication review journals ( which accept and publish all manuscripts under the assumption that readers will review them later ) .
One should not automatically trust all documents formatted as a scientific paper .
Don ’ t real journals publish fraud and nonsense too ?
Yes , but once the fraud is discovered @ @ @ @ @ @ @ though far too many do not ) .
So far , more than 30 articles on COVID-19 have been retracted .
My paper and the one citing it have not , and never will .
Silver lining : they can be used in science ethics classes to educate others about predatory publishing , and have inspired some researchers , such as Carthage College ’ s Adam Larson , to write Pokémon papers themselves .
How , then , to catch a predator , besides checking Beall ’ s List ?
First , assume @ @ @ @ @ @ @ unsolicited submission invitations are predatory , especially if they are outside your field , cover overly broad subjects , promise rapid review , or flatter you with compliments such as “ eminent researcher.
” Any journal with multiple email domains is predatory , as are absolutely all journals that list the worthless “ Index Copernicus ” number on their website .
There are no shortcuts in science .
If you want to be taken seriously as an academic , do not give predatory journals your business , especially as institutes wise up to @ @ @ @ @ @ @ on CVs or applications .
Although , if any institute wants to grant me an honorary degree in Pokémon Studies for my eminence in the field , I would cheerfully accept .
Editors Note ( November 1 , 2020 ) - The American Journal of Biomedical Science & Research has informed Shelomi that it will be removing the paper that serves as the subject of this piece as he has not paid the publication fees .
Matan Shelomi , who writes fake articles under the pseudonym Mattan Schlomi , is an assistant professor @ @ @ @ @ @ @ Trademarks here are for the purposes of education and parody under fair use .

ABOVE: SONJA PINCK
On March 18, 2020, the American Journal of Biomedical Science & Research published my paper claiming that eating a bat-like Pokémon sparked the spread of COVID-19. This paper, “Cyllage City COVID-19 outbreak linked to Zubat consumption,” blames a fictional creature for an outbreak in a fictional city, cites fictional references (including one from author Bruce Wayne in Gotham Forensics Quarterly on using bats to fight crime), and is cowritten by fictional authors such as Pokémon’s Nurse Joy and House, MD. Nonetheless, four days after submission, editor Catherine Nichols was “cheerful to inform” me via email that it had “received positive review comments” and was accepted for publication.
They appear legitimate, but practice no peer review, no editing, not even a reality check.
It’s not the only fake paper on Pokémon I’ve had published or accepted for publication, covering creatures from Pikachu to Porygon. Some would argue that editors cannot recognize Pokémon names, but lines in the text such as “a journal publishing this paper does not practice peer review and must therefore be predatory” or “this invited article is in a predatory journal that likely does not practice peer review” would have tipped off anyone who bothered to read the articles. These papers did not slip in under the radar; they were welcomed in blindly.
The journals that accepted my papers are predatory. They appear legitimate, but practice no peer review, no editing, not even a reality check. Publishers such as BiomedGrid (which publishes American Journal of Biomedical Science & Research), OMICS, or Longdom Publishing will accept anything so long as authors agree to pay the open access fees, which range from less than $100 to several thousand dollars. (I have not paid a penny so far, as some of these journals publish submitted manuscripts before receiving payment.) Predatory journals are just expensive blogs, no more reliable as sources of scientific information than a celebrity’s Twitter feed, yet unfortunately equally trusted in some circles.
Adapted from a figure that appeared in another paper, “ Expression of the Pokemon gene and pikachurin protein in the pokémon Pikachu ,” that Shelomi got published in the Academia Journal of Scientific Research this July. SONJA PINCK
To make matters worse, my Pokémon-inspired paper on the novel coronavirus has already been cited. A physicist based in Tunisia published “The COVID-19 outbreak’s multiple effects,” which claimed that COVID-19 was human-made and is treatable with “provincial herbs,” in another predatory journal, The International Journal of Engineering Research and Technology. He not only cited my article, but also cited one of my made-up references, “Signs and symptoms of Pokérus infection,” as the paper that first identified SARS-CoV-2. When I asked the author how this happened, he failed to see any problem with citing a paper he never read while writing a paper outside his field, and was unaware of the difference between open access and predatory journals. The difference—editing and peer review—is critical: when it comes to public health, fake journals are a real danger.
While evidence shows that the majority of authors publishing in predatory journals are naive researchers from developing countries, ample opportunity exists to use such venues deliberately to push fraud and misinformation. What is stopping someone, using their real name or a fake name (or your name!), from publishing a paper claiming that kale juice prevents AIDS, that vaccines cause transsexualism, that certain races are inferior, or any other equally eroneous drivel, and then publicly citing that paper as evidence? The answer is nothing. It’s been done, with quacks promoting the thoroughly debunked, fraudulent, fake diagnosis of “chronic Lyme” in predatory and post-publication review journals (which accept and publish all manuscripts under the assumption that readers will review them later). One should not automatically trust all documents formatted as a scientific paper.
Don’t real journals publish fraud and nonsense too? Yes, but once the fraud is discovered, they can retract the paper (though far too many do not). So far, more than 30 articles on COVID-19 have been retracted. My paper and the one citing it have not, and never will. Silver lining: they can be used in science ethics classes to educate others about predatory publishing, and have inspired some researchers, such as Carthage College’s Adam Larson, to write Pokémon papers themselves.
How, then, to catch a predator, besides checking Beall’s List? First, assume all journals or conferences that email you unsolicited submission invitations are predatory, especially if they are outside your field, cover overly broad subjects, promise rapid review, or flatter you with compliments such as “eminent researcher.” Any journal with multiple email domains is predatory, as are absolutely all journals that list the worthless “Index Copernicus” number on their website.
There are no shortcuts in science. If you want to be taken seriously as an academic, do not give predatory journals your business, especially as institutes wise up to the problem and stop accepting such articles on CVs or applications. Although, if any institute wants to grant me an honorary degree in Pokémon Studies for my eminence in the field, I would cheerfully accept.
Editor's Note (November 1, 2020) - The American Journal of Biomedical Science & Research has informed Shelomi that it will be removing the paper that serves as the subject of this piece as he has not paid the publication fees.
Matan Shelomi, who writes fake articles under the pseudonym Mattan Schlomi, is an assistant professor of entomology at National Taiwan University. Trademarks here are for the purposes of education and parody under fair use.


thescientist--2020-11-01--How a Centipede Survives its Own Species’ Venom

ABOVE : The front set of legs of centipedes such as Scolopendra subspinipes have evolved into venom-injecting pincers.. © ISTOCK.COM , KIRISA99 S. Yang et al.
, “ Target switch of centipede toxins for antagonistic switch , ” Sci Adv , 6 : eabb5734 , 2020 .
While it ’ s handy to be able to neutralize prey or would-be predators with a bite or sting , being a venomous animal can be dangerous .
Usually critters avoid the effects of their own venom “ by keeping it in glands where it doesn ’ t go into the bloodstream and @ @ @ @ @ @ @ explains evolutionary biologist Kevin Arbuckle of Swansea University in the UK .
But because accidents happen , it ’ s also advantageous to be able to survive exposure to one ’ s own toxic concoction—often by lacking the receptors the venom ’ s components bind to .
The centipede Scolopendra subspinipes both kills prey with its venom and uses it to temporarily stun conspecifics during fights for dominance .
Ren Lai of the Kunming Institute of Zoology in China writes in an email to The Scientist that he and his colleagues wanted to @ @ @ @ @ @ @ .
In several of the centipede ’ s prey species , including mice , a venom component known as spooky toxin binds to potassium channels , including one called shaker , wreaking havoc on the nerves that control breathing and heartbeat .
Lai ’ s team found the shaker channel in S. subspinipes cells carries a single amino acid change that protects the species from the worst effects of the venom .
Injecting the centipedes with venom from other S. subspinipes , Lai and his colleagues confirmed that the arthropods were only temporarily @ @ @ @ @ @ @ .
Cell culture experiments revealed that spooky toxin inhibited the shal channel , which affects both neurons and the vascular system and most likely explains the centipedes ’ immobilization .
The experiments , says Arbuckle , who was not involved in the study , are “ a really cool integration ” of molecular-level work on venom and observations of the different purposes for which it ’ s used .

