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Tuesday, 7 April 2020

One Step Closer to Quantum Spin Liquids


A recent discovery by University of Arkansas physicists could help researchers establish the existence of quantum spin liquids, a new state of matter. They’ve been a mystery since they were first proposed in the 1970s. If proven to exist, quantum spin liquids would be a step toward much faster, next-generation quantum computing.

Scientists have focused attention and research on the so-called Kitaev-type of spin liquid, named in honor of the Russian scientist, Alexei Kitaev, who first proposed it. In particular, they have looked extensively at two materials – RuCl3  and Na2IrO – as candidates for this type. Both have small quantum spin numbers.

“Traditional candidates are pretty limited to only these two,” said Changsong Xu, a researcher in the Department of Physics and first author of a paper published in the journal Physical Review Letters.

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In their recent work, U of A physicists have greatly expanded the number of materials that might be candidates as Kitaev quantum spin liquids by looking at materials with higher quantum spin numbers, and by putting materials under physical strain to tune their magnetic states.

“Suddenly, we realize there are dozens of candidates we can propose,” said Xu.

Quantum spin liquids are defined by their unusual magnetic arrangement. Magnets have a north and south pole, which combined are called dipoles. These are typically produced by the quantum spin of electrons. Inside a magnetic material, dipoles tend to all be parallel to each other (ferromagnetism) or periodically alternate their up and down direction (antiferromagnetism).

In the case of hypothetical quantum spin liquids, dipoles aren’t as well ordered. Instead, they exhibit unusual ordering within a small distance of each other. Different ordering creates different types of spin liquids.



Quantum spin liquids (QSLs) form an extremely unusual magnetic state in which the spins are highly correlated and fluctuate coherently down to the lowest temperatures, but without symmetry breaking and without the formation of any static long-range-ordered magnetism. Such intriguing phenomena are not only of great fundamental relevance in themselves, but also hold promise for quantum computing and quantum information.

Xu, along with Distinguished Professor of Physics Laurent Bellaiche and colleagues in China and Japan, used computational models to predict a Kitaev quantum spin liquid state in materials such as chromium iodide and chromium germanium telluride. The work, which was supported by grants from the Arkansas Research Alliance and the Department of Energy, will give researchers many more materials to study in a search to prove the existence of quantum spin liquids, said Xu.


Bibliography:

Changsong Xu, Junsheng Feng, Mitsuaki Kawamura, Youhei Yamaji, Yousra Nahas, Sergei Prokhorenko, Yang Qi, Hongjun Xiang, L. Bellaiche.

Possible Kitaev Quantum Spin Liquid State in 2D Materials with S=3/2.

Physical Review Letters, 2020; 124 (8)

DOI: 10.1103/PhysRevLett.124.087205

Monday, 6 April 2020

Tooth be told: Earless seals existed in ancient Australia


A fossilised seal tooth found on a Victorian beach could hold the key to uncovering the history and geography of earless seals that graced Australia's shores three million years ago.

This prehistoric specimen is only the second earless seal fossil ever discovered in Australia, and proves the country's local fur seals and sea lions were preceded by a group of sea mammals, known as monachines, now long extinct in Australia.

The study also highlights the current dangers of climate change to Earth's existing wildlife, with falling sea levels likely to have played a role in the extinction of these ancient seals.

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The history of this rare specimen was published today (Friday 3 April) in the Journal of Vertebrate Paleontology by a team of scientists from Monash University's School of Biological Sciences and Department of Anatomy and Developmental Biology, and Museums Victoria, led by PhD candidate James Rule.

"This tooth, roughly three million years old, tells a story similar to what occurred in South Africa and South America in the past. Earless monachine seals used to dominate southern beaches and waters, and then suddenly disappeared, with eared seals replacing them," Mr Rule said.

"Since seal fossils are rare globally, this discovery makes a vital contribution to our understanding of this iconic group of sea mammals."



An Australian citizen scientist and amateur fossil collector discovered the tooth while strolling along the beach at Portland, western Victoria.

But it wasn't until he donated the fossil to Museums Victoria many years later that it was found to have been a tooth from an extinct group of earless seals.

The research team compared the tooth to other pinnipeds -- a group that includes earless seals, fur seals, sea lions and the walrus.

They found the tooth possessed characteristics of monachines and shed light on how these seals lived and what they ate.

"This seal lived in shallow waters close to the shore, likely hunting fish and squid. As monachines cannot use their limbs to walk on land, it would have required flat, sandy beaches when it came ashore to rest," Mr Rule said.

Researchers believe drastic changes in the Earth's climate fundamentally altered Australia's environment by eliminating the beaches used by earless seals to rest.

"These changes in the past have led to the extinction of Australia's ancient earless seals," Dr David Hocking, co-author and Research Fellow in Monash University's School of Biological Sciences, said.



"Our living fur seals and sea lions will likely face similar challenges as the Earth continues to warm, with melting polar ice leading to rising sea levels.

"Over time, this may lead to the eventual loss of islands that these species currently rely upon to rest and raise their young."


Bibliography:

James P. Rule, David P. Hocking, Erich M. G. Fitzgerald.

Pliocene monachine seal (Pinnipedia: Phocidae) from Australia constrains timing of pinniped turnover in the Southern Hemisphere.

Journal of Vertebrate Paleontology, 2020; e1734015

DOI: 10.1080/02724634.2019.1734015

Sunday, 5 April 2020

Worldwide Study Unlocks Genetic Secrets of Gray Matter


The cerebral cortex is the relatively thin, folded, outer "gray matter" layer of the brain crucial for thinking, information processing, memory, and attention. Not much has been revealed about the genetic underpinnings that influence the size of the cortex's surface area and its thickness, both of which have previously been linked to various psychiatric traits, including schizophrenia, bipolar disorder, depression, attention deficit hyperactivity disorder (ADHD), and autism.

Now, for the first time, more 360 scientists from 184 different institutions -- including UNC-Chapel Hill -- have contributed to a global effort to find more than 200 regions of the genome and more than 300 specific genetic variations that affect the structure of the cerebral cortex and likely play important roles in psychiatric and neurological conditions.

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The study, published in Science, was led by co-senior authors Jason Stein, PhD, assistant professor in the Department of Genetics at the UNC School of Medicine; Sarah Medland, PhD, senior research fellow at the QIMR Berghofer Medical Research Institute in Australia; and Paul Thompson, PhD, associate director of the Mark and Mary Stevens Neuroimaging and Informatics Institute at the University of Southern California. Ten years ago, these scientists cofounded the ENIGMA Consortium, an international research network that has brought together hundreds of imaging genomics researchers to understand brain structure, function, and disease based on brain imaging and genetic data.

"This study was only possible due to a huge scientific collaboration of more than 60 sites involved in MRI scanning and genotyping participants," Stein said. "This study is the crown jewel of the ENIGMA Consortium, so far."

The researchers studied MRI scans and DNA from more than 50,000 people to identify 306 genetic variants that influence brain structure in order to shed light on how genetics contribute to differences in the cerebral cortex of individuals. Genetic variants or variations are simply the slight genetic differences that make us unique. Generally speaking, some variants contribute to differences such as hair color or blood type. Some are involved in diseases. Most of the millions of genetic variants, though, have no known significance. This is why pinpointing genetic variants associated with cortex size and structure is a big deal. Stein and colleagues consider their new genetic roadmap of the brain a sort of "Rosetta stone" that will help translate how some genes impact physical brain structure and neurological consequences for individuals.



