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Tempe, Ariz., January 10, 2020 - According to the World Wildlife Fund, there are only an estimated 1,500 Bornean elephants in the wild, with populations mostly concentrated in Sabah, Malaysian Borneo--a region that has historically experienced unprecedentedly high rates of deforestation. Due to the conversion of Bornean forests for agriculture, elephants were forced from their natural habitats into human-dominated landscapes, increasing incidences of conflicts between people and elephants, such as ivory poaching and crop raids. These conflicts have resulted in rising elephant deaths, cementing this vulnerable species' Endangered status on the IUCN Red List.

To give elephants the space they need to roam freely without coming into contact with people, conservation scientists seek to create protected wildlife corridors, areas of land that allow elephants to travel between their habitats safely. But to create these paths, scientists must first determine how much space elephants need to roam as well as the kinds of habitats they prefer -- and avoid.

In collaboration with scientists from Danau Girang Field Centre, Harvard University, and the South East Asia Rainforest Research Partnership, scientists from the Arizona State University Center for Global Discovery and Conservation Science (GDCS) led the broadest study to date that assesses how elephants utilize different landscapes in Sabah. The research study was published on January 10, 2020, in the journal Global Ecology and Conservation.

The research site was located in the Malaysian state of Sabah, an area encompassing the majority of the Bornean elephant's range within forests and tree plantations. Between 2010-2017, the team fitted the elephants with GPS collars. Data from these collars were combined with topological and LiDAR data obtained by GDCS's Global Airborne Observatory (GAO) to track how natural and anthropogenic factors such as forest quality, topology, urbanization, and connectivity between landscapes influenced the elephant's movements and behaviors.

"This study has utilized a vast array of locational and remote sensing data to provide nuanced behavioral insight for elephant populations at severe risk of decline and even extinction," noted lead author Luke Evans, a postdoctoral researcher of GDCS director, Greg Asner.

The researchers discovered that elephants actively avoided urbanized areas, such as roads and villages, and moved more quickly and directly in areas with less vegetation. "Our study showed overall active avoidance of urbanized areas by elephants despite increasing levels of human-elephant conflict throughout Sabah. This suggests that the increase in Bornean elephant mortality is not adequately explained without significant increases in incidences of active hunting and ivory poaching, as well as incidences of poisoning in agricultural landscapes," said Benoit Goossens from Cardiff University and Danau Girang Field Centre.

The researchers also found that elephants preferred to travel along ridgelines, suggesting that these pathways should feature in future protected areas such as wildlife corridors.

"Together, the airborne and field-based observations helped us to untangle how this keystone species utilizes landscapes, providing vital insight into best practices for implementing effective large-scale management plans," said author Greg Asner.

Hummingbirds are some of the most brightly-colored things in the entire world. Their feathers are iridescent-- light bounces off them like a soap bubble, resulting in shimmering hues that shift as you look at them from different angles. While other birds like ducks can have bright feathers, nothing seems to come close to hummingbirds, and scientists weren't sure why. But a new study in Evolution shows that while hummingbird feathers have the same basic makeup as other birds', the special shape of their pigment-containing structures enables them to reflect a rainbow of light.

"The big question that keeps me up at night is, why are some groups of birds more colorful than others?" says Chad Eliason, the paper's first author and a postdoctoral researcher at the Field Museum in Chicago. "You can look out your window and see drab brown birds, and then you have this glittering gem flutter to your hummingbird feeder. Why are hummingbirds so colorful? Is it the environment, is it sexual selection? Or is it something about the internal mechanisms, the physics and the way colors are produced?"

To answer these questions, Eliason and his international team of colleagues conducted the largest-ever optical study of hummingbird feathers. They examined the feathers of 35 species of hummingbirds with transmission electron microscopes and compared them with the feathers of other brightly-colored birds, like green-headed mallard ducks, to look for differences in their make-up.

All birds' feathers are made of keratin, the same material as our hair and nails, and they're structured like tiny trees, with parts resembling a trunk, branches, and leaves. The "leaves," called feather barbules, are made up of cells that contain pigment-producing organelles called melanosomes. We have melanosomes too-- they produce the dark melanin pigment that colors our hair and skin. But pigment isn't the only way to get color. The shape and arrangement of melanosomes can influence the way light bounces off them, producing bright colors.