ABOVE: The front set of legs of centipedes such as Scolopendra subspinipes have evolved into venom-injecting pincers..
© ISTOCK.COM, KIRISA99
EDITOR’S CHOICE IN CELL & MOLECULAR BIOLOGY
The paper
S. Yang et al., “Target switch of centipede toxins for antagonistic switch,” Sci Adv, 6:eabb5734, 2020.
While it’s handy to be able to neutralize prey or would-be predators with a bite or sting, being a venomous animal can be dangerous. Usually critters avoid the effects of their own venom “by keeping it in glands where it doesn’t go into the bloodstream and doesn’t affect them,” explains evolutionary biologist Kevin Arbuckle of Swansea University in the UK. But because accidents happen, it’s also advantageous to be able to survive exposure to one’s own toxic concoction—often by lacking the receptors the venom’s components bind to.
The centipede Scolopendra subspinipes both kills prey with its venom and uses it to temporarily stun conspecifics during fights for dominance. Ren Lai of the Kunming Institute of Zoology in China writes in an email to The Scientist that he and his colleagues wanted to understand why prey and conspecifics react differently.
In several of the centipede’s prey species, including mice, a venom component known as spooky toxin binds to potassium channels, including one called shaker, wreaking havoc on the nerves that control breathing and heartbeat. Lai’s team found the shaker channel in S. subspinipes cells carries a single amino acid change that protects the species from the worst effects of the venom. Injecting the centipedes with venom from other S. subspinipes, Lai and his colleagues confirmed that the arthropods were only temporarily immobilized; they recovered within 10 minutes. Cell culture experiments revealed that spooky toxin inhibited the shal channel, which affects both neurons and the vascular system and most likely explains the centipedes’ immobilization.
The experiments, says Arbuckle, who was not involved in the study, are “a really cool integration” of molecular-level work on venom and observations of the different purposes for which it’s used.


Reconsidering Life’s Origin

Whenever a living organism is good at something , there ’ s the understandable temptation to explain matters by invoking natural selection .
The insight that organisms are more likely to pass on traits to offspring if those traits help with surviving and reproducing sheds light on many aspects of biological form and function , from quirks of anatomy down to the fine points of how proteins are assembled .
It is a little bit dangerous , though , to get in the habit of telling these stories about every bit of biology .
As I wrote in my new @ @ @ @ @ @ @ , recent theoretical progress warns against such a rush to judgment .
What is becoming increasingly clear is that interacting collectives of “ dumb ” particles can evolve into specialized structures with fine-tuned relationships to their environment even in circumstances where there is no self-copying entity in the system to enable natural selection .
This dissipative adaptation is a broadly applicable physical mechanism based on the simple idea that energy both helps collections of particles to change their state of assembly , and is processed differently by a system depending on its current @ @ @ @ @ @ @ these two facts leads to a feedback loop , whereby a set of building blocks can perform an exploration of possible combinations guided by how well each combination absorbs energy .
Already , researchers have identified examples of dissipative adaptation that lead to a range of energy-harvesting or computing-like behaviors in disorderly material collectives that are subject to patterned sources of energy in their environment .
A network of entangled masses and springs , for example , can “ learn ” to resonate at the particular frequency of an oscillating force from the @ @ @ @ @ @ @ energy absorption increases over time .
Many , if not most , proteins must be thought of as metastable tangles whose conformational changes and mobility are a function both of what else they are bound to and of how much ATP or other energy-bearing substrate is being processed in their particular configuration .
Many proteins function in a state that is highly managed by the activity of ATPase molecular chaperones that burn through chemical fuel as they chomp down on substrate proteins until those proteins are knocked into the right shape .
What @ @ @ @ @ @ @ cell as a self-organizing machine capable of adaptive emergence that may reflect complex “ learned ” responses to recent environmental patterns of energy input .
Understanding how fine-tuned adaptive relationships between system and environment can arise without natural selection potentially restructures science ’ s vision of the ingredients needed for life to come together .
Initially uncoordinated molecules can form a society of sorts that already looks like it is making accurate predictions about its surrounding world or optimizing access to sources of energy .
This system , then , has a richer @ @ @ @ @ @ @ “ random soup ” often imagined as primordial conditions .
Furthermore , there are practical implications in the present-day study of living things that we can also derive from the same physics .
An emerging literature in experimental cell biology has revealed many membraneless cellular compartments that seem to self-organize in response to a wide variety of stress conditions and other environmental changes .
We tend to think of organelles as being genetically programmed , fixed features of architecture that form according to static rules .
But there appears to be a spectrum @ @ @ @ @ @ @ together as needed under a wide variety of conditions .
So how much of what is going on had to be carefully optimized by the slow process of Darwinian selection , and how much might have been available in some first-draft version just from the self-organizing properties of a motley mixture of fuel-burning protein complexes ?
Although experimental science is just beginning to open up the necessary frontier for this discussion , it is exciting to consider that there may be a great deal of plasticity and intelligence in the components of life @ @ @ @ @ @ @ respond to stimuli based on how they are built .
Developing a coherent understanding of the physics of such systems could help us ask questions that will make detecting such phenomena possible .
Jeremy England is senior director in artificial intelligence at GlaxoSmithKline , principal research scientist at Georgia Tech , and the former Thomas D. and Virginia W. Cabot career development associate professor of physics at MIT .
Read an excerpt of Every Life Is on Fire .

ABOVE: © ISTOCK.COM, Ruslana Chub
Whenever a living organism is good at something, there’s the understandable temptation to explain matters by invoking natural selection. The insight that organisms are more likely to pass on traits to offspring if those traits help with surviving and reproducing sheds light on many aspects of biological form and function, from quirks of anatomy down to the fine points of how proteins are assembled.
It is a little bit dangerous, though, to get in the habit of telling these stories about every bit of biology.
As I wrote in my new book, Every Life Is on Fire, recent theoretical progress warns against such a rush to judgment. What is becoming increasingly clear is that interacting collectives of “dumb” particles can evolve into specialized structures with fine-tuned relationships to their environment even in circumstances where there is no self-copying entity in the system to enable natural selection. This dissipative adaptation is a broadly applicable physical mechanism based on the simple idea that energy both helps collections of particles to change their state of assembly, and is processed differently by a system depending on its current state of assembly. The combination of these two facts leads to a feedback loop, whereby a set of building blocks can perform an exploration of possible combinations guided by how well each combination absorbs energy.
Already, researchers have identified examples of dissipative adaptation that lead to a range of energy-harvesting or computing-like behaviors in disorderly material collectives that are subject to patterned sources of energy in their environment. A network of entangled masses and springs, for example, can “learn” to resonate at the particular frequency of an oscillating force from the environment, so that the rate of energy absorption increases over time.
Many, if not most, proteins must be thought of as metastable tangles whose conformational changes and mobility are a function both of what else they are bound to and of how much ATP or other energy-bearing substrate is being processed in their particular configuration. Many proteins function in a state that is highly managed by the activity of ATPase molecular chaperones that burn through chemical fuel as they chomp down on substrate proteins until those proteins are knocked into the right shape. What emerges is a vivid picture of the cell as a self-organizing machine capable of adaptive emergence that may reflect complex “learned” responses to recent environmental patterns of energy input.
Understanding how fine-tuned adaptive relationships between system and environment can arise without natural selection potentially restructures science’s vision of the ingredients needed for life to come together. Initially uncoordinated molecules can form a society of sorts that already looks like it is making accurate predictions about its surrounding world or optimizing access to sources of energy. This system, then, has a richer toolbox to work with than the naive “random soup” often imagined as primordial conditions.
Furthermore, there are practical implications in the present-day study of living things that we can also derive from the same physics. An emerging literature in experimental cell biology has revealed many membraneless cellular compartments that seem to self-organize in response to a wide variety of stress conditions and other environmental changes. We tend to think of organelles as being genetically programmed, fixed features of architecture that form according to static rules. But there appears to be a spectrum of organelle-like subcellular structures that can come together as needed under a wide variety of conditions.
So how much of what is going on had to be carefully optimized by the slow process of Darwinian selection, and how much might have been available in some first-draft version just from the self-organizing properties of a motley mixture of fuel-burning protein complexes? Although experimental science is just beginning to open up the necessary frontier for this discussion, it is exciting to consider that there may be a great deal of plasticity and intelligence in the components of life. Perhaps some cells or molecules automatically respond to stimuli based on how they are built. Developing a coherent understanding of the physics of such systems could help us ask questions that will make detecting such phenomena possible.
Jeremy England is senior director in artificial intelligence at GlaxoSmithKline, principal research scientist at Georgia Tech, and the former Thomas D. and Virginia W. Cabot career development associate professor of physics at MIT. Read an excerpt of Every Life Is on Fire.