Among the findings of the research published in Science:

  • Some genetic variants are associated with cortical folding, measured as surface area, while other genetic variants are associated with the thickness of the cortex.

  • Genes that determine surface area are related to very early development in the fetal cortex, while thickness appears to be driven by genes active in the adult cortex.

  • People at genetic risk for depression or insomnia are genetically inclined toward having lower surface area, while people with a genetic risk for Parkinson's disease tend to have higher surface area.

  • The vast scale of the project allowed the discovery of specific genes that drive brain development and aging in people worldwide.

"Most of our previous understanding of genes affecting the brain are from model systems, like mice," Stein said. "With mice, we can find genes, knock out genes, or over express genes to see how they influence the structure or function of the brain. But there are a couple of problems with this."

One problem is, quite simply, a mouse is not a human. There are many human-specific features that scientists can only study in the human brain.

"The genetic basis for a mouse is very different than the genetic basis for humans," Stein said, "especially in in the noncoding regions of the genome."

Genes contain DNA, the basic human code that, when translated into action, creates proteins that "do" things, such as help your finger muscles type or your heart beat or your liver process toxins. But only about 3 percent of the human genome codes for proteins. The vast majority of the human genome is called the noncoding genome. Much of this region is not shared between mice and humans. This noncoding genome consists of tiny molecular switches that can modulate the expression of other genes. These switches don't directly alter the function of a protein, but they can affect the amounts of a protein that is expressed. Turns out, most genetic variants associated with psychiatric disorders are found in the noncoding region of the genome.

These findings can now be a resource for scientists to help answer important questions about the genetic influences on the brain and how they relate to numerous conditions.



Aysenil Berger, PhD, director of Psychiatry Neuroimaging Research and director of the Frank Porter Graham Child Development Institute at UNC-Chapel Hill, is a co-author on the study.

The study was funded by national and international public and private funding agencies, including the National Institutes of Health, the Australian National Health and Medical Research Council, the Michael J. Fox Foundation, and the Kavli Foundation.


Bibliography:

Katrina L. Grasby et al.

The genetic architecture of the human cerebral cortex.

Science, 2020; 367 (6484): eaay6690

DOI: 10.1126/science.aay6690

Friday, 3 April 2020

Trial drug can significantly block early stages of COVID-19 in engineered human tissues


An international team led by University of British Columbia researcher Dr. Josef Penninger has found a trial drug that effectively blocks the cellular door SARS-CoV-2 uses to infect its hosts.

The findings, published today in Cell, hold promise as a treatment capable of stopping early infection of the novel coronavirus that, as of April 2, has affected more than 981,000 people and claimed the lives of 50,000 people worldwide.

The study provides new insights into key aspects of SARS-CoV-2, the virus that causes COVID-19, and its interactions on a cellular level, as well as how the virus can infect blood vessels and kidneys.

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"We are hopeful our results have implications for the development of a novel drug for the treatment of this unprecedented pandemic," says Penninger, professor in UBC's faculty of medicine, director of the Life Sciences Institute and the Canada 150 Research Chair in Functional Genetics at UBC.

"This work stems from an amazing collaboration among academic researchers and companies, including Dr. Ryan Conder's gastrointestinal group at STEMCELL Technologies in Vancouver, Nuria Montserrat in Spain, Drs. Haibo Zhang and Art Slutsky from Toronto and especially Ali Mirazimi's infectious biology team in Sweden, who have been working tirelessly day and night for weeks to better understand the pathology of this disease and to provide breakthrough therapeutic options."



ACE2 -- a protein on the surface of the cell membrane -- is now at centre-stage in this outbreak as the key receptor for the spike glycoprotein of SARS-CoV-2. In earlier work, Penninger and colleagues at the University of Toronto and the Institute of Molecular Biology in Vienna first identified ACE2, and found that in living organisms, ACE2 is the key receptor for SARS, the viral respiratory illness recognized as a global threat in 2003. His laboratory also went on to link the protein to both cardiovascular disease and lung failure.

While the COVID-19 outbreak continues to spread around the globe, the absence of a clinically proven antiviral therapy or a treatment specifically targeting the critical SARS-CoV-2 receptor ACE2 on a molecular level has meant an empty arsenal for health care providers struggling to treat severe cases of COVID-19.

"Our new study provides very much needed direct evidence that a drug -- called APN01 (human recombinant soluble angiotensin-converting enzyme 2 -- hrsACE2) -- soon to be tested in clinical trials by the European biotech company Apeiron Biologics, is useful as an antiviral therapy for COVID-19," says Dr. Art Slutsky, a scientist at the Keenan Research Centre for Biomedical Science of St. Michael's Hospital and professor at the University of Toronto who is a collaborator on the study.

In cell cultures analyzed in the current study, hrsACE2 inhibited the coronavirus load by a factor of 1,000-5,000. In engineered replicas of human blood vessel and kidneys -- organoids grown from human stem cells -- the researchers demonstrated that the virus can directly infect and duplicate itself in these tissues. This provides important information on the development of the disease and the fact that severe cases of COVID-19 present with multi-organ failure and evidence of cardiovascular damage. Clinical grade hrsACE2 also reduced the SARS-CoV-2 infection in these engineered human tissues.

"Using organoids allows us to test in a very agile way treatments that are already being used for other diseases, or that are close to being validated. In these moments in which time is short, human organoids save the time that we would spend to test a new drug in the human setting," says Núria Montserrat, ICREA professor at the Institute for Bioengineering of Catalonia in Spain.



"The virus causing COVID-19 is a close sibling to the first SARS virus," adds Penninger. "Our previous work has helped to rapidly identify ACE2 as the entry gate for SARS-CoV-2, which explains a lot about the disease. Now we know that a soluble form of ACE2 that catches the virus away, could be indeed a very rational therapy that specifically targets the gate the virus must take to infect us. There is hope for this horrible pandemic."

This research was supported in part by the Canadian federal government through emergency funding focused on accelerating the development, testing, and implementation of measures to deal with the COVID-19 outbreak.


Bibliography:

Vanessa Monteil, Hyesoo Kwon, Patricia Prado, Astrid Hagelkrüys, Reiner A. Wimmer, Martin Stahl, Alexandra Leopoldi, Elena Garreta, Carmen Hurtado Del Pozo, Felipe Prosper, J.p. Romero, Gerald Wirnsberger, Haibo Zhang, Arthur S. Slutsky, Ryan Conder, Nuria Montserrat, Ali Mirazimi, Josef M. Penninger.

Inhibition of SARS-CoV-2 infections in engineered human tissues using clinical-grade soluble human ACE2.

Submitted to Cell, 2020

DOI: 10.1016/j.cell.2020.04.004

Engineers create shape-changing, free-roaming soft robot


A new type of robot combines traditional and soft robotics, making it safe but sturdy. Once inflated, it can change shape and move without being attached to a source of energy or air.