"We call these iridescent colors 'structural colors' because they depend on the structural dimensions," says co-author Matthew Shawkey of Belgium's University of Ghent. "A good analogy would be like a soap bubble. If you just look at a little bit of soap, it's going to be colorless. But if you structure it the right way, if you spread it out really thin to form the shell of a bubble, you get those shimmering rainbow colors around the edges. It works the same way with melanosomes: with the right structure, you can turn something colorless into something really colorful."

"In mammals, the melanin isn't organized in any fancy way inside of the hairs, but in birds, you get these layers of melanosomes, and when light bounces off the different layers, we see bright colors," says Eliason.

But even among birds, hummingbird melanosomes are special. Ducks have log-shaped melanosomes without any air inside, but hummingbirds' melanosomes are pancake-shaped and contain lots of tiny air bubbles. The flattened shape and air bubbles of hummingbird melanosomes create a more complex set of surfaces. When light glints off those surfaces, it bounces off in a way that produces iridescence.

The researchers also found that the different traits that make hummingbird feathers special-- like melanosome shape and the thickness of the feather lining-- are traits that evolved separately, allowing hummingbirds to mix and match a wider variety of traits. It's kind of like how you can make more outfit combinations with three shirts and three pairs of pants than you can with three dresses. All in all, hummingbird feathers are super complex, and that's what makes them so much more colorful than other birds.

And, the authors note, this project opens the door to a greater understanding of why hummingbirds develop the specific colors that they do. "Not all hummingbird colors are shiny and structural--some species have drab plumage, and in many species, the females are less colorful than the males," notes co-author Rafael Maia, a biologist and data scientist at Instacart.

"In this paper we describe a model of how all these variations can be achieved within feathers. Now other wonderful questions appear. For example, if it is possible to display a wide variety of colors, why are many hummingbirds green? Whether this reflects historical events, predation, or female variation in preferences are still open and challenging questions," says co-author Juan Parra from Colombia's Universidad de Antioquia.

"This study sets the stage for really understanding how color patterns are developed. Now that we have a better idea of how feather structure maps to color, we can really parse out which genes are underlying those really crazy colors in birds," says Eliason.

Placing a checkmark on the to-do list is an extremely liberating feeling for many eager list lovers, especially when the task has been postponed for a long time. But what happens in our brain when we have completed a postponed task? Will it be deactivated? If so, how? A team of scientists from the Collaborative Research Centre 940 "Volition and Cognitive Control" at TU Dresden, together with two leading international experts, Julie Bugg and Michael Scullin, investigated these questions in a systematic review article.

Headed by Dr. Marcus Möschl from the Chair of General Psychology at TU Dresden, the team analysed 20 years of research on intention deactivation and so-called aftereffects of completed intentions across different research fields.

There are many everyday examples of postponed intentions: children who put off tidying up their room until later, people planning to call their best friend tomorrow rather than now, and so on. Intentions have been proven to influence our thoughts and actions until they are completed. Afterwards, they could be deactivated and removed from our mental to-do list.

"To our surprise, however, the studies we reviewed have repeatedly shown that completed intentions are sometimes not deactivated immediately, but continue to affect people. For instance, when implementing new intentions," explains Marcus Möschl.

In particular, this happens, when an action has been postponed until a certain salient event or stimulus function as a reminder. Elderly or sick people, for instance, may postpone taking medication until they receive a calendar notification on their mobile. If this alarm accidently rings again after having taken the medication, they may not only recall their intention, in drastic cases, they even might take their medication again.

However, as the studies suggest, such drastic cases of aftereffects are rather rare. "Often, intentions seem to be deactivated as soon as they are completed," continues Dr. Möschl. "However, this deactivation does not always work perfectly like switching the light on and off. In some cases, connections between a stimulus and a completed action have to be dissolved step by step until the event or stimulus no longer trigger the retrieval of the completed intention."