thescientist--2020-11-01--Chelsea Wood Tracks Parasites Around the World

Chelsea Wood once imagined she ’ d study dolphins , so it was a surprise , she says , to realize “ there were much more charismatic things living inside the dolphins.
” As an undergraduate at Dartmouth University , Wood worked alongside James Byers , an ecologist then at the University of New Hampshire , who encouraged her to study parasites .
“ I went to his lab like a little mercenary trying to get marine biology experience , having little to no interest in the parasites , ” Wood says .
But along the way , she recognized @ @ @ @ @ @ @ .
For her undergraduate thesis , Wood studied how infection with a parasitic flatworm ( Cryptocotyle lingua ) changed the grazing habits of the marine snail Littorina littorea , and how those effects rippled through the local ecosystem .
After earning her bachelor ’ s degree in 2006 , Wood spent two years as an editor of Frontiers in Ecology and the Environment , where she realized that she most enjoyed reading papers about parasitology .
She decided to pursue the topic for her graduate research .
Wood began her PhD at Stanford @ @ @ @ @ @ @ 2008 , focusing on how fishing affects fish parasites .
Studying communities off the coast of Chile and around the Line Islands , south of Hawaii , she showed that parasite assemblages largely track their hosts in abundance and diversity—in heavily fished areas , many parasites are , like their fish hosts , less abundant and diverse .
However , certain parasites fared better than others .
Species that spread through direct contact were more abundant than ones with complex , multi-host life cycles .
As Wood was completing her dissertation , her @ @ @ @ @ @ @ attention of Pieter Johnson , a disease ecologist at the University of Colorado Boulder who studies how parasites structure aquatic communities .
It was rare to see work that looked holistically at multiple organisms , as Wood ’ s did , Johnson says .
After meeting Wood at a conference , “ I essentially headhunted her , ” he tells The Scientist , encouraging Wood to join his lab for a postdoc .
When she showed up in Boulder in 2013 and began working in new ecosystems , Johnson says , Wood “ @ @ @ @ @ @ @ research “ like a dynamo.
” Together , the two studied how aquatic bird diversity affects parasite diversity .
Wood and Johnson added perches , nesting material , and bird decoys to attract a greater variety of bird species to some ponds while leaving others as controls ; two years later , they looked at the parasites in each pond .
As she ’ d observed in fish , more-diverse bird populations correlated with more-diverse parasites , but again , the effects were different across species .
After wrapping up her postdoc in @ @ @ @ @ @ @ the University of Michigan , where she studied a group of flatworms called schistosomes that infect humans through a snail host and cause a disease called schistosomiasis .
Wood used drones to search for areas where the snails ’ preferred habitat—submerged water plants—bordered on human settlements in Senegal , helping to identify communities at the greatest risk of schistosomiasis outbreaks .
In 2016 , Wood accepted a faculty position at the University of Washington , where she now runs her own parasite ecology lab .
Several of her current initiatives involve historical ecology @ @ @ @ @ @ @ records to track parasites over time .
Wood ’ s first publication using museum data followed a species of nematode worm ( Clavinema mariae ) infecting English sole ( Parophrys vetulus ) in the Puget Sound between 1930 and 2016 ( J Appl Ecol , 56:190–200 , 2019 ) .
During that time , she found , the number of nematodes per fish increased eightfold .
Her ongoing work will reconstruct a broader assemblage of parasites that have infected 10 economically important fish species , including herring , hake , and rockfish , @ @ @ @ @ @ @ is an amazing treasure trove of information hidden away in our natural [ history ] museums , ” Katrina Lohan , a parasite ecologist with the Smithsonian ’ s Environmental Research Center , tells The Scientist .
Without historical data , researchers can only estimate how disease outbreaks might change in the future , says Lohan , who praises Wood ’ s creative method of using museum specimens to answer pressing questions .
“ I ’ m really excited to see what [ she and her team ] come up with , ” @ @ @ @ @ @ @ s current priorities is convincing societies around the globe to prevent parasite extinction .
It ’ s not an easy sell , she concedes ; most people ’ s interactions with parasites are unpleasant .
To others , parasites are “ not beautiful , they ’ re not cute , they ’ re not charismatic , but they .
.
.
are vitally ecologically important , ” Wood says .
“ If we want functioning ecosystems , we have to decide to conserve parasites .
”

ABOVE: Mark Stone, University of Washington
Chelsea Wood once imagined she’d study dolphins, so it was a surprise, she says, to realize “there were much more charismatic things living inside the dolphins.”
As an undergraduate at Dartmouth University, Wood worked alongside James Byers, an ecologist then at the University of New Hampshire, who encouraged her to study parasites. “I went to his lab like a little mercenary trying to get marine biology experience, having little to no interest in the parasites,” Wood says. But along the way, she recognized how beautiful the freeloading organisms could be. For her undergraduate thesis, Wood studied how infection with a parasitic flatworm (Cryptocotyle lingua) changed the grazing habits of the marine snail Littorina littorea, and how those effects rippled through the local ecosystem.
After earning her bachelor’s degree in 2006, Wood spent two years as an editor of Frontiers in Ecology and the Environment, where she realized that she most enjoyed reading papers about parasitology. She decided to pursue the topic for her graduate research.
Wood began her PhD at Stanford University’s Hopkins Marine Station in 2008, focusing on how fishing affects fish parasites. Studying communities off the coast of Chile and around the Line Islands, south of Hawaii, she showed that parasite assemblages largely track their hosts in abundance and diversity—in heavily fished areas, many parasites are, like their fish hosts, less abundant and diverse. However, certain parasites fared better than others. Species that spread through direct contact were more abundant than ones with complex, multi-host life cycles.
As Wood was completing her dissertation, her undergraduate work on L. littorea caught the attention of Pieter Johnson, a disease ecologist at the University of Colorado Boulder who studies how parasites structure aquatic communities. It was rare to see work that looked holistically at multiple organisms, as Wood’s did, Johnson says. After meeting Wood at a conference, “I essentially headhunted her,” he tells The Scientist, encouraging Wood to join his lab for a postdoc. When she showed up in Boulder in 2013 and began working in new ecosystems, Johnson says, Wood “was just fearless,” attacking her research “like a dynamo.” Together, the two studied how aquatic bird diversity affects parasite diversity. Wood and Johnson added perches, nesting material, and bird decoys to attract a greater variety of bird species to some ponds while leaving others as controls; two years later, they looked at the parasites in each pond. As she’d observed in fish, more-diverse bird populations correlated with more-diverse parasites, but again, the effects were different across species.
After wrapping up her postdoc in 2014, Wood completed a fellowship at the University of Michigan, where she studied a group of flatworms called schistosomes that infect humans through a snail host and cause a disease called schistosomiasis. Wood used drones to search for areas where the snails’ preferred habitat—submerged water plants—bordered on human settlements in Senegal, helping to identify communities at the greatest risk of schistosomiasis outbreaks.
In 2016, Wood accepted a faculty position at the University of Washington, where she now runs her own parasite ecology lab. Several of her current initiatives involve historical ecology: delving into museum specimens and historical records to track parasites over time. Wood’s first publication using museum data followed a species of nematode worm (Clavinema mariae) infecting English sole (Parophrys vetulus) in the Puget Sound between 1930 and 2016 (J Appl Ecol, 56:190–200, 2019). During that time, she found, the number of nematodes per fish increased eightfold. Her ongoing work will reconstruct a broader assemblage of parasites that have infected 10 economically important fish species, including herring, hake, and rockfish, over the last century.
“There is an amazing treasure trove of information hidden away in our natural [history] museums,” Katrina Lohan, a parasite ecologist with the Smithsonian’s Environmental Research Center, tells The Scientist. Without historical data, researchers can only estimate how disease outbreaks might change in the future, says Lohan, who praises Wood’s creative method of using museum specimens to answer pressing questions. “I’m really excited to see what [she and her team] come up with,” Lohan says.
One of Wood’s current priorities is convincing societies around the globe to prevent parasite extinction. It’s not an easy sell, she concedes; most people’s interactions with parasites are unpleasant. To others, parasites are “not beautiful, they’re not cute, they’re not charismatic, but they . . . are vitally ecologically important,” Wood says. “If we want functioning ecosystems, we have to decide to conserve parasites.”


Ten Minute Sabbatical

7 .
Order , as of the nucleotide bases in a DNA molecule 8 .
Living in a state of @ @ @ @ @ a DNA package 10 .
Produce offspring from stocks not related 11 .
Gregor Mendel @ @ @ @ @ .
Relating to the nose 15 .
Cell formed by the union of two gametes @ @ @ @ @ directly above the pelvis 18 .
Sudden variation in an inheritable characteristic 20 .
Niels @ @ @ @ @ is just an atom ’ s way of looking at itself ” 21 .
Number @ @ @ @ @ forces 22 .
Dangerous mistake in self-medication

ACROSS 7. Order, as of the nucleotide bases in a DNA molecule
8. Living in a state of nature
9. Shape of a DNA package
10. Produce offspring from stocks not related
11. Gregor Mendel’s middle name
13. Relating to the nose
15. Cell formed by the union of two gametes
17. Of the vertebrae directly above the pelvis
18. Sudden variation in an inheritable characteristic
20. Niels who said “A physicist is just an atom’s way of looking at itself”
21. Number of classical elements or fundamental forces
22. Dangerous mistake in self-medication