Advances in soft robotics could someday allow robots to work alongside humans, helping them lift heavy objects or carrying them out of danger. As a step toward that future, Stanford University researchers have developed a new kind of soft robot that, by borrowing features from traditional robotics, is safe while still retaining the ability to move and change shape.

"A significant limitation of most soft robots is that they have to be attached to a bulky air compressor or plugged into a wall, which prevents them from moving," said Nathan Usevitch, a graduate student in mechanical engineering at Stanford. "So, we wondered: What if we kept the same amount of air within the robot all the time?"

From that starting point, the researchers ended up with a human-scale soft robot that can change its shape, allowing it to grab and handle objects and roll in controllable directions. Their invention is described in a paper published March 18 in Science Robotics.

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"The casual description of this robot that I give to people is Baymax from the movie Big Hero 6 mixed with Transformers. In other words, a soft, human-safe robot mixed with robots that can dramatically change their shape," said Usevitch.

A combination of many robots

The simplest version of this squishy robot is an inflated tube that runs through three small machines that pinch it into a triangle shape. One machine holds the two ends of the tube together; the other two drive along the tube, changing the overall shape of the robot by moving its corners. The researchers call it an "isoperimetric robot" because, although the shape changes dramatically, the total length of the edges -- and the amount of air inside -- remains the same.

The isoperimetric robot is a descendent of three types of robots: soft robots, truss robots and collective robots. Soft robots are lightweight and compliant, truss robots have geometric forms that can change shape and collective robots are small robots that work together, making them particularly strong in the face of single-part failures.



"We're basically manipulating a soft structure with traditional motors," said Sean Follmer, assistant professor of mechanical engineering and co-senior author of the paper. "It makes for a really interesting class of robots that combines many of the benefits of soft robots with all of the knowledge we have about more classic robots."

To make a more complex version of the robot, the researchers simply attach several triangles together. By coordinating the movements of the different motors, they can cause the robot to perform different behaviors, such as picking up a ball by engulfing it on three sides or altering the robot's center of mass to make it roll.

"A key understanding we developed was that to create motion with a large, soft pneumatic robot, you don't actually need to pump air in and out," said Elliot Hawkes, assistant professor of mechanical engineering at the University of California, Santa Barbara and co-senior author of the paper. "You can use the air you already have and just move it around with these simple motors; this method is more efficient and lets our robot move much more quickly."


From outer space to your living room

The field of soft robotics is relatively young, which means people are still figuring out the best applications for these new creations. Their safe-but-sturdy softness may make them useful in homes and workplaces, where traditional robots could cause injury. Squishy robots are also appealing as tools for disaster response.

Other exciting possibilities for the isoperimetric robot could lie off-planet. "This robot could be really useful for space exploration -- especially because it can be transported in a small package and then operates untethered after it inflates," said Zachary Hammond, a graduate student in mechanical engineering at Stanford and co-lead author of the paper, with Usevitch. "On another planet, it could use its shape-changing ability to traverse complicated environments, squeezing through tight spaces and spreading over obstacles."

For now, the researchers are experimenting with different shapes for their supple robot and considering plopping it in water to see if it can swim. They are also exploring even more new soft robot types, each with their own features and benefits.



"This research highlights the power of thinking about how to design and build robots in new ways," said Allison Okamura, professor of mechanical engineering and co-author of the paper. "The creativity of robot design is expanding with this type of system and that's something we'd really like to encourage in the robotics field."

This research was funded by the National Science Foundation and the Defense Advanced Research Projects Agency.


Bibliography:

Nathan S. Usevitch, Zachary M. Hammond, Mac Schwager, Allison M. Okamura, Elliot W. Hawkes, Sean Follmer.

An untethered isoperimetric soft robot.

Science Robotics, 2020; 5 (40): eaaz0492

DOI: 10.1126/scirobotics.aaz0492

New Nanosensors could offer early detection of lung tumors


People who are at high risk of developing lung cancer, such as heavy smokers, are routinely screened with computed tomography (CT), which can detect tumors in the lungs. However, this test has an extremely high rate of false positives, as it also picks up benign nodules in the lungs.

Researchers at Massachusetts Institute of Technology (MIT) have developed a nanoparticle-based approach that allows the early diagnosis of lung cancer through a simple urine test. The strategy detects biomarkers resulting from the interaction of peptide-coated nanoparticles with disease-associated proteases in the tumor microenvironment.

Experiments in two different mouse models of lung cancer showed that the urine test could detect tumors as small as 2.8 mm3. The researchers hope that this type of noninvasive diagnosis could reduce the number of false positives associated with an existing test method, and help to detect more tumors in the early stages of the disease.

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“If you look at the field of cancer diagnostics and therapeutics, there’s a renewed recognition of the importance of early cancer detection and prevention,” said study lead Sangeeta Bhatia, PhD, who is the John and Dorothy Wilson professor of health sciences and technology and electrical engineering and computer science, and a member of MIT’s Koch Institute for Integrative Cancer Research and the Institute for Medical Engineering and Science. “We really need new technologies that are going to give us the capability to see cancer when we can intercept it and intervene early.” Bhatia and colleagues report on development of the test in Science Translational Medicine Journal.

MIT engineers have developed nanoparticles that can be delivered to the lungs, where tumor-associated proteases cut peptides on the surface of the particles, releasing reporter molecules. Those reporters can be detected by a urine test.

Lung cancer is the most common cause of cancer-related death (25.3%) in the United States the authors wrote, and has a “dismal” five-year survival rate of 18.6%. Early detection is key, as the five-year survival rates are 6- to 13-fold higher in patients whose tumors are detected before they spread to distal sites in the body. People in the United States who are at high risk of developing lung cancer, such as heavy smokers, are routinely screened using low-dose computed tomography (LDCT), which can detect tumors in the lungs.

However, this test has an extremely high rate of false positives, as it also picks up benign nodules in the lungs. There is then a “considerable burden of complications incurred during unnecessary follow-up procedures,” the investigators stated, and the method isn’t routinely used in other countries. “As a result of these complications, screening by LDCT has not been widely adopted outside of the United States, and there is “an urgent need to develop diagnostic tests that increase the effectiveness of lung cancer screening.”

The approach taken by the MIT researchers is based on the use of what they call “activity-based sensors” that monitor for disease and intensify disease-associated signals, which can then be detected in urine. “Activity-based nanosensors leverage dysregulated protease activity to overcome the insensitivity of previous biomarker assays, amplifying disease-associated signals generated in the tumor microenvironment and providing a concentrated urine-based readout,” the team explained.



Bhatia’s lab has for several years been developing such nanoparticles that can detect cancer by interacting with proteases. These enzymes help tumor cells to escape their original locations by cutting through proteins of the extracellular matrix. To find the cancer-associated proteases Bhatia created nanoparticles coated with peptides that are targeted by the cancer-related proteases. The particles accumulate at tumor sites, where the peptides are cleaved, releasing biomarkers that can then be detected in a urine sample.

The Bhatia lab has previously developed sensors for colon and ovarian cancer, and in their new study, the researchers applied the technology to lung cancer, which kills about 150,000 people in the United States every year. They project that the test could be applied to confirm cancer in patients who have had a positive CT scan. These patients would commonly undergo a biopsy or other invasive test to search for lung cancer, but in some cases, this procedure can cause complications, so a noninvasive follow-up test could be useful to determine which patients actually need a biopsy, Bhatia said.