Now the scientists want to investigate in which situations it could be advantageous if completed intentions remain activated and whether these aftereffects play a role in learning new routines.

Engineers need to get more creative in their approach to design and additive manufacturing (AM) systems, by taking inspiration from the way humans grow and develop, say researchers at the University of Birmingham.

In a new paper, published in The International Journal of Advanced Manufacturing Technology, teams from the University's School of Engineering and Centre for Reproductive Science have proposed a design approach for AM, otherwise known as 3D printing, which opens a world of potential for the development of new materials and products.

Dr Lauren Thomas-Seale, lecturer in Engineering Design and Principle Investigator of the project, explains: "Although we refer to it as additive manufacturing, traditionally engineers learn to design parts based on a long history of subtractive manufacturing. This leads to well-acknowledged constraints in design creativity. Additive manufacturing has to break out of this inertia if it is to reach its full potential in both design and as a fundamental technique."

Dr Jackson Kirkman-Brown, Reader in Human Reproductive Biology, and co-author on the paper, says: "Whilst using biological inspiration in engineering design is commonplace, studying the growth of humans and translating this to advanced manufacturing systems offers a whole new perspective. The way in which biological systems develop from incrementally adding cells to form tissues and organs, which both grow and modulate each other to function in synergy, is the epitome of sophisticated AM."

The study outlines how growth processes of the foetus change over time i.e. the duration of pregnancy. These processes are fundamental to the development of the human. Yet, the "growth" of an AM part during manufacture, is limited to where the material is deposited or fused. Therefore time can be considered an unutilised variable in design for AM. The authors propose Temporal Design for AM as a new approach that will unleash the potential of time through the additive build, to create new materials and parts for AM.

Dr Thomas-Seale elaborates "Looking towards radically different avenues for inspiration, is required not only to create real change in the way we approach design but also represents a more holistic approach, which is important to avoid the fragmented development of the technique that ultimately mean new products face a much more difficult and costly route towards commercialisation."

NASA's Aqua satellite provided a look at the remnant clouds and storms associated with Ex-tropical Cyclone Blake as it continues to move through Western Australia and generate rainfall over desert areas. Blake's rainfall has triggered four area flood warnings in some parts of southeastern Western Australia. The remnants have dropped over 10 inches of rain in the Sandy Desert.

Slow moving ex-Tropical Cyclone Blake is continuing to track south southeast and is expected to weaken sometime on Friday.

On January 10, 2020, the Moderate Imaging Spectroradiometer or MODIS instrument that flies aboard NASA's Aqua satellite provided a visible image of Blake. The MODIS image revealed the elongated shape of the remnants that stretched from the central part of Western Australia to the southeastern corner of the region.

The Australian Government Bureau of Meteorology (ABM) in Western Australia issued several flood warnings at 10:47 a.m. WST on Friday Jan. 10. Flood Warnings were in effect for four areas. There is a Major Flood Warning for the De Grey River Catchment and a Flood Warning for the Fortescue River, Salt Lakes District Rivers, and southwestern parts the Sandy Desert Catchment.

ABM said, "Major flooding is occurring in the Nullagine River in the De Grey river catchment. Most upstream locations have now peaked with minor to moderate flooding expected to continue during Friday before flooding starts to ease throughout the area over the weekend. Heavy rainfall from ex-Tropical Cyclone Blake has resulted in in rapid river level rises, and areas of flooding throughout the De Grey river catchment. Flooding has adversely impacted road conditions particularly at floodways resulting in multiple road closures."

Rainfall totals over 24 hours in the De Grey catchment indicated 1.30 inches (33 mm) at Nullagine.

On Jan. 10, areas of flooding were occurring in the Fortescue River upstream of Roy Hill. Twenty-four hour rainfall totals recorded over Fortescue River catchment include 0.4 inches (9.4 mm) at Newman Airport and at Upper Portland. ABM expects flooding to continue in the Fortescue River catchment during Friday. Flooding could adversely affect road conditions particularly at floodways. Some roads may become impassable and some communities may become isolated.