Looming Change

In this topsy-turvy year , the world has been waylaid by a viral pandemic .
But a larger and more intractable menace churns in the background , continuing to wreak havoc while humanity ’ s attention is diverted .
Climate change remains arguably the most pressing threat we face as a species .
And despite signs of hope earlier this year as lockdowns in response to the COVID-19 pandemic grounded airplanes , shuttered businesses , and garaged cars , the problem is not abating .
Humanity must be able to fight disease while simultaneously keeping our sights trained on the @ @ @ @ @ @ @ .
If we are not up to this task , the hell of 2020 will pale in comparison to the challenges we ’ ll face .
The first few months of the pandemic provided a glimpse of what a planet given respite from the relentless pressure of modern human inhabitance might look like .
In April , people in Punjab , India , snapped photos of the Himalayas , more than 100 miles away , a sight usually obscured by smoggy skies .
The International Energy Agency published a report that same month @ @ @ @ @ @ @ reduce CO emissions by 8 percent compared to 2019 levels—an unprecedented drop .
All this sounded like a rare spot of good news in an otherwise disconcerting year .
But alas , the sense that nature might be able to quickly heal over the scars of human activity was short-lived .
As economies reopened , we took back to our petroleum-fueled modes of transportation , and fossil fuel–powered factories revved back up to continue their belching of greenhouse gases into the atmosphere .
By mid-May , levels of several air pollutants in China @ @ @ @ @ @ @ and fine particulate matter , had rebounded to concentrations above levels recorded in April and May of last year , according to an analysis by the Finland-based Centre for Research on Energy and Clean Air .
And globally , CO emissions have been creeping back up as the planet ’ s human inhabitants return to something close to business as usual .
By early June , global emissions had rebounded to within 5 percent of mean 2019 levels , up from an average 17 percent reduction in early April , according to data @ @ @ @ @ @ @ .
There have also been negative effects of the COVID-19 pandemic on the environment .
Pre-pandemic , humans were already dumping an unbelievable amount of plastic—8 million metric tons per year—into our oceans , the eventual destination for much of our waste .
But with the uptick in the use of products such as disposable plastic packaging , bags , and cutlery as well as personal protective equipment , this year is set to outpace 2019 ’ s outflow of plastic waste by 30 percent , according to a paper published in June @ @ @ @ @ @ @ a pandemic the size and scope of COVID-19 demands immediate attention , action on climate change and other environmental crises can not be shelved .
Wildfires in the western US and hurricanes in the South remind us that even though we ’ re busy trying to address a pressing public health emergency , global warming isn ’ t put on pause .
This persistent concern should inform how we strategically emerge from the COVID-19 pandemic and enter a world where we live with the chronic problem of SARS-CoV-2 and likely future epidemics .
@ @ @ @ @ @ @ help economies fully rebound need to focus on zero-carbon climate resilient investments that address unemployment but avoid locking us into a new high-carbon future , ” Bob Ward , a policy director at the Grantham Research Institute on Climate Change at the London School of Economics , told The Guardian in June .
I was heartened to see that , in both the US presidential debate and the US vice presidential debate that have been held as of this writing , climate change questions were posed to the candidates , something that did @ @ @ @ @ @ @ to the 2016 US election .
After the worst of the COVID-19 pandemic is behind us , humanity must learn to navigate a world changed by the ravages of a novel virus at the same time that we address not-so-novel problems with how Homo sapiens affects our planet and the organisms we share it with .

ABOVE: © istock.com, KOLDUNOV
In this topsy-turvy year, the world has been waylaid by a viral pandemic. But a larger and more intractable menace churns in the background, continuing to wreak havoc while humanity’s attention is diverted. Climate change remains arguably the most pressing threat we face as a species. And despite signs of hope earlier this year as lockdowns in response to the COVID-19 pandemic grounded airplanes, shuttered businesses, and garaged cars, the problem is not abating. Humanity must be able to fight disease while simultaneously keeping our sights trained on the persistent and snowballing effects of global warming. If we are not up to this task, the hell of 2020 will pale in comparison to the challenges we’ll face.
The first few months of the pandemic provided a glimpse of what a planet given respite from the relentless pressure of modern human inhabitance might look like. In April, people in Punjab, India, snapped photos of the Himalayas, more than 100 miles away, a sight usually obscured by smoggy skies. The International Energy Agency published a report that same month that the globe was on track to reduce CO 2 emissions by 8 percent compared to 2019 levels—an unprecedented drop.
All this sounded like a rare spot of good news in an otherwise disconcerting year. But alas, the sense that nature might be able to quickly heal over the scars of human activity was short-lived. As economies reopened, we took back to our petroleum-fueled modes of transportation, and fossil fuel–powered factories revved back up to continue their belching of greenhouse gases into the atmosphere. By mid-May, levels of several air pollutants in China, including ozone, sulfur dioxide, and fine particulate matter, had rebounded to concentrations above levels recorded in April and May of last year, according to an analysis by the Finland-based Centre for Research on Energy and Clean Air. And globally, CO 2 emissions have been creeping back up as the planet’s human inhabitants return to something close to business as usual. By early June, global emissions had rebounded to within 5 percent of mean 2019 levels, up from an average 17 percent reduction in early April, according to data published by the Integrated Carbon Observation System.
ANDRZEJ KRAUZE
There have also been negative effects of the COVID-19 pandemic on the environment. Pre-pandemic, humans were already dumping an unbelievable amount of plastic—8 million metric tons per year—into our oceans, the eventual destination for much of our waste. But with the uptick in the use of products such as disposable plastic packaging, bags, and cutlery as well as personal protective equipment, this year is set to outpace 2019’s outflow of plastic waste by 30 percent, according to a paper published in June in Environmental Science & Technology.
While a pandemic the size and scope of COVID-19 demands immediate attention, action on climate change and other environmental crises cannot be shelved. Wildfires in the western US and hurricanes in the South remind us that even though we’re busy trying to address a pressing public health emergency, global warming isn’t put on pause. This persistent concern should inform how we strategically emerge from the COVID-19 pandemic and enter a world where we live with the chronic problem of SARS-CoV-2 and likely future epidemics. “Any economic recovery packages designed to help economies fully rebound need to focus on zero-carbon climate resilient investments that address unemployment but avoid locking us into a new high-carbon future,” Bob Ward, a policy director at the Grantham Research Institute on Climate Change at the London School of Economics, told The Guardian in June.
I was heartened to see that, in both the US presidential debate and the US vice presidential debate that have been held as of this writing, climate change questions were posed to the candidates, something that did not occur in the debates running up to the 2016 US election. After the worst of the COVID-19 pandemic is behind us, humanity must learn to navigate a world changed by the ravages of a novel virus at the same time that we address not-so-novel problems with how Homo sapiens affects our planet and the organisms we share it with.
Bob Grant
Editor-in-Chief


thescientist--2020-11-01--Microbes Find Their Niche in Underwater Shipwrecks

ABOVE : Microbiologist Erin Field ( center ) holds a shipwreck core that maritime archaeologist Nathan Richards ( left ) drilled from the hull of the Pappy Lane , while Field ’ s student Kyra Price holds a sterile bag for its collection .
JOHN MCCORD , UNC COASTAL STUDIES INSTITUTE Armed with a battery-powered underwater drill , maritime archaeologist Nathan Richards ducked his face into the Atlantic Ocean .
It was a sunny afternoon in September 2017 , and Richards was standing in waist-deep water atop a wrecked ship called the Pappy Lane , which ran aground off the @ @ @ @ @ @ @ .
With students looking on , Richards peered through his mask and skillfully applied pressure to push the 1.5-inch circular drill bit into the ship ’ s steel hull under his feet .
As the director of maritime studies at East Carolina University ( ECU ) , Richards had studied hundreds of shipwrecks over the years , and had even drilled core samples of some , but this was the first time he ’ d gone in search of microbes .
Richards has been interested in this particular wreck for the better part @ @ @ @ @ @ @ investigation—funded primarily by the North Carolina Department of Transportation because a planned bridge project would run right by the wreck—revealed it to be an amphibious assault vessel from the Second World War that had apparently been converted to an oil barge before being intentionally run aground to help rescue some other barges stranded in a storm .
Despite having been sitting on the seafloor for just half a century , the wreck is extremely corroded compared with other sunken vessels in the area , Richards notes .
Like many marine archaeologists , he @ @ @ @ @ @ @ occur on shipwrecks as the boats ’ metals exchange electrons with one another once submerged in the conductive seawater .
“ But that ’ s an electrochemical process that doesn ’ t really take into account all that much microbes .
.
.
.
And [ we ’ ve ] always known that there ’ s a microbial component to corrosion.
” So this time , Richards was drilling for microbes to see if he and his students could shed light on the Pappy Lane ’ s particularly rapid deterioration .
Along with @ @ @ @ @ @ @ his students drilled a total of six core samples of the ship ’ s steel hull—containing both the metal structure itself and the concrete-like layer of bacteria and their secretions on either side—from the bow to the stern .
The team also collected pieces of loose debris from the ship , as well as seawater and sediment samples , all of which were placed into a cooler for the trip back to the lab for genetic analysis .
The data revealed pronounced differences in microbial communities—in terms of both the species makeup and @ @ @ @ @ @ @ the shipwreck and in the surrounding water and sediment .
“ I often think about it in terms of the human micro-biome , ” Field says .
“ We have microbes that live all over and in our bodies , but you won ’ t find the same microbes in your gut that you will on your skin because the environments are different.
” Field was particularly interested in how iron-oxidizing bacteria , which eat iron from the ship ’ s metal and produce rust as a waste product , were contributing to @ @ @ @ @ @ @ In the lab , Field and her team cultured bacteria from the debris and core samples and found that iron-oxidizing bacteria such as Zetaproteobacteria were present in every sample , and particularly abundant in samples with visible rust .
“ It ’ s possible that their presence could indicate early detection for future corrosion , ” Field says .
She also notes that Zetaproteobacteria , as some of the first to settle on shipwrecks , may make the environment more hospitable to other microbes .
For example , they deplete the immediate surroundings @ @ @ @ @ @ @ that grow well in anoxic conditions to further corrode the ship ’ s steel , Field speculates .
The findings could have implications for preservation strategies not just for shipwrecks , but for any aquatic steel structure , she notes .
“ Most [ current ] preservation methods are not accounting for the microbial role .
.
.
so we ’ re still missing that piece of the puzzle .
And we ’ re finding that microbes are definitely affecting the deterioration or preservation of these wrecks.
” The University of Southern Mississippi @ @ @ @ @ @ @ been studying the microbiomes of deep-sea wrecks for a decade but was not involved in the Pappy Lane work , says that it ’ s exciting that the team was able to take core samples to search for microbial life on the shipwreck itself .
“ In that way , you can ask those really specific questions of : How does microbial life exist on these human-made surfaces ?
” She adds that she was not surprised that the microbial communities varied in and around the wreck .
“ We definitely see parallels @ @ @ @ @ @ @ work on deep-sea wrecks .
Analyzing samples of the surrounding sediment , her team recently found an increasing abundance of cellulose- and hemicellulose-degrading bacteria with proximity to two newly discovered wooden wrecks—one around 500 meters deep and the other nearly 1,800 meters down—in the Gulf of Mexico , says Hamdan , who presented the data at the Ocean Sciences Meeting in San Diego in February .
Hamdan joins Field as one of the few microbiologists to focus on shipwrecks .
In her first such project , Hamdan and colleagues navigated a remotely operated @ @ @ @ @ @ @ , all located between 140 meters and 2,000 meters deep , to collect samples that could help them understand the effects of the 2010 Deepwater Horizon oil spill on the microbes in and around the wrecks .
She ’ s also studied how the shipwrecks themselves affect the microbial communities surrounding them .
Most recently , she and her team placed pieces of wood near wrecks in the deep sea that they later retrieved , using an acoustic signal to trigger a flotation device to bring them to a research vessel at the @ @ @ @ @ @ @ grown on them .
The results support the idea that the composition of microbial communities changes with distance from wrecks , she says .
“ We ’ ve seen a .
.
.
definitive signature of increased biodiversity in a ring around the shipwreck Anona , ” a yacht that sank in the Gulf of Mexico in 1944 , “ and we ’ re also seeing this pattern emerge around one of the two wooden shipwrecks that we studied last summer.
” Hamdan says these results will be published soon .
“ Looking @ @ @ @ @ @ @ something new , ” says Kirstin Meyer-Kaiser , a marine biologist at Woods Hole Oceanographic Institution who studies invertebrate communities that live on shipwrecks .
She suspects that , with more research on the microbial communities in and around shipwrecks , scientists will learn about how those communities interact with invertebrates , too .
Just as the material of the ship appears to affect which bacteria settle where , she speculates , perhaps the biofilms those bacteria form affect which invertebrates take up residence .
Hamdan says it ’ s very likely microbes @ @ @ @ @ @ @ communities at shipwrecks .
“ For you to be able to see any corals and tube worms and all of this gorgeous stuff that grows on shipwrecks , the microbes have to get there first .
”