“The CT scan is a good tool that can see a lot of things,” she said. “The problem with it is that 95% of what it finds is not cancer, and right now you have to biopsy too many patients who test positive.”

To customize their sensors for lung cancer, the researchers analyzed data in The Cancer Genome Atlas, and identified proteases that are abundant in lung cancer. They created a panel of 14 peptide-coated nanoparticles that could interact with these enzymes.

The researchers then tested the sensors in two different genetic mouse models, “driven by either Kras/Trp53 (KP) mutations, or Eml4-Alk (EA) fusion,” that spontaneously develop lung cancer. To help prevent background noise that could come from other organs or the bloodstream, the researchers injected the particles directly into the animals’ airways. The researchers carried out their diagnostic test using the sensors at 5 weeks, 7.5 weeks, and 10.5 weeks after tumor growth began. To make the diagnoses more accurate, they used machine learning to train an algorithm to distinguish between data from mice that had tumors and from mice that did not.

Using this approach, the researchers found that they could accurately detect tumors in one of the mouse models as early as 7.5 weeks, when the tumors were only 2.8 mm3, on average. In the other strain of mice, tumors could be detected at 5 weeks. The sensors’ success rate was also comparable to or better than the success rate of CT scans performed at the same time points.

“Intrapulmonary administration of the nanosensors to a Kras- and Trp53-mutant lung adenocarcinoma mouse model confirmed the role of metalloproteases in lung cancer and enabled accurate detection of localized disease, with 100% specificity and 81% sensitivity,” they reported. “Furthermore, this approach generalized to an alternative autochthonous model of lung adenocarcinoma, where it detected cancer with 100% specificity and 95% sensitivity and was not confounded by lipopolysaccharide-driven lung inflammation.”

Importantly, the sensors could distinguish between early-stage cancer and noncancerous inflammation of the lungs, a common condition in smokers, and one of the reasons that CT scans produce so many false positives. “Activity-based nanosensors may have clinical utility as a rapid, safe, and cost-effective follow-up to LDCT, reducing the number of patients referred for invasive testing,” the authors concluded. “With further optimization and validation studies, activity-based nanosensors may one day provide an accurate, noninvasive, and radiation-free strategy for lung cancer testing.”

The authors acknowledged that their study was carried out in mouse models, which do not fully recapitulate human disease, and there were other study limitations that will need to be addressed. Clinical trials will be needed to fully validate the use of activity-based nanosensors for detecting lung cancer and distinguishing malignant from benign and extrapulmonary disease, they pointed out.



Bhatia envisions that the nanoparticle sensors could be used as a noninvasive diagnostic for people who get a positive result on a screening test, potentially eliminating the need for a biopsy. For use in humans, her team is working on a form of the particles that could be inhaled as a dry powder or through a nebulizer. Another possible application is using the sensors to monitor how well lung tumors respond to treatment, such as drugs or immunotherapies. “A great next step would be to take this into patients who have known cancer, and are being treated, to see if they’re on the right medicine,” Bhatia said.


Bibliography:

Urinary detection of lung cancer in mice via noninvasive pulmonary protease profiling

Jesse D. Kirkpatrick, Andrew D. Warren, Ava P. Soleimany, Peter M. K. Westcott1, Justin C. Voog, Carmen Martin-Alonso, Heather E. Fleming, Tuomas Tammela, Tyler Jacks and Sangeeta N. Bhatia.

Science Translational Medicine  01 Apr 2020:
Vol. 12, Issue 537, eaaw0262

DOI: 10.1126/scitranslmed.aaw0262

Thursday, 2 April 2020

Scientists identify microbe that could help degrade polyurethane-based plastics


A strain of an extremophile group of bacteria is capable of ingesting toxic organic compounds as its sole source of carbon, nitrogen and energy.

There may be a small answer to one of the biggest problems on the planet. German researchers report in the journal Frontiers in Microbiology that they have identified and characterized a strain of bacteria capable of degrading some of the chemical building blocks of polyurethane.

“The bacteria can use these compounds as a sole source of carbon, nitrogen and energy,” said Dr. Hermann J. Heipieper, a senior scientist at the Helmholtz Centre for Environmental Research-UFZ in Leipzig, Germany and co-author of the new paper. “This finding represents an important step in being able to reuse hard-to-recycle PU products.”

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In 2015, polyurethane products alone accounted for 3.5 million tons of the plastics produced in Europe. Polyurethane is used in everything from refrigerators and buildings to footwear and furniture to numerous other applications that can leverage its lightweight, insulating and flexible properties.

Unfortunately, polyurethane is difficult and energy-intensive to recycle or destroy as most of these kinds of plastics are thermosetting polymers that do not melt when heated. The waste mostly ends up in landfills where it releases a number of toxic chemicals, some of which are carcinogenic.



The use of microorganisms like bacteria and fungi to break down oil-based plastics is an ongoing area of research. However, few studies have addressed biodegradation of polyurethanes like the current paper.

The team out of Germany managed to isolate a bacterium, Pseudomonas sp. TDA1, from a site rich in brittle plastic waste that shows promise in attacking some of the chemical bonds that make up polyurethane plastics.

The researchers performed a genomic analysis to identify the degradation pathways at work. They made preliminary discoveries about the factors that help the microbe metabolize certain chemical compounds in plastic for energy. They also conducted other analyses and experiments to understand the bacterium’s capabilities.

This particular strain is part of a group of bacteria that are well-known for their tolerance of toxic organic compounds and other forms of stress, according to Dr. Christian Eberlein with the Helmholtz Centre for Environmental Research-UFZ. He is a co-author on the paper who coordinated and supervised the work.

“That trait is also named solvent-tolerance and is one form of extremophilic microorganisms,” he said.

The research is part of a European Union scientific program dubbed P4SB (From Plastic waste to Plastic value using Pseudomonas putida Synthetic Biology), which is attempting to find useful microorganisms that can bioconvert oil-based plastics into fully biodegradable ones. As the name implies, the project has focused on a bacterium known as Pseudomonas putida.

In addition to polyurethane, the P4SB consortium, which includes the Helmholtz Centre for Environmental Research-UFZ, is also testing the efficacy of microbes to degrade plastics made of polyethylene terephthalate (PET), which is widely used in plastic water bottles.

Heipieper said that the first step of any future research on Pseudomonas sp. TDA1 will be to identify the genes that code for the extracellular enzymes that are capable of breaking down certain chemical compounds in polyester-based polyurethanes. Extracellular enzymes, also called exoenzymes, are proteins secreted outside of a cell that cause a biochemical reaction.

However, there is no immediate plan to engineer these or other enzymes using synthetic biology techniques for bioplastic production. That could involve, for instance, genetically converting the bacteria into mini-factories capable of transforming oil-based chemical compounds into biodegradable ones for planet-friendly plastics.



Heipieper said more “fundamental knowledge” like the one gathered in the current study is needed before scientists can make that technological and commercial leap.

One small step at a time.


Bibliography:

María José Cárdenas Espinosa, Andrea Colina Blanco, Tabea Schmidgall, Anna Katharina Atanasoff-Kardjalieff, Uwe Kappelmeyer, Dirk Tischler, Dietmar H. Pieper, Hermann J. Heipieper, Christian Eberlein.