Flooding in the southwestern parts of the Sandy Desert Catchment is expected to affect road conditions. In the 24 hours to 9 a.m. WST today, Jan. 10, rainfall totals recorded over the Sandy Desert Catchment include 10.6 inches (270 mm) at Carnegie, 5.8 inches (148 mm) at Prenit Downs and 5.6 inches (142 mm) and 2.8 inches (71 mm) at Gruyere mine Airport.

In the Salt Lakes District, ABM issued a Flood Warning for the Salt Lakes District Rivers as flooding is occurring due to heavy rainfall. ABM's forecast calls for rainfall for the next 24 hours is 0.4 to 1.2 inches (10-30 mm) in the central and southern part of the district, with the possibility of isolated totals of 2 inches (50 mm). Flooding is expected to continue in the Salt Lakes District during Friday.

Blake is continuing to track slowly south-southeast over the Salt Lakes District and is expected weaken during the day.

NASA's Aqua satellite is one in a fleet of NASA satellites that provide data for hurricane research.

Tropical cyclones/hurricanes are the most powerful weather events on Earth. NASA's expertise in space and scientific exploration contributes to essential services provided to the American people by other federal agencies, such as hurricane weather forecasting.

ITHACA, NY, January 10, 2020]] -- Nematodes are tiny, ubiquitous roundworms that infect plant roots, causing more than $100 billion in crop damage worldwide each year. New research has found that plants manipulate the worms' pheromones to repel infestations, providing insights into how farmers could fight these pests.

Led by Boyce Thompson Institute faculty member Frank Schroeder, the group studied a group of chemicals called ascarosides, which the worms produce and secrete to communicate with each other. As described in a paper published in Nature Communications on January 10, the researchers have shown that plants also "talk" to nematodes by metabolizing ascarosides and secreting the metabolites back into the soil.

"It's not only that the plant can 'sense' or 'smell' a nematode," Schroeder said. "It's that the plant learns a foreign language, and then broadcasts something in that language to spread propaganda that 'this is a bad place'. Plants mess with nematodes' communications system to drive them away."

The study built on the team's previous work showing that plants react to ascr#18 - the predominant ascaroside secreted by plant-infecting nematodes - by bolstering their own immune defenses, thereby protecting them against many types of pests and pathogens.

In those earlier studies, "We also saw that when ascr#18 was given to plants, the chemical disappears over time," according to lead author Murli Manohar, a senior research associate at BTI.

That observation, along with published literature suggesting plants could modify pest metabolites, led the team to hypothesize that "plants and nematodes interact via small molecule signaling and alter one another's messages," Schroeder said.

To probe that idea, the team treated three plant species - Arabidopsis, wheat and tomato - with ascr#18 and compared compounds found in treated and untreated plants. They identified three ascr#18 metabolites, the most abundant of which was ascr#9.

The researchers also found Arabidopsis and tomato roots secreted the three metabolites into the soil, and that a mixture of 90% ascr#9 and 10% ascr#18 added to the soil steered nematodes away from the plant's roots, thereby reducing infection.

The team hypothesized that nematodes in the soil perceive the mixture as a signal, sent by plants already infected with nematodes, to "go away" and prevent overpopulation of a single plant. Worms may have evolved to hijack plant metabolism to send this signal. Plants, in turn, may have evolved to tamper with the signal to appear as heavily infected as possible, thereby fooling would-be invaders.

"This is a dimension of their relationship that no one has seen before," said Manohar. "And plants may have similar types of chemical communication with other pests."

Although the mixture of ascr#9 and ascr#18 could serve as a crop protectant, Schroeder said there should be no detriment to using straight ascr#18 on crops, as described in the team's earlier research.

"Ascr#18 mainly primes the plant to respond more quickly and strongly to a pathogen, rather than fully inducing the defensive response itself," he said. "So there should be no cost to the plant in terms of reduced growth, yield or other problems."

The team also showed that plants metabolize ascr#18 via the peroxisomal β-oxidation pathway, a system conserved across many plant species.

"This paper uncovers an ancient interaction," Schroeder said. "All nematodes make ascarosides, and plants have had millions of years to learn how to manipulate these molecules."