ABOVE: Microbiologist Erin Field (center) holds a shipwreck core that maritime archaeologist Nathan Richards (left) drilled from the hull of the Pappy Lane, while Field’s student Kyra Price holds a sterile bag for its collection.
JOHN MCCORD, UNC COASTAL STUDIES INSTITUTE
Armed with a battery-powered underwater drill, maritime archaeologist Nathan Richards ducked his face into the Atlantic Ocean. It was a sunny afternoon in September 2017, and Richards was standing in waist-deep water atop a wrecked ship called the Pappy Lane, which ran aground off the coast of North Carolina in the 1960s. With students looking on, Richards peered through his mask and skillfully applied pressure to push the 1.5-inch circular drill bit into the ship’s steel hull under his feet. As the director of maritime studies at East Carolina University (ECU), Richards had studied hundreds of shipwrecks over the years, and had even drilled core samples of some, but this was the first time he’d gone in search of microbes.
Richards has been interested in this particular wreck for the better part of the past decade. His exhaustive investigation—funded primarily by the North Carolina Department of Transportation because a planned bridge project would run right by the wreck—revealed it to be an amphibious assault vessel from the Second World War that had apparently been converted to an oil barge before being intentionally run aground to help rescue some other barges stranded in a storm.
We’ve always known that there’s a microbial component to corrosion. —Nathan Richards, East Carolina University
Despite having been sitting on the seafloor for just half a century, the wreck is extremely corroded compared with other sunken vessels in the area, Richards notes. Like many marine archaeologists, he has studied the galvanic corrosion known to occur on shipwrecks as the boats’ metals exchange electrons with one another once submerged in the conductive seawater. “But that’s an electrochemical process that doesn’t really take into account all that much microbes. . . . And [we’ve] always known that there’s a microbial component to corrosion.” So this time, Richards was drilling for microbes to see if he and his students could shed light on the Pappy Lane’s particularly rapid deterioration.
Along with ECU microbiologist Erin Field, Richards and his students drilled a total of six core samples of the ship’s steel hull—containing both the metal structure itself and the concrete-like layer of bacteria and their secretions on either side—from the bow to the stern. The team also collected pieces of loose debris from the ship, as well as seawater and sediment samples, all of which were placed into a cooler for the trip back to the lab for genetic analysis.
The data revealed pronounced differences in microbial communities—in terms of both the species makeup and the metabolic functionalities—on the different materials of the shipwreck and in the surrounding water and sediment. “I often think about it in terms of the human micro-biome,” Field says. “We have microbes that live all over and in our bodies, but you won’t find the same microbes in your gut that you will on your skin because the environments are different.”
A BOAT FULL OF BUGS: The Pappy Lane was intentionally run aground in the 1960s off the coast of North Carolina. Now it’s home to a diverse community of microbes. JOHN MCCORD, UNC COASTAL STUDIES INSTITUTE
Field was particularly interested in how iron-oxidizing bacteria, which eat iron from the ship’s metal and produce rust as a waste product, were contributing to the Pappy Lane’s deterioration. In the lab, Field and her team cultured bacteria from the debris and core samples and found that iron-oxidizing bacteria such as Zetaproteobacteria were present in every sample, and particularly abundant in samples with visible rust. “It’s possible that their presence could indicate early detection for future corrosion,” Field says. She also notes that Zetaproteobacteria, as some of the first to settle on shipwrecks, may make the environment more hospitable to other microbes. For example, they deplete the immediate surroundings of oxygen, possibly inviting sulfate bacteria that grow well in anoxic conditions to further corrode the ship’s steel, Field speculates.
The findings could have implications for preservation strategies not just for shipwrecks, but for any aquatic steel structure, she notes. “Most [current] preservation methods are not accounting for the microbial role . . . so we’re still missing that piece of the puzzle. And we’re finding that microbes are definitely affecting the deterioration or preservation of these wrecks.”
The University of Southern Mississippi’s Leila Hamdan, who has been studying the microbiomes of deep-sea wrecks for a decade but was not involved in the Pappy Lane work, says that it’s exciting that the team was able to take core samples to search for microbial life on the shipwreck itself. “In that way, you can ask those really specific questions of: How does microbial life exist on these human-made surfaces?” She adds that she was not surprised that the microbial communities varied in and around the wreck. “We definitely see parallels there,” she says of her work on deep-sea wrecks. Analyzing samples of the surrounding sediment, her team recently found an increasing abundance of cellulose- and hemicellulose-degrading bacteria with proximity to two newly discovered wooden wrecks—one around 500 meters deep and the other nearly 1,800 meters down—in the Gulf of Mexico, says Hamdan, who presented the data at the Ocean Sciences Meeting in San Diego in February.
UNDERWATER ACTION: Maritime archaeologist Nathan Richards drills a core from the hull of the Pappy Lane shipwreck. JOHN MCCORD, UNC COASTAL STUDIES INSTITUTE
Hamdan joins Field as one of the few microbiologists to focus on shipwrecks. In her first such project, Hamdan and colleagues navigated a remotely operated vehicle to six Gulf of Mexico wrecks, all located between 140 meters and 2,000 meters deep, to collect samples that could help them understand the effects of the 2010 Deepwater Horizon oil spill on the microbes in and around the wrecks. She’s also studied how the shipwrecks themselves affect the microbial communities surrounding them. Most recently, she and her team placed pieces of wood near wrecks in the deep sea that they later retrieved, using an acoustic signal to trigger a flotation device to bring them to a research vessel at the surface, to see what microbes had grown on them.
The results support the idea that the composition of microbial communities changes with distance from wrecks, she says. “We’ve seen a . . . definitive signature of increased biodiversity in a ring around the shipwreck Anona,” a yacht that sank in the Gulf of Mexico in 1944, “and we’re also seeing this pattern emerge around one of the two wooden shipwrecks that we studied last summer.” Hamdan says these results will be published soon.
“Looking at microbial communities on shipwrecks is definitely something new,” says Kirstin Meyer-Kaiser, a marine biologist at Woods Hole Oceanographic Institution who studies invertebrate communities that live on shipwrecks. She suspects that, with more research on the microbial communities in and around shipwrecks, scientists will learn about how those communities interact with invertebrates, too. Just as the material of the ship appears to affect which bacteria settle where, she speculates, perhaps the biofilms those bacteria form affect which invertebrates take up residence.
Hamdan says it’s very likely microbes are playing a role in shaping macrofaunal communities at shipwrecks. “For you to be able to see any corals and tube worms and all of this gorgeous stuff that grows on shipwrecks, the microbes have to get there first.”