Toward Biorecycling: Isolation of a Soil Bacterium That Grows on a Polyurethane Oligomer and Monomer.

Frontiers in Microbiology, 2020; 11

DOI: 10.3389/fmicb.2020.00404

Wednesday, 1 April 2020

Early Mars Had Multiple Water Sources, New Study Shows

An analysis of two Martian meteorites — Northwest Africa (NWA) 7034 and Allan Hills (ALH) 84001 — shows that Mars likely received water from at least two vastly different sources early in its history; the variability implies that Mars, unlike Earth and the Moon, never had a global ocean of magma.

A close view of the surface of Mars. What lies below continues to intrigue.

“These two different sources of water in Mars’ interior might be telling us something about the kinds of objects that were available to coalesce into the inner, rocky planets,” said Dr. Jessica Barnes, a researcher at NASA’s Johnson Space Center and the Lunar and Planetary Laboratory at the University of Arizona.

“Two distinct planetesimals with vastly different water contents could have collided and never fully mixed. This context is also important for understanding the past habitability and astrobiology of Mars.”

Dr. Barnes and colleagues were able to piece together Mars’ water history by looking for clues in two isotopes of hydrogen: light hydrogen and deuterium.

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The researchers analyzed samples they knew were originated from the Martian crust: NWA 7034 (also known as the Black Beauty meteorite) and ALH 84001 meteorites.

Black Beauty was especially helpful because it’s a mashup of surface material from many different points in Mars’ history.

“This allowed us to form an idea of what Mars’ crust looked like over several billions of years,” Dr. Barnes said.

The isotopic ratios of the meteorite samples fell about midway between the value for Earth rocks and Mars’ atmosphere.

When the team’s findings were compared with previous studies, including results from NASA’s Curiosity rover, it seems that this was the case for most of Mars’ 4 billion-plus-year history.



“We thought, ok this is interesting, but also kind of weird. How do we explain this dichotomy where the Martian atmosphere is being fractionated, but the crust is basically staying the same over geological time?” Dr. Barnes said.

The scientists also grappled with trying to explain why the crust seemed so different from the Martian mantle, the rock later which lies below.

“If you try and explain this fairly constant isotopic ratio of Mars’ crust, you really can’t use the atmosphere to do that. But we know how crusts are formed. They’re formed from molten material from the interior that solidifies on the surface,” Dr. Barnes said.

“The prevailing hypothesis before we started this work was that the interior of Mars was more Earthlike and unfractionated, and so the variability in hydrogen isotope ratios within Martian samples was due to either terrestrial contamination or atmospheric implantation as it made its way off Mars.”

Illustration showing the present-day hydrogen reservoirs in and on Mars. The mass fractions (pie chart) of Martian water are based on the mass of water in the bulk crust (C), the mantle (M) and the combined inventory (A) of the atmosphere and polar ice deposits (PID). The mantle mass fraction is the combination of depleted shergottites (DS) and enriched shergottites (ES). Image credit: Barnes et al, doi: 10.1038/s41561-020-0552-y.

The idea that Mars’ interior was Earthlike in composition came from one study of a Martian meteorite thought to have originated from the mantle — the interior between the planet’s core and its surface crust.

“However, Martian meteorites basically plot all over the place, and so trying to figure out what these samples are actually telling us about water in the mantle of Mars has historically been a challenge,” Dr. Barnes said.

“The fact that our data for the crust was so different prompted us to go back through the scientific literature and scrutinize the data.”

The study authors found that two geochemically different types of Martian volcanic rocks — enriched shergottites and depleted shergottites — contain water with different hydrogen isotope ratios.

Enriched shergottites contain more deuterium than the depleted shergottites, which are more Earth-like, they found.



“It turns out that if you mix different proportions of hydrogen from these two kinds of shergottites, you can get the crustal value,” Dr. Barnes said.

“We think that the shergottites are recording the signatures of two different hydrogen — and by extension, water — reservoirs within Mars. The stark difference hints to them that more than one source might have contributed water to Mars and that Mars did not have a global magma ocean.”


Bibliography:

Multiple early-formed water reservoirs in the interior of Mars

Jessica J. Barnes, Francis M. McCubbin, Alison R. Santos, James M. D. Day, Jeremy W. Boyce, Susanne P. Schwenzer, Ulrich Ott, Ian A. Franchi, Scott Messenger, Mahesh Anand & Carl B. Agee

Nat. Geosci. (2020).

https://doi.org/10.1038/s41561-020-0552-y

Tuesday, 31 March 2020

Old human cells rejuvenated with stem cell technology


Old human cells return to a more youthful and vigorous state after being induced to briefly express a panel of proteins involved in embryonic development, according to a new study by researchers at the Stanford University School of Medicine.

The researchers also found that elderly mice regained youthful strength after their existing muscle stem cells were subjected to the rejuvenating protein treatment and transplanted back into their bodies.

The proteins, known as Yamanaka factors, are commonly used to transform an adult cell into what are known as induced pluripotent stem cells, or iPS cells. Induced pluripotent stem cells can become nearly any type of cell in the body, regardless of the cell from which they originated. They've become important in regenerative medicine and drug discovery.

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The study found that inducing old human cells in a lab dish to briefly express these proteins rewinds many of the molecular hallmarks of aging and renders the treated cells nearly indistinguishable from their younger counterparts.

"When iPS cells are made from adult cells, they become both youthful and pluripotent," said Vittorio Sebastiano, PhD, assistant professor of obstetrics and gynecology and the Woods Family Faculty Scholar in Pediatric Translational Medicine. "We've wondered for some time if it might be possible to simply rewind the aging clock without inducing pluripotency. Now we've found that, by tightly controlling the duration of the exposure to these protein factors, we can promote rejuvenation in multiple human cell types."

Sebastiano is the senior author of the study, which will be published online March 24 in Nature Communications. Former graduate student Tapash Sarkar, PhD, is the lead author of the article.

"We are very excited about these findings," said study co-author Thomas Rando, MD, PhD, professor of neurology and neurological sciences and the director of Stanford's Glenn Center for the Biology of Aging. "My colleagues and I have been pursuing the rejuvenation of tissues since our studies in the early 2000s revealed that systemic factors can make old tissues younger. In 2012, Howard Chang and I proposed the concept of using reprogramming factors to rejuvenate cells and tissues, and it is gratifying to see evidence of success with this approach." Chang, MD, PhD, is a professor of dermatology and of genetics at Stanford.



Exposure to proteins

Researchers in Sebastiano's laboratory make iPS cells from adult cells, such as those that compose skin, by repeatedly exposing them over a period of about two weeks to a panel of proteins important to early embryonic development. They do so by introducing daily, short-lived RNA messages into the adult cells. The RNA messages encode the instructions for making the Yamanaka proteins. Over time, these proteins rewind the cells' fate -- pushing them backward along the developmental timeline until they resemble the young, embryonic-like pluripotent cells from which they originated.

During this process the cells not only shed any memories of their previous identities, but they revert to a younger state. They accomplish this transformation by wiping their DNA clean of the molecular tags that not only differentiate, say, a skin cell from a heart muscle cell, but of other tags that accumulate as a cell ages.