He added: "Plants aren't passive green things. They are active participants in an interactive dialog with the surrounding environment, and we will continue to decipher this dialog."

Antimicrobial tolerance can promote the evolution of antimicrobial resistance even under combination drug treatments widely used and expected to prevent it from occurring, a new study finds. The results suggest the need to consider drug tolerance when designing antibiotic treatments to prevent antibiotic-resistant pathogens. The rise of antimicrobial resistance in potentially life-threatening infections is a growing concern worldwide. In the United States alone, more than 2.8 million antibiotic-resistant infections were identified in 2019, resulting in more than 35,000 deaths. To improve patient outcomes as well as to reduce the potential for the emergence of resistance, it's become common clinical practice to use combinations of antimicrobial drugs to treat the most serious and stubborn infections. Whereas antimicrobial resistance renders microbes invulnerable to the drugs designed to kill them, they can also become more tolerant of them, which is often associated with the failure of antibiotic treatments and the relapse of infections. Previous studies have demonstrated the rapid emergence of tolerance during single antibiotic treatments, which can subsequently promote the evolution of resistance. However, the effect of tolerance on the emergence of resistance when drug combinations are used remains unclear. Jiafeng Liu and colleagues closely monitored the evolutionary trajectory of life-threatening methicillin-resistant Staphylococcus aureus isolated from patients undergoing combination treatment for persistent MRSA blood infections. Liu et al. observed the rapid emergence of tolerance in microbial populations that was followed by the development of resistance, despite combination treatment. According to the authors, once tolerance was established for just one of the drugs, the benefits of using drug combinations were lost. Experiments using different classes of antibiotics produced similar results. "Although these results suggest that many benefits are lost when microbes become tolerant, additional studies assessing clinical outcomes in patients with antimicrobial-tolerant infections will be necessary to guide clinical decision making," write Andrew Berti and Elizabeth Hirsch in a related Perspective.

Researchers at Harvard Medical School and the New York State Department of Health have discovered how a common plasticizer associated with human reproductive abnormalities likely does its damage at the molecular level.

For years, scientists have linked exposure to DEHP, short for di(2-ethylhexyl) phthalate--a chemical added to many plastics to make them flexible--to increased risk of health problems, including reproductive abnormalities such as birth defects and male infertility.

Various U.S. federal and state agencies responded by passing laws limiting the percentage of DEHP and other phthalates in children's toys, food packaging, drinking water and other items, although DEHP can still be found in everyday products ranging from medical devices to rain gear to shampoo.

Meanwhile, it remains unclear what exactly DEHP does to the body and how much exposure can be considered safe.

To help answer those questions, Monica Colaiácovo, professor of genetics in the Blavatnik Institute at Harvard Medical School, and colleagues turned to Caenorhabditis elegans, worms that are a common model organism for studying human genetics and biology.

The findings, reported Jan. 9 in PLoS Genetics, show that DEHP disrupts meiosis--the type of cell division that results in eggs and sperm--in several ways, leading to defects during egg formation and very early embryonic development.

"These are completely new findings and hopefully will shed some light as to how this phthalate impacts human reproductive health," said Colaiácovo, who is senior author of the paper.

The insights could have implications for those who are pregnant or of reproductive age, for regulation of DEHP and other phthalates and for the ongoing development of "green chemicals" intended to replace phthalates.

Double trouble

Colaiácovo's lab had previously adapted a strategy in which C. elegans eggs glow green if they develop abnormal numbers of chromosomes. In people, such abnormalities cause more than 35 percent of miscarriages and 4 percent of stillbirths as well as infertility and conditions such as Down syndrome.

In 2019, Colaiácovo used the worms to quickly screen dozens of common chemicals for those that altered worm egg chromosomes and were therefore most likely to cause similar abnormalities in humans.

DEHP appeared high on the list, along with several other phthalates.

In the new study, the team discovered that DEHP causes trouble in two ways.

First, DEHP causes an excessive number of double-strand DNA breaks as the worms' "parental" genetic material recombined in their eggs. The chemical appears to do this by altering chromosome length and relaxing the normally tightly wound structure of chromatin, exposing more DNA to potential breakage.