thescientist--2020-11-02--Baking Soda Boosts T Cells' Ability to Fight Leukemia

Patients with acute myeloid leukemia who relapse after stem cell transplantation have just a small chance of survival : doctors can give them additional donor T cells to fight the cancer , but only about 20 percent of patients go back into remission .
Scientists didn ’ t know why these T cells aren ’ t working against AML , but a paper published in Science Translational Medicine on October 28 uncovers the mechanism , as well as a simple , inexpensive treatment that can reactivate them : sodium bicarbonate , otherwise known as baking soda .
“ This is @ @ @ @ @ @ @ Nataliya Buxbaum , who researches T cell metabolism at the National Cancer Institute and who wasn ’ t involved in this study .
“ Relapsed AML is very difficult to treat , so if something rudimentary , like sodium bicarb , which is available at every hospital , can augment the immune response , it ’ s certainly interesting.
” AML is a disease that attacks the blood-forming cells of the bone marrow , and physicians treat it with chemotherapy to kill the leukemia cells .
But if a high dose of chemotherapy @ @ @ @ @ @ @ bone marrow , and the patient will need a stem cell transplant to generate new blood-forming and immune cell–forming cells .
The donor T cells from the transplant recognize the leukemia cells as foreign and attack them , a phenomenon known as graft-versus-leukemia effect , which , along with the chemotherapy , can send the patient into remission .
If the leukemia comes back even after these procedures , patients can receive a donor lymphocyte infusion of additional T cells , but it is rarely successful .
Robert Zeiser , a transplant physician @ @ @ @ @ @ @ , wanted to see whether leukemia cells alter T cell function , so he examined T cells from patients with AML after stem cell transplantation , when the AML was in remission , and after subsequent relapse .
He found that relapsed patients ’ T cells had reduced glycolysis and oxidative phosphorylation , and less cytotoxicity .
In other words , their metabolism and ability to kill other cells was diminished .
Zeiser moved his experiments into AML mouse models , where he found that genes involved in glycolysis were down-regulated in mouse @ @ @ @ @ @ @ cells also had reduced metabolic fitness and proliferation .
Transferring T cells previously exposed to AML into AML mice couldn ’ t get rid of the leukemia , whereas T cells not exposed to AML did attack the leukemia , showing that AML cells release some factor that reduces T cells ’ ability to fight leukemia .
The team used magnetic resonance imaging and mass spectrometry to identity possible metabolites from the leukemia cells that could have caused the changes in T cell function .
After five years testing various metabolites , one @ @ @ @ @ @ @ acid ( LA ) .
LA was elevated in AML cultures , and also in patients with AML relapse after stem cell transplantation , but not in the same patients during remission .
To test lactic acid ’ s effect on T cells , they added it to T cell culture and saw it reduced the activity of glycolysis-related enzymes , damaged T cells ’ ability to proliferate , and reduced their capacity to kill leukemia cells .
“ Lactic acid paralyzes the T cells , and that helps the leukemia cells to @ @ @ @ @ @ @ system , ” says Zeiser .
He says it ’ s not clear which comes first , the relapse or the lower pH caused by excess LA .
Zeiser tried a few different buffers to see whether they reduced acidosis , including sodium bicarbonate ( NaBi ) , which is used to counteract metabolic acidosis caused by a variety of reasons , such as diet , diarrhea , or poor kidney function .
Zeiser and his colleagues found that adding NaBi to T cells treated with lactic acid reversed the effects of the @ @ @ @ @ @ @ metabolism and proliferation were restored , and the low pH inside the cells was returned to normal .
When they added NaBi to the drinking water of mice with AML and transplanted additional T cells after a stem cell transplant , the animals lived longer .
When they added NaBi to healthy human T cells challenged with lactic acid , glycolysis was restored .
Zeiser and his team prescribed an oral NaBi treatment for one week to 10 AML patients receiving a donor lymphocyte infusion after they experienced a relapse following a stem @ @ @ @ @ @ @ recipients ’ blood was less acidic than before the baking soda treatment , and that T cell metabolism improved .
In addition , the T cells “ produced more cytokines and they were more aggressive against leukemia cells after the treatment , ” says Zeiser .
The team is preparing for a larger clinical trial of the treatment to look at patient outcomes , which they didn ’ t report in their study .
Richard Stone , a physician who studies leukemia at Dana-Farber Cancer Institute in Boston , asks , “ What @ @ @ @ @ @ @ provided to the patient to decrease the relapse rate ?
How long does it have to be given , what would be the side effects ?
The devil is in the details .
Is it specific to certain genetic subtypes ?
AML is very heterogeneous , and one person ’ s AML is not another person ’ s AML.
” Still , he says , “ I think it ’ s very intriguing.
” F.M .
Uhl et al.
, “ Metabolic reprogramming of donor T cells enhances graft-versus-leukemia effects in mice and @ @ @ @ @ @ @ 12 : eabb8969 , 2020 .

ABOVE: © ISTOCK.COM, JARUN011
Patients with acute myeloid leukemia who relapse after stem cell transplantation have just a small chance of survival: doctors can give them additional donor T cells to fight the cancer, but only about 20 percent of patients go back into remission. Scientists didn’t know why these T cells aren’t working against AML, but a paper published in Science Translational Medicine on October 28 uncovers the mechanism, as well as a simple, inexpensive treatment that can reactivate them: sodium bicarbonate, otherwise known as baking soda.
“This is an elegant study,” says physician-scientist Nataliya Buxbaum, who researches T cell metabolism at the National Cancer Institute and who wasn’t involved in this study. “Relapsed AML is very difficult to treat, so if something rudimentary, like sodium bicarb, which is available at every hospital, can augment the immune response, it’s certainly interesting.”
AML is a disease that attacks the blood-forming cells of the bone marrow, and physicians treat it with chemotherapy to kill the leukemia cells. But if a high dose of chemotherapy is required, it can destroy the bone marrow, and the patient will need a stem cell transplant to generate new blood-forming and immune cell–forming cells. The donor T cells from the transplant recognize the leukemia cells as foreign and attack them, a phenomenon known as graft-versus-leukemia effect, which, along with the chemotherapy, can send the patient into remission.
If the leukemia comes back even after these procedures, patients can receive a donor lymphocyte infusion of additional T cells, but it is rarely successful. Robert Zeiser, a transplant physician at the University of Freiburg in Germany, wanted to see whether leukemia cells alter T cell function, so he examined T cells from patients with AML after stem cell transplantation, when the AML was in remission, and after subsequent relapse. He found that relapsed patients’ T cells had reduced glycolysis and oxidative phosphorylation, and less cytotoxicity. In other words, their metabolism and ability to kill other cells was diminished.
Zeiser moved his experiments into AML mouse models, where he found that genes involved in glycolysis were down-regulated in mouse T cells cultured with AML; the cells also had reduced metabolic fitness and proliferation. Transferring T cells previously exposed to AML into AML mice couldn’t get rid of the leukemia, whereas T cells not exposed to AML did attack the leukemia, showing that AML cells release some factor that reduces T cells’ ability to fight leukemia.
The team used magnetic resonance imaging and mass spectrometry to identity possible metabolites from the leukemia cells that could have caused the changes in T cell function. After five years testing various metabolites, one candidate rose to the top: lactic acid (LA). LA was elevated in AML cultures, and also in patients with AML relapse after stem cell transplantation, but not in the same patients during remission. To test lactic acid’s effect on T cells, they added it to T cell culture and saw it reduced the activity of glycolysis-related enzymes, damaged T cells’ ability to proliferate, and reduced their capacity to kill leukemia cells.
The authors’ proposed mechanism for how sodium bicarbonate can overcome the impaired ability of T cells to destroy leukemia cells in the context of excess lactic acid reprinted with permission from F.M. Uhl et al., “Metabolic reprogramming of donor T cells enhances graft-versus-leukemia effects in mice and humans,” Sci Transl Med , 12:eabb8969, 2020.
“Lactic acid paralyzes the T cells, and that helps the leukemia cells to escape from the control by the immune system,” says Zeiser. He says it’s not clear which comes first, the relapse or the lower pH caused by excess LA.
Zeiser tried a few different buffers to see whether they reduced acidosis, including sodium bicarbonate (NaBi), which is used to counteract metabolic acidosis caused by a variety of reasons, such as diet, diarrhea, or poor kidney function. Zeiser and his colleagues found that adding NaBi to T cells treated with lactic acid reversed the effects of the lactic acid: the T cells’ metabolism and proliferation were restored, and the low pH inside the cells was returned to normal. When they added NaBi to the drinking water of mice with AML and transplanted additional T cells after a stem cell transplant, the animals lived longer. When they added NaBi to healthy human T cells challenged with lactic acid, glycolysis was restored.
Zeiser and his team prescribed an oral NaBi treatment for one week to 10 AML patients receiving a donor lymphocyte infusion after they experienced a relapse following a stem cell transplantation. They found that the recipients’ blood was less acidic than before the baking soda treatment, and that T cell metabolism improved. In addition, the T cells “produced more cytokines and they were more aggressive against leukemia cells after the treatment,” says Zeiser.
The team is preparing for a larger clinical trial of the treatment to look at patient outcomes, which they didn’t report in their study. Richard Stone, a physician who studies leukemia at Dana-Farber Cancer Institute in Boston, asks, “What level of sodium bicarbonate needs to be provided to the patient to decrease the relapse rate? How long does it have to be given, what would be the side effects? The devil is in the details. Is it specific to certain genetic subtypes? AML is very heterogeneous, and one person’s AML is not another person’s AML.” Still, he says, “I think it’s very intriguing.”
F.M. Uhl et al., “Metabolic reprogramming of donor T cells enhances graft-versus-leukemia effects in mice and humans,” Sci Transl Med, 12:eabb8969, 2020.