Recently researchers have begun to wonder whether exposing the adult cells to Yamanaka proteins for days rather than weeks could trigger this youthful reversion without inducing full-on pluripotency. In fact, researchers at the Salk Institute for Biological Studies found in 2016 that briefly expressing the four Yamanaka factors in mice with a form of premature aging extended the animals' life span by about 20%. But it wasn't clear whether this approach would work in humans.

Sarkar and Sebastiano wondered whether old human cells would respond in a similar fashion, and whether the response would be limited to just a few cell types or generalizable for many tissues. They devised a way to use genetic material called messenger RNA to temporarily express six reprogramming factors -- the four Yamanaka factors plus two additional proteins -- in human skin and blood vessel cells. Messenger RNA rapidly degrades in cells, allowing the researchers to tightly control the duration of the signal.

The researchers then compared the gene-expression patterns of treated cells and control cells, both obtained from elderly adults, with those of untreated cells from younger people. They found that cells from elderly people exhibited signs of aging reversal after just four days of exposure to the reprogramming factors. Whereas untreated elderly cells expressed higher levels of genes associated with known aging pathways, treated elderly cells more closely resembled younger cells in their patterns of gene expression.



When the researchers studied the patterns of aging-associated chemical tags called methyl groups, which serve as an indicator of a cell's chronological age, they found that the treated cells appeared to be about 1½ to 3½ years younger on average than untreated cells from elderly people, with peaks of 3½ years (in skin cells) and 7½ years (in cells that line blood vessels).

Comparing hallmarks of aging

Next they compared several hallmarks of aging -- including how cells sense nutrients, metabolize compounds to create energy and dispose of cellular trash -- among cells from young people, treated cells from old people and untreated cells from old people.

"We saw a dramatic rejuvenation across all hallmarks but one in all the cell types tested," Sebastiano said. "But our last and most important experiment was done on muscle stem cells. Although they are naturally endowed with the ability to self-renew, this capacity wanes with age. We wondered, Can we also rejuvenate stem cells and have a long-term effect?"

When the researchers transplanted old mouse muscle stem cells that had been treated back into elderly mice, the animals regained the muscle strength of younger mice, they found.

Finally, the researchers isolated cells from the cartilage of people with and without osteoarthritis. They found that the temporary exposure of the osteoarthritic cells to the reprogramming factors reduced the secretion of inflammatory molecules and improved the cells' ability to divide and function.



The researchers are now optimizing the panel of reprogramming proteins needed to rejuvenate human cells and are exploring the possibility of treating cells or tissues without removing them from the body.

"Although much more work needs to be done, we are hopeful that we may one day have the opportunity to reboot entire tissues," Sebastiano said. "But first we want to make sure that this is rigorously tested in the lab and found to be safe."


Bibliography:

Tapash Jay Sarkar, Marco Quarta, Shravani Mukherjee, Alex Colville, Patrick Paine, Linda Doan, Christopher M. Tran, Constance R. Chu, Steve Horvath, Lei S. Qi, Nidhi Bhutani, Thomas A. Rando, Vittorio Sebastiano.

Transient non-integrative expression of nuclear reprogramming factors promotes multifaceted amelioration of aging in human cells. 

Nature Communications, 2020; 11 (1)

DOI: 10.1038/s41467-020-15174-3

Too much salt weakens the immune system


A diet rich in salt weakens the antibacterial immune defense

A high-salt diet is not only bad for one's blood pressure, but also for the immune system. This is the conclusion of a current study under the leadership of the University Hospital Bonn. Mice fed a high-salt diet were found to suffer from much more severe bacterial infections. Human volunteers who consumed an additional six grams of salt per day also showed pronounced immune deficiencies. This amount corresponds to the salt content of two fast food meals. The results are published in the journal "Science Translational Medicine".

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Five grams a day, no more: This is the maximum amount of salt that adults should consume according to the recommendations of the World Health Organization (WHO). It corresponds approximately to one level teaspoon. In reality, however, many Germans exceed this limit considerably: Figures from the Robert Koch Institute suggest that on average men consume ten, women more than eight grams a day.



This means that we reach for the salt shaker much more than is good for us. After all, sodium chloride, which is its chemical name, raises blood pressure and thereby increases the risk of heart attack or stroke. But not only that: "We have now been able to prove for the first time that excessive salt intake also significantly weakens an important arm of the immune system," explains Prof. Dr. Christian Kurts from the Institute of Experimental Immunology at the University of Bonn.

Graph showing the level of bacteria present in the spleen in the case of an infection with L. monocytogenes . In black for a low salt diet, and in blue for a high salt diet. Credits: Katarzyna Jobin et al. 2020


This finding is unexpected, as some studies point in the opposite direction. For example, infections with certain skin parasites in laboratory animals heal significantly faster if these consume a high-salt diet: The macrophages, which are immune cells that attack, eat and digest parasites, are particularly active in the presence of salt. Several physicians concluded from this observation that sodium chloride has a generally immune-enhancing effect.

The skin serves as a salt reservoir

"Our results show that this generalization is not accurate," emphasizes Katarzyna Jobin, lead author of the study, who has since transferred to the University of Würzburg. There are two reasons for this: Firstly, the body keeps the salt concentration in the blood and in the various organs largely constant. Otherwise important biological processes would be impaired. The only major exception is the skin: It functions as a salt reservoir of the body. This is why the additional intake of sodium chloride works so well for some skin diseases.

However, other parts of the body are not exposed to the additional salt consumed with food. Instead, it is filtered out by the kidneys and excreted in the urine. And this is where the second mechanism comes into play: The kidneys have a sodium chloride sensor that activates the salt excretion function. As an undesirable side effect, however, this sensor also causes so-called glucocorticoids to accumulate in the body. And these in turn inhibit the function of granulocytes, the most common type of immune cell in the blood.

Charts showing the levels of hormones and urea in the body for a low-salt diet (black) and a high-salt diet (blue). Credits: Katarzyna Jobin et al. 2020


Granulocytes, like macrophages, are scavenger cells. However, they do not attack parasites, but mainly bacteria. If they do not do this to a sufficient degree, infections proceed much more severely. "We were able to show this in mice with a listeria infection," explains Dr. Jobin. "We had previously put some of them on a high-salt diet. In the spleen and liver of these animals we counted 100 to 1,000 times the number of disease-causing pathogens." Listeria are bacteria that are found for instance in contaminated food and can cause fever, vomiting and sepsis. Urinary tract infections also healed much more slowly in laboratory mice fed a high-salt diet.

Sodium chloride also appears to have a negative effect on the human immune system. "We examined volunteers who consumed six grams of salt in addition to their daily intake," says Prof. Kurts. "This is roughly the amount contained in two fast food meals, i.e. two burgers and two portions of French fries." After one week, the scientists took blood from their subjects and examined the granulocytes. The immune cells coped much worse with bacteria after the test subjects had started to eat a high-salt diet.



In human volunteers, the excessive salt intake also resulted in increased glucocorticoid levels. That this inhibits the immune system is not surprising: The best-known glucocorticoid cortisone is traditionally used to suppress inflammation. "Only through investigations in an entire organism were we able to uncover the complex control circuits that lead from salt intake to this immunodeficiency," stresses Kurts. "Our work therefore also illustrates the limitations of experiments purely with cell cultures."