DEHP then compounds the problem by interfering with the system that's supposed to shut down excess breakage during meiosis.

The results: breaks aren't properly repaired during meiosis, chromosomes have abnormal morphology, eggs contain the wrong number of chromosomes and embryos are less viable, the team found.

Problems persisted past meiosis and into the first round of mitotic cell division in the worm embryos. The researchers did not investigate changes beyond this stage of development.

Low dose, high impact

Analyses showed that the worms were exposed to, and metabolized, low levels of DEHP, comparable to levels that have been detected in urine samples from the general human population. The discovery concerns the researchers because it reveals that even small amounts of DEHP can disrupt meiosis.

The findings also suggest that the worms process DEHP similarly to how mammals do, bolstering their usefulness as a model, said Colaiácovo.

Notably, the effects of DEHP exposure varied from worm to worm.

"Not every worm is affected, nor affected to the same degree," said Colaiácovo. But that is a feature, not a bug, of the experiment, she said.

"Not everyone metabolizes DEHP in the same way," she explained. "The route and duration of exposure, a person's age and diet, these are just some of the factors that can result in some people being more affected by low-level exposure to a given chemical than other people."

"You need large numbers to get a complete picture of what a chemical like DEHP may be doing, and we can easily achieve that using worms," she said.

More work will be needed to determine whether the worm findings hold true for humans. In the meantime, Colaiácovo will continue to investigate how various chemicals alter reproductive biology--one piece of the puzzle of how they affect human health overall.

An international team led by Argonne has visualized the elusive, ultrafast proton transfer process following the ionization of water.

Understanding how ionizing radiation interacts with water — like in water-cooled nuclear reactors and other water-containing systems — requires glimpsing some of the fastest chemical reactions ever observed.

In a new study from a worldwide collaboration led by scientists at the U.S. Department of Energy’s (DOE) Argonne National Laboratory, Nanyang Technological University, Singapore (NTU Singapore), the German research center DESY, and conducted at SLAC National Accelerator Laboratory, researchers have witnessed for the first time the ultrafast proton transfer reaction following ionization of liquid water.

“The truly exciting thing is that we’ve witnessed the fastest chemical reaction in ionized water.” — Argonne distinguished fellow Linda Young

The proton transfer reaction is a process of great significance to a wide range of fields, including nuclear engineering, space travel and environmental remediation. The observation was made possible by the availability of ultrafast X-ray free-electron-laser pulses, and is basically unobservable by other ultrafast methods. While studying the fastest chemical reactions is interesting in its own right, this observation for water also has important practical implications.

“The truly exciting thing is that we’ve witnessed the fastest chemical reaction in ionized water, which leads to the birth of the hydroxyl radical,” said Argonne distinguished fellow Linda Young, the senior corresponding author of the study. “The hydroxyl radical is itself of considerable importance, as it can diffuse through an organism, including our bodies, and damage virtually any macromolecule including DNA, RNA, and proteins.”

By understanding the time scale for the formation of the chemically aggressive hydroxyl radical and, thereby, gaining a deeper mechanistic understanding of the radiolysis of water, it may ultimately become possible to develop strategies to suppress this key step which can lead to radiation damage.

When radiation with sufficient energy hits a water molecule, it triggers a set of virtually instantaneous reactions. First, the radiation ejects an electron, leaving a positively charged water molecule (H2O+) in its wake. H2O+ is extremely short-lived — so short-lived, in fact, that it is virtually impossible to see directly in experiments. Within a fraction of a trillionth of a second, H2O+ gives up a proton to another water molecule, creating hydronium (H3O+) and a hydroxyl (OH) radical.

Scientists had long known of this reaction, with a first sighting in the 1960s when scientists at Argonne first detected the electron ejected from water by radiolysis. However, without a sufficiently fast X-ray probe like that provided by the Linac Coherent Light Source (LCLS) at SLAC, a DOE Office of Science User Facility, researchers had no way to observe the residual positively charged ion, the other half of the reaction pair.