thescientist--2020-11-02--Bio-Rad Launches Three StarBright Dyes for Flow Cytometry

Bio-Rad Laboratories , Inc. ( NYSE : BIO and BIOb ) , a global leader of life science research and clinical diagnostic products , today launched three StarBright Dyes specifically developed for flow cytometry .
StarBright Blue 700 , StarBright Violet 440 , and StarBright Violet 610 are fluorescent nanoparticles that are conjugated to Bio-Rad ’ s highly validated flow antibodies , providing maximal brightness and improved resolution .
Brighter than other fluorescent dyes with similar excitation and emission spectra , the StarBright dyes provide researchers with an alternative for flow cytometry panels .
The brightness of the dyes combined @ @ @ @ @ @ @ improved resolution of rare populations and low-density antigens and easily integrate into multiplex panels .
“ StarBright Dyes offer exceptional brightness with specific excitation and emission , allowing researchers to build brighter flow cytometry panels to enable better resolution of positive populations from background without the need for special buffers , ” said Mike Blundell , Bio-Rad Product Manager , Life Science Group .
“ The unique profile of these dyes combined with Bio-Rad ’ s high-quality antibodies provides flexibility and offers a reliable alternative for incorporation into flow cytometry protocols.
” Resistant @ @ @ @ @ @ @ lot-to-lot variation , enabling researchers to achieve consistent and reproducible staining • Work with all common staining buffers , including special polymer dye staining buffers , for easy integration into multicolor panels • The unique chemistry ensures no loss of signal in fixation • Offer narrow excitation and emission profiles for improved resolution in new and existing flow cytometry experiments StarBright Dyes are compatible with Bio-Rad ’ s ZE5 Cell Analyzer , S3e Cell Sorter , as well as other conventional and spectral flow cytometers .

Bio-Rad Laboratories, Inc. (NYSE: BIO and BIOb), a global leader of life science research and clinical diagnostic products, today launched three StarBright Dyes specifically developed for flow cytometry.
StarBright Blue 700, StarBright Violet 440, and StarBright Violet 610 are fluorescent nanoparticles that are conjugated to Bio-Rad’s highly validated flow antibodies, providing maximal brightness and improved resolution. Brighter than other fluorescent dyes with similar excitation and emission spectra, the StarBright dyes provide researchers with an alternative for flow cytometry panels. The brightness of the dyes combined with precise excitation and emission profiles offer improved resolution of rare populations and low-density antigens and easily integrate into multiplex panels.
“StarBright Dyes offer exceptional brightness with specific excitation and emission, allowing researchers to build brighter flow cytometry panels to enable better resolution of positive populations from background without the need for special buffers,” said Mike Blundell, Bio-Rad Product Manager, Life Science Group. “The unique profile of these dyes combined with Bio-Rad’s high-quality antibodies provides flexibility and offers a reliable alternative for incorporation into flow cytometry protocols.”
Key Benefits of StarBright Dyes
Resistant to photobleaching and highly stable with minimal lot-to-lot variation, enabling researchers to achieve consistent and reproducible staining
Work with all common staining buffers, including special polymer dye staining buffers, for easy integration into multicolor panels
The unique chemistry ensures no loss of signal in fixation
Offer narrow excitation and emission profiles for improved resolution in new and existing flow cytometry experiments
StarBright Dyes are compatible with Bio-Rad’s ZE5 Cell Analyzer, S3e Cell Sorter, as well as other conventional and spectral flow cytometers.


thescientist--2020-11-02--First Alzheimer's Blood Test Rolled Out for Clinical Use in US

The first blood test designed to assist physicians in determining whether a patient has Alzheimer ’ s disease is now available in most US states , the company C N Diagnostics announced October 29 .
The test measures biomarkers that frequently reflect the presence of amyloid plaques in the brain—a hallmark of Alzheimer ’ s—as well as the presence of a gene variant that increases the risk of the disease .
“ I ’ m very excited about it , ” says Suzanne Schindler , a neurologist at the Washington University School of Medicine in St. Louis who was involved @ @ @ @ @ @ @ assay but is not connected to C N. While there are two other tests for Alzheimer ’ s-associated brain changes , she notes , both have logistical and financial challenges : one that collects biomarkers in the cerebrospinal fluid ( CSF ) requires a spinal tap , while the other , a scan called amyloid PET , involves injecting a radioactive tracer , costs thousands of dollars , and is only performed at specialized centers .
“ I think patients really like the idea of a blood test , ” she says .
@ @ @ @ @ @ @ has the potential to allow us to do a lot more testing than we have done in the past.
” The price of the test is $ 1,250 , says C N CEO Joel Braunstein , but patients who qualify for financial assistance will be charged between $ 25 and $ 400 .
Health insurance companies don ’ t currently pay for the test , he adds , but qualifying for this reimbursement “ is a very high priority ” for the company .
“ If you asked me [ five or ten @ @ @ @ @ @ @ be a blood test for Alzheimer ’ s , I would have been very skeptical , ” says Howard Fillit , the executive director and chief science officer of the Alzheimer ’ s Drug Discovery Foundation , which invested in C N ’ s development of the test .
“ So the fact that this is on the market now is just amazing.
” Fillit wasn ’ t alone in thinking that , due to the blood-brain barrier , biomarkers from the brain wouldn ’ t be found in peripheral blood in sufficient @ @ @ @ @ @ @ analytical techniques have advanced in sensitivity in recent years , allowing small amounts of biomarkers in the blood to be detected .
See “ The Hunt for a Blood Test for Alzheimer ’ s Disease ” The C N test relies on the ratio of two isoforms of the amyloid-β protein , Aβ42 and Aβ40 , that aggregate to form amyloid plaques in the brain , combined with the presence of isoforms of apolipoprotein E ( ApoE ) that reflect whether the patient caries a genetic variant associated with Alzheimer ’ s risk @ @ @ @ @ @ @ score that indicates the probability that a patient would be found to have amyloid plaques if they were to undergo an amyloid PET scan .
Doctors can then consider the test results along with other information about the patient to arrive at a diagnosis .
According to data posted on the company ’ s website , a study in 686 patients with cognitive impairment found that those with scores above a certain cutoff point had a positive amyloid PET scan 92 percent of the time , while those with scores below a certain @ @ @ @ @ @ @ having a negative result on the PET scan .
While no drugs have yet been approved to treat Alzheimer ’ s , being able to distinguish it from other possible causes of cognitive impairment is nonetheless valuable , Fillit and Schindler say .
As a clinician , Schindler says , “ I want to know what my patients have.
” That can be complicated because in many cases , “ they don ’ t just have memory impairment , they ’ re taking multiple medications , they have all sorts of health issues @ @ @ @ @ @ @ sometimes it ’ s really hard to know whether the symptoms they ’ re experiencing are due to something like Alzheimer ’ s or something else.
” Symptom-based diagnosis of Alzheimer ’ s disease is only about 70 percent accurate , notes Colin Masters of the Florey Institute of Neuroscience and Mental Health in Australia who was part of the team that first characterized the amyloid plaques in the disease .
If a clinician suspects the disease but the blood test returns a negative result , this “ will force the clinicians to @ @ @ @ @ @ @ of dementia , ” says Masters , who collaborates with one of the test ’ s developers but has no ties to C N. He adds that once an amyloid-targeting Alzheimer ’ s drug is approved , the test will be useful in determining who should receive it .
Such a treatment may not be far off : the Biogen drug candidate aducanumab is set for review by a US Food and Drug Administration panel later this week .
The blood test is also likely to be a boon for clinical trials to @ @ @ @ @ @ @ make it easier to screen patients for recruitment , Fillit says .
“ Screening and enrollment represents up to fifty percent of the cost of clinical trials in Alzheimer ’ s disease , and one Phase 3 trial costs three to four hundred million dollars , ” he says , calling the blood test a “ huge advance in clinical trials.
” See “ New Tracer Gives Clear Picture of Alzheimer ’ s and Other Dementias ” Clarification ( November 2 ) : This article has been amended to state Masters ’ s @ @ @ @ @ @ @ ’ s developers .