Bibliography:

Katarzyna Jobin, Natascha E. Stumpf, Sebastian Schwab, Melanie Eichler, Patrick Neubert, Manfred Rauh, Marek Adamowski, Olena Babyak, Daniel Hinze, Sugirthan Sivalingam, Christina K. Weisheit, Katharina Hochheiser, Susanne Schmidt, Mirjam Meissner, Natalio Garbi, Zeinab Abdullah, Ulrich Wenzel, Michael Hölzel, Jonathan Jantsch and Christian Kurts.

A high-salt diet compromises antibacterial neutrophil responses through hormonal perturbation.

Science Translational Medicine, 2020

DOI: 10.1126/scitranslmed.aay3850

Friday, 27 March 2020

As the ocean warms, marine species relocate toward the poles


Since pre-industrial times, the world's oceans have warmed by an average of one degree Celsius (1°C). Now researchers report in Current Biology on March 26th that those rising temperatures have led to widespread changes in the population sizes of marine species. The researchers found a general pattern of species having increasing numbers on their poleward sides and losses toward the equator.

"The main surprise is how pervasive the effects were," says senior author Martin Genner, an evolutionary ecologist at the University of Bristol. "We found the same trend across all groups of marine life we looked at, from plankton to marine invertebrates, and from fish to seabirds."

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The new study builds on earlier evidence for a prevailing effect of climate change on the distributions, abundance, and seasonality of marine species. Based on those findings, Genner's team reasoned that marine species should be doing well at the leading (poleward) edge of their ranges but poorly at their trailing (equatorward) side. They also realized that existing databases of global species distributions could be used to test this hypothesis.

Based on a thorough search of available data in the literature, the researchers now report on a global analysis of abundance trends for 304 widely distributed marine species over the last century. The results show that -- just as predicted -- abundance increases have been most prominent where sampling has taken place at the poleward side of species ranges, while abundance declines have been most prominent where sampling has taken place at the equatorward side of species ranges.



The findings show that large-scale changes in the abundance of species are well underway. They also suggest that marine species haven't managed to adapt to warmer conditions. The researchers therefore suggest that projected sea temperature increases of up to 1.5°C over pre-industrial levels by 2050 will continue to drive the latitudinal abundance shifts in marine species, including those of importance for coastal livelihoods.

"This matters because it means that climate change is not only leading to abundance changes, but intrinsically affecting the performance of species locally," Genner says. "We see species such as Emperor penguin becoming less abundant as water becomes too warm at their equatorward edge, and we see some fish such as European seabass thriving at their poleward edge where historically they were uncommon."

The findings show that climate change is affecting marine species in a highly consistent and non-trivial way. "While some marine life may benefit as the ocean warms, the findings point toward a future in which we will also see continued loss of marine life," Genner says.

The long-term data included in the study primarily represent the most well-studied regions of the world. The researchers say that more work is needed to understand how climate change has affected marine life in all regions of the world in greater detail.

"We aim to get a better understanding of precisely how marine climate change drives abundance shifts," Genner says. "Is this mainly related to the physiological limits of the species, or instead due to changes in the species with which they interact?"



The work was supported by the Natural Environment Research Council and the UK Government Office for Science.


Bibliography:

Reuben A. Hastings, Louise A. Rutterford, Jennifer J. Freer, Rupert A. Collins, Stephen D. Simpson, Martin J. Genner.

Climate Change Drives Poleward Increases and Equatorward Declines in Marine Species. 

Current Biology, 2020;

DOI: 10.1016/j.cub.2020.02.043

New mathematical model can more effectively track epidemics



As COVID-19 spreads worldwide, leaders are relying on mathematical models to make public health and economic decisions.

A new model developed by Princeton and Carnegie Mellon researchers improves tracking of epidemics by accounting for mutations in diseases. Now, the researchers are working to apply their model to allow leaders to evaluate the effects of countermeasures to epidemics before they deploy them.

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“We want to be able to consider interventions like quarantines, isolating people, etc., and then see how they affect an epidemic’s spread when the pathogen is mutating as it spreads,” said H. Vincent Poor, one of the researchers on this study and Princeton’s interim dean of engineering.

The models currently used to track epidemics use data from doctors and health workers to make predictions about a disease’s progression. Poor, the Michael Henry Strater University Professor of Electrical Engineering, said the model most widely used today is not designed to account for changes in the disease being tracked. This inability to account for changes in the disease can make it more difficult for leaders to counter a disease’s spread. Knowing how a mutation could affect transmission or virulence could help leaders decide when to institute isolation orders or dispatch additional resources to an area.



“In reality, these are physical things, but in this model, they are abstracted into parameters that can help us more easily understand the effects of policies and of mutations,” Poor said.

If the researchers can correctly account for measures to counter the spread of disease, they could give leaders critical insights into the best steps they could take in the face of pandemics. The researchers are building on work published March 17 in the Proceedings of the National Academy of Sciences. In that article, they describe how their model is able to track changes in epidemic spread caused by mutation of a disease organism. The researchers are now working to adapt the model to account for public health measures taken to stem an epidemic as well.

The researchers’ work stems from their examination of the movement of information through social networks, which has remarkable similarities to the spread of biological infections. Notably, the spread of information is affected by slight changes in the information itself. If something becomes slightly more exciting to recipients, for example, they might be more likely to pass it along or to pass it along to a wider group of people. By modeling such variations, one can see how changes in the message change its target audience.

“The spread of a rumor or of information through a network is very similar to the spread of a virus through a population,” Poor said. “Different pieces of information have different transmission rates. Our model allows us to consider changes to information as it spreads through the network and how those changes affect the spread.”

“Our model is agnostic with regard to the physical network of connectivity among individuals,” said Poor, an expert in the field of information theory whose work has helped establish modern cellphone networks. “The information is being abstracted into graphs of connected nodes; the nodes might be information sources or they might be potential sources of infection.”



Obtaining accurate information is extremely difficult during an ongoing pandemic when circumstances shift daily, as we have seen with the COVID-19 virus. “It’s like a wildfire. You can’t always wait until you collect data to make decisions — having a model can help fill this void,” Poor said.

 “Hopefully, this model could give leaders another tool to better understand the reasons why, for example, the COVID-19 virus is spreading so much more rapidly than predicted, and thereby help them deploy more effective and timely countermeasures,” Poor said.


Bibliography:

Rashad Eletreby, Yong Zhuang, Kathleen M. Carley, Osman Yağan, H. Vincent Poor.

The effects of evolutionary adaptations on spreading processes in complex networks. 

Proceedings of the National Academy of Sciences, 2020; 117 (11): 5664

DOI: 10.1073/pnas.1918529117

Tuesday, 24 March 2020

Ancestor of all animals identified in Australian fossils


A team led by UC Riverside geologists has discovered the first ancestor on the family tree that contains most familiar animals today, including humans.

The tiny, wormlike creature, named Ikaria wariootia, is the earliest bilaterian, or organism with a front and back, two symmetrical sides, and openings at either end connected by a gut. The paper is published today in Proceedings of the National Academy of Sciences.