“Being part of this highly collaborative and world-class group was just as exciting as watching water molecules dance in slow motion following ionization,” said SLAC instrument scientist Bill Schlotter, who with Young led the conceptual design of the experiment. “The keys to capturing the water in action are the ultrashort X-ray pulses at LCLS. By adjusting the ‘color’ of these X-ray pulses, we can distinguish between the specific ions and molecules that participate.”

The “freeze-frame” technology offered by LCLS offered researchers the first opportunity to watch the time evolution of the hydroxyl radical. While according to Young, the researchers would have liked to isolate the spectroscopic signature of the H2O+ radical cation as well, its lifetime is so short that its presence was only inferred from the OH spectroscopy measurements.

The ultrafast proton transfer that creates the hydroxyl radical gives rise to a special spectroscopic signature that indicates the rise of the hydroxyl radical and is a “time stamp” for the initial creation of the H2O+. According to Young, the spectra of both species is accessible because they exist in a “water window” where liquid water does not absorb light.

“The major accomplishment here is the development of a method to watch elementary proton transfer reactions in water and to have a clean probe for the hydroxyl radical,” Young said. “No one knew the time scale of proton transfer, so now we’ve measured it. No one had a way to follow the hydroxyl radical in complex systems on ultrafast timescales, and now we have a way to do that as well.”

Understanding the formation of the hydroxyl radical could be of particular interest in aqueous environments containing salts or other minerals that might, in turn, react with ionized water or its byproducts. Such environments could include nuclear waste repositories or other places in need of environmental remediation.

The development of the theory behind the experiment was led by Robin Santra of the Center for Free-Electron Laser Science at DESY in Germany. Santra showed that through ultrafast X-ray absorption, scientists could detect the structural dynamics — both in terms of electron and nuclear motion — near the ionization and proton transfer site.

“We could show that the X-ray data actually contain information on the dynamics of the water molecules that enable the proton transfer,” said Santra, who is a lead scientist at DESY and principal investigator at the Hamburg Centre for Ultrafast Imaging, a cluster of excellence at the University of Hamburg and DESY. “In just 50 quadrillionths of a second, the surrounding water molecules literally move in on the ionized H2O+ until one of them comes close enough to grab one of its protons in a sort of handshake, turning into hydronium H3O+ and leaving behind the hydroxyl radical OH.”

This work was motivated by earlier research by Zhi-Heng Loh from NTU Singapore, the lead author and co-corresponding author for this paper.

“Since joining NTU nine years ago, I and the members of my group have been studying the ultrafast dynamics that accompany the ionization of molecules, both in the gas phase and in aqueous medium, using femtosecond laser pulses spanning the infrared to the extreme ultraviolet. Our earlier work on ionized liquid water provided a glimpse of the lifetime of the H2O+ radical cation, albeit via indirect probing in the near-infrared,” Loh said. “We realized that a definitive experiment to observe the H2O+ radical cation would require soft X-ray probing, which however, lies beyond the capability of most tabletop femtosecond light sources. So when Linda approached me after hearing my talk on ionized water at a meeting in 2016, and wanted to collaborate on an experiment at the LCLS X-ray free-electron laser, I was absolutely thrilled.”

Psoriasis is a frequent skin inflammatory disorder affecting 3% of the population. Psoriasis is characterized by hyperproliferation and defect of epidermal differentiation, leading to the scaly appearance of the skin. The psoriasis skin also presents an increase in blood vessels, leading to the redness of the skin lesions and is associated with immune infiltration.

The cross talk between immune cells, blood vessels and keratinocytes have been previously shown to be crucial for psoriasis development. However, the respective role of each of these populations in the psoriasis initiation has been a matter of debates. Vascular endothelial growth factor A (VEGFA) is the principal factor responsible for the formation of new blood vessels.

Despite the well-known role of VEGFA in promoting psoriasis, it remains unclear whether VEGFA acts only on blood vessels, which in turns mediate recruitment of inflammatory cells and defect of epidermis differentiation or whether VEGFA also acts directly on the skin epidermis to orchestrate psoriasis development.

In a study published in Science Advances, researchers lead by Pr. Cédric Blanpain, MD/PhD, WELBIO investigator and Professor at the Université libre de Bruxelles, Belgium now provide evidence that targeting VEGFA signaling in the epidermis prevents psoriasis development.