ABOVE: © ISTOCK.COM, YACOBCHUKOLENA
Update (April 21, 2022): In research published today in JAMA Network Open, C2N Diagnostics scientists and their colleagues report that the company’s blood test had an overall accuracy of 81 percent in predicting whether adults with cognitive impairment would show amyloid plaques on a PET scan.
The first blood test designed to assist physicians in determining whether a patient has Alzheimer’s disease is now available in most US states, the company C 2 N Diagnostics announced October 29. The test measures biomarkers that frequently reflect the presence of amyloid plaques in the brain—a hallmark of Alzheimer’s—as well as the presence of a gene variant that increases the risk of the disease.
“I’m very excited about it,” says Suzanne Schindler, a neurologist at the Washington University School of Medicine in St. Louis who was involved in testing an earlier version of the assay but is not connected to C 2 N. While there are two other tests for Alzheimer’s-associated brain changes, she notes, both have logistical and financial challenges: one that collects biomarkers in the cerebrospinal fluid (CSF) requires a spinal tap, while the other, a scan called amyloid PET, involves injecting a radioactive tracer, costs thousands of dollars, and is only performed at specialized centers. “I think patients really like the idea of a blood test,” she says. “And I think that it really has the potential to allow us to do a lot more testing than we have done in the past.”
The price of the test is $1,250, says C 2 N CEO Joel Braunstein, but patients who qualify for financial assistance will be charged between $25 and $400. Health insurance companies don’t currently pay for the test, he adds, but qualifying for this reimbursement “is a very high priority” for the company.
“If you asked me [five or ten] years ago if there would ever be a blood test for Alzheimer’s, I would have been very skeptical,” says Howard Fillit, the executive director and chief science officer of the Alzheimer’s Drug Discovery Foundation, which invested in C 2 N’s development of the test. “So the fact that this is on the market now is just amazing.”
Fillit wasn’t alone in thinking that, due to the blood-brain barrier, biomarkers from the brain wouldn’t be found in peripheral blood in sufficient quantities to deliver a diagnosis. But analytical techniques have advanced in sensitivity in recent years, allowing small amounts of biomarkers in the blood to be detected.
The C 2 N test relies on the ratio of two isoforms of the amyloid-β protein, Aβ42 and Aβ40, that aggregate to form amyloid plaques in the brain, combined with the presence of isoforms of apolipoprotein E (ApoE) that reflect whether the patient caries a genetic variant associated with Alzheimer’s risk. The results are combined into a score that indicates the probability that a patient would be found to have amyloid plaques if they were to undergo an amyloid PET scan. Doctors can then consider the test results along with other information about the patient to arrive at a diagnosis. According to data posted on the company’s website, a study in 686 patients with cognitive impairment found that those with scores above a certain cutoff point had a positive amyloid PET scan 92 percent of the time, while those with scores below a certain cutoff had a 77 percent chance of having a negative result on the PET scan.
While no drugs have yet been approved to treat Alzheimer’s, being able to distinguish it from other possible causes of cognitive impairment is nonetheless valuable, Fillit and Schindler say. As a clinician, Schindler says, “I want to know what my patients have.” That can be complicated because in many cases, “they don’t just have memory impairment, they’re taking multiple medications, they have all sorts of health issues,” she says. “And sometimes it’s really hard to know whether the symptoms they’re experiencing are due to something like Alzheimer’s or something else.”
Symptom-based diagnosis of Alzheimer’s disease is only about 70 percent accurate, notes Colin Masters of the Florey Institute of Neuroscience and Mental Health in Australia who was part of the team that first characterized the amyloid plaques in the disease. If a clinician suspects the disease but the blood test returns a negative result, this “will force the clinicians to go and look harder for other causes of dementia,” says Masters, who collaborates with one of the test’s developers but has no ties to C 2 N. He adds that once an amyloid-targeting Alzheimer’s drug is approved, the test will be useful in determining who should receive it. Such a treatment may not be far off: the Biogen drug candidate aducanumab is set for review by a US Food and Drug Administration panel later this week.
The blood test is also likely to be a boon for clinical trials to develop other drugs, as it will make it easier to screen patients for recruitment, Fillit says. “Screening and enrollment represents up to fifty percent of the cost of clinical trials in Alzheimer’s disease, and one Phase 3 trial costs three to four hundred million dollars,” he says, calling the blood test a “huge advance in clinical trials.”
Clarification (November 2): This article has been amended to state Masters’s working relationship with one of the test’s developers.


thescientist--2020-11-02--Extended range of services supports accelerated drug discovery and development using predictive 3D L

Extended range of services supports accelerated drug discovery and development using predictive 3D Liver-on-Chip technology

CN Bio , a leading 3D cell culture company , that has developed single and multi-organ microphysiological systems ( MPS ) to improve the accuracy and efficiency of drug discovery , today announced the commercial launch of its Drug Metabolism and Safety Toxicity Testing Services .
Liver toxicity is a principal safety concern during drug discovery and development , with the potential to terminate expensive clinical trials already underway .
The new services will incorporate the Company ’ s advanced Liver-on-Chip technology and expertise in the field to enable researchers to generate predictive and human-relevant data , improving the translatability @ @ @ @ @ @ @ new drugs to market .
Based on the success of CN Bio ’ s Non-Alcoholic Fatty Liver Disease ( NAFLD ) and Non-Alcoholic Steatohepatitis ( NASH ) Fee-For-Service offerings , the new toxicity testing services also provide researchers with additional support and bandwidth during the COVID-19 pandemic , when laboratories are not at full capacity .
Similarly to the NAFLD/NASH Fee-For-Service , all studies use the Company ’ s PhysioMimix™ Organ-on-Chip system and in vitro 3D Liver-on-Chip model ; replicating the physiological and mechanical microenvironment of the liver to fast-track lead targets and @ @ @ @ @ @ @ reproducible , and cost-effective versus animal studies .
CN Bio ’ s extended portfolio of services offers solutions to many existing workflow challenges including : drug metabolism testing , to study the human metabolism of lead candidates , identify metabolites and correlation with cell health - even for low clearance compounds , and safety toxicity testing , to provide in-depth analysis of acute or chronic drug-induced liver injury using a wide range of endpoints to determine causality and mechanism of toxicity .
The Company also provides complimentary service capabilities to support industry and @ @ @ @ @ @ @ the COVID-19 pandemic .
Dr David Hughes , CEO , CN Bio , said : “ One in ten drugs successfully reach clinical trials , with safety concerns being the principal cause for subsequent failure .
Through our enhanced drug metabolism and safety toxicity testing services , we enable scientists to take a step beyond what is currently possible with 2D cell culture and animal studies to improve their chances of clinical success .
Our technologies are on the cutting-edge of research to simulate human biological conditions , in vitro , and we @ @ @ @ @ @ @ customers in developing tomorrow ’ s medicines , especially at this challenging time .
”

CN Bio, a leading 3D cell culture company, that has developed single and multi-organ microphysiological systems (MPS) to improve the accuracy and efficiency of drug discovery, today announced the commercial launch of its Drug Metabolism and Safety Toxicity Testing Services. Liver toxicity is a principal safety concern during drug discovery and development, with the potential to terminate expensive clinical trials already underway. The new services will incorporate the Company’s advanced Liver-on-Chip technology and expertise in the field to enable researchers to generate predictive and human-relevant data, improving the translatability from discovery to clinic, and accelerating new drugs to market.
Based on the success of CN Bio’s Non-Alcoholic Fatty Liver Disease (NAFLD) and Non-Alcoholic Steatohepatitis (NASH) Fee-For-Service offerings, the new toxicity testing services also provide researchers with additional support and bandwidth during the COVID-19 pandemic, when laboratories are not at full capacity. Similarly to the NAFLD/NASH Fee-For-Service, all studies use the Company’s PhysioMimix™ Organ-on-Chip system and in vitro 3D Liver-on-Chip model; replicating the physiological and mechanical microenvironment of the liver to fast-track lead targets and generate actionable data in weeks that is reproducible, and cost-effective versus animal studies.
CN Bio’s extended portfolio of services offers solutions to many existing workflow challenges including: drug metabolism testing, to study the human metabolism of lead candidates, identify metabolites and correlation with cell health - even for low clearance compounds, and safety toxicity testing, to provide in-depth analysis of acute or chronic drug-induced liver injury using a wide range of endpoints to determine causality and mechanism of toxicity. The Company also provides complimentary service capabilities to support industry and biotechnology organisations that have been impacted by the COVID-19 pandemic.
Dr David Hughes, CEO, CN Bio, said: “One in ten drugs successfully reach clinical trials, with safety concerns being the principal cause for subsequent failure. Through our enhanced drug metabolism and safety toxicity testing services, we enable scientists to take a step beyond what is currently possible with 2D cell culture and animal studies to improve their chances of clinical success. Our technologies are on the cutting-edge of research to simulate human biological conditions, in vitro, and we are confident in our ability to support customers in developing tomorrow’s medicines, especially at this challenging time.”