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The earliest multicellular organisms, such as sponges and algal mats, had variable shapes. Collectively known as the Ediacaran Biota, this group contains the oldest fossils of complex, multicellular organisms. However, most of these are not directly related to animals around today, including lily pad-shaped creatures known as Dickinsonia that lack basic features of most animals, such as a mouth or gut.

The development of bilateral symmetry was a critical step in the evolution of animal life, giving organisms the ability to move purposefully and a common, yet successful way to organize their bodies. A multitude of animals, from worms to insects to dinosaurs to humans, are organized around this same basic bilaterian body plan.



Evolutionary biologists studying the genetics of modern animals predicted the oldest ancestor of all bilaterians would have been simple and small, with rudimentary sensory organs. Preserving and identifying the fossilized remains of such an animal was thought to be difficult, if not impossible.

For 15 years, scientists agreed that fossilized burrows found in 555 million-year-old Ediacaran Period deposits in Nilpena, South Australia, were made by bilaterians. But there was no sign of the creature that made the burrows, leaving scientists with nothing but speculation.

Scott Evans, a recent doctoral graduate from UC Riverside; and Mary Droser, a professor of geology, noticed miniscule, oval impressions near some of these burrows. With funding from a NASA exobiology grant, they used a three-dimensional laser scanner that revealed the regular, consistent shape of a cylindrical body with a distinct head and tail and faintly grooved musculature. The animal ranged between 2-7 millimeters long and about 1-2.5 millimeters wide, with the largest the size and shape of a grain of rice -- just the right size to have made the burrows.

"We thought these animals should have existed during this interval, but always understood they would be difficult to recognize," Evans said. "Once we had the 3D scans, we knew that we had made an important discovery."

A 3D laser scan of an Ikaria wariootia impression. (Droser Lab/UCR)


The researchers, who include Ian Hughes of UC San Diego and James Gehling of the South Australia Museum, describe Ikaria wariootia, named to acknowledge the original custodians of the land. The genus name comes from Ikara, which means "meeting place" in the Adnyamathanha language. It's the Adnyamathanha name for a grouping of mountains known in English as Wilpena Pound. The species name comes from Warioota Creek, which runs from the Flinders Ranges to Nilpena Station.

"Burrows of Ikaria occur lower than anything else. It's the oldest fossil we get with this type of complexity," Droser said. "Dickinsonia and other big things were probably evolutionary dead ends. We knew that we also had lots of little things and thought these might have been the early bilaterians that we were looking for."

In spite of its relatively simple shape, Ikaria was complex compared to other fossils from this period. It burrowed in thin layers of well-oxygenated sand on the ocean floor in search of organic matter, indicating rudimentary sensory abilities. The depth and curvature of Ikaria represent clearly distinct front and rear ends, supporting the directed movement found in the burrows.



The burrows also preserve crosswise, "V"-shaped ridges, suggesting Ikaria moved by contracting muscles across its body like a worm, known as peristaltic locomotion. Evidence of sediment displacement in the burrows and signs the organism fed on buried organic matter reveal Ikaria probably had a mouth, anus, and gut.

"This is what evolutionary biologists predicted," Droser said. "It's really exciting that what we have found lines up so neatly with their prediction."


Bibliography:

Scott D. Evans, Ian V. Hughes, James G. Gehling, and Mary L. Droser.

Discovery of the oldest bilaterian from the Ediacaran of South Australia.

PNAS, March 23, 2020

DOI: 10.1073/pnas.2001045117

Monday, 23 March 2020

Some Blood Types May Be Slightly More Susceptible to COVID-19, Paper Suggests


As governments take increasingly stringent containment measures to stop the spread of the coronavirus, researchers are still trying to better understand the dynamics of the latter. Recently, a team of Chinese immunologists suggested that not all blood groups were equal in the face of the virus. Indeed, type A would be more likely to contract the infection, while group O would be less. While these results are interesting for a better understanding of SARS-CoV-2, they have not yet been the subject of a peer-review procedure and should therefore be taken with caution.

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The study was undertaken by Chinese researchers and focused on 2,173 patients with COVID-19 from three hospitals in Wuhan and Shenzhen. The team looked at the distribution of blood types in the normal population in each area, and then compared it to their sample of patients with the virus, again in each area.

"Meta-analyses on the pooled data showed that blood group A had a significantly higher risk for COVID-19 compared with non-A blood groups," the researchers write in their paper. "Whereas blood group O had a significantly lower risk for the infectious disease compared with non-O blood groups."



Blood groups potentially affected differently by SARS-CoV-2 coronavirus

But the paper also clearly states that although the results were significant, it's not an all-or-nothing result.

As per the study, the normal population in Wuhan has a blood type distribution of 31 percent type A, 24 percent type B, 9 percent type AB, and 34 percent type O. Those with the virus, by comparison, were distributed as follows: 38 percent type A, 26 percent type B, 10 percent type AB, and 25 percent type O. Similar differences were observed in Shenzhen.

The different blood groups and their antigenic structure. Credits: Maxicours

As you can see, the percentages between the normal population and those with the virus have some differences - but it doesn't mean that people with type O blood type are immune; and not everyone who gets the virus is going to be type A. Far from it.

So, these relatively small differences, if replicated in studies with larger data pools, could lead to slight changes in the way we manage the spread of the disease; but even so, it probably won't change anything about the way we individually should be trying to limit the spread of the virus.

So, that's the low-down on the study. But this raises another fascinating topic - how our blood types can change the way we are affected by certain viruses is interesting in itself.

Norovirus is a stomach flu, and people will usually be infected through the digestive system. Those antigens on our blood cells are also on the surface of cells that line the intestine, and norovirus requires certain antigens to latch on to.

"This difference in susceptibility [to norovirus] has an interesting consequence," microbiologist Patricia Foster writes for The Conversation. "When an outbreak occurs, for example, on a cruise ship, roughly a third of the people may escape infection.

"Because they do not know the underlying reason for their resistance, I think spared people engage in magical thinking – for example, 'I didn't get sick because I drank a lot of grape juice'. Of course, these mythical evasive techniques will not work if the next outbreak is a strain to which the individual is susceptible."

So, how might the new coronavirus exploit our different blood types? At this point, we simply don't know.

The authors of the blood group paper uploaded to medRxiv aren't sure, but they suggest that maybe it has to do with the anti-A antibodies that both type B and type O have. That's just a hypothesis for now, and until we find out more, don't take it as gospel.



But it is a great example of how we are learning new information about the virus every single day. There's currently a vaccine being trialled in humans; many are doing everything they can to flatten the curve; and while the pandemic is stopping the world in its tracks, communities are swapping supplies and helping those in need.


Bibliography:

Relationship between the ABO Blood Group and the COVID-19 Susceptibility

Jiao Zhao, Yan Yang, Han-Ping Huang, Dong Li, Dong-Feng Gu, Xiang-Feng Lu, Zheng Zhang, Lei Liu, Ting Liu, Yu-Kun Liu, Yun-Jiao He, Bin Sun, Mei-Lan Wei, Guang-Yu Yang, Xinghuan Wang, Li Zhang, Xiao-Yang Zhou, Ming-Zhao Xing, Peng George Wang

doi: https://doi.org/10.1101/2020.03.11.20031096

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