To address this key question, Benhadou and colleagues used a mouse model overexpressing VEGFA, which induces a psoriatic like disease recapitulating the hallmarks of human psoriasis. By combining VEGFA overexpression and the genetic deletion of VEGFA receptor (VEGFR1) and co-receptor (Nrp1) in the skin epidermis, the authors demonstrate that the deletion of Nrp1 or Flt1 prevents psoriasis development. "It was very surprising to find that inhibiting VEGFA signaling only in the epidermis was sufficient to completely prevent psoriasis development including immune cell infiltration and increase in blood vessel formation mediated by VEGFA overexpression" comments Dr Farida Benhadou, the first author of this study.

To assess whether inhibiting Nrp1/Vegfa interaction can be of therapeutic relevance for the treatment of psoriasis, Benhadou and colleagues administrated a therapeutic anti-Nrp1 antibody that block the interaction between Vegfa and Nrp1 to mice presenting psoriasis. Administration of Nrp1 blocking antibodies induced a rapid disappearance of psoriatic lesions. "These data demonstrate the therapeutic benefit of blocking Vegfa/Nrp1 interaction in the treatment of psoriatic disease, which may be safer for the treatment of psoriasis as compared to other therapeutic modalities that can be associated with serious side effects" comments Cédric Blanpain, the senior author of this study.

Altogether this new study demonstrates the essential role of Flt1 and Nrp1expression in the skin epidermis to mediate psoriasis development. The results of this study have important implications for the understanding of mechanisms leading to psoriasis, one of the most frequent inflammatory diseases, and for the treatment of patients with psoriasis.

Totipotent cells own the highest differentiation potential of all cells. They can only be found shortly after fertilization in an early embryonic state and are capable of producing all cell types. Pluripotent cells, also called embryonic stem cells, on the contrary have lost some of this potential as they have already further developed. In order to be able re-program their initial totipotency, it is crucial to have a broad knowledge about the differences between pluripotent and totipotent cells as the elimination of these differences might lead to totipotency. One of the possible differences, which so far has not been investigated, is whether totipotent and pluripotent cells have different metabolic needs and activities.

Adding metabolites for more potential

To find an answer to this question, the researchers in a first step compared the gene expression of pluripotent and totipotent-like cells, which are also referred to as "2-cell-like cells", in culture. They discovered differences in metabolic enzymes and regulators involved in glycolysis, TCA-cycle, electron transport and glutamine metabolism. To dig deeper into these differences, Diego Rodriguez-Terrones from the Institute of Epigenetics and Stem Cells and Götz Hartleben from the Institute for Diabetes and Cancer teamed up to be able to measure oxygen consumption in 2-cell like cells, which was thus far not possible. They found that totipotent-like cells consume different amounts of oxygen compared to pluripotent cells. In addition, they observed differences in mitochondria morphology and reactive oxygen species (ROS) levels between pluripotent and totipotent-like cells. These findings led to the hypothesis that by adding specific metabolites pluripotent cells could re-programmed in a way to induce totipotent-like cells. Indeed, after analyzing 20 different metabolites, the group successfully identified 3 metabolites which are shown for the first time to induce totipotent-like cells in culture.

"Totipotent-like cells are invaluable to gain more knowledge about cellular plasticity. With these manipulated cells, we might be able to study and recreate the molecular features of totipotency in vitro.

Also, they open up the possibility for us to study very early developmental events during mammalian embryogenesis," says Rodriguez-Terrones. "In future, totipotent-like cells could be very important for cell replacement therapies. The ability to generate them efficiently with metabolites paves the way for further research and innovation."

Multi-disciplinary collaboration fundamental for scientific success

The study joined forces and expertise of the Institute of Epigenetics and Stem Cells and the Institute for Diabetes and Cancer at Helmholt Zentrum München. The hybrid collaboration made it possible to analyze the emergence of 2-cell-like cells in culture from another perspective. The work was partly funded by the Helmholtz Association and the German Research Council (CRC 1064)

"We did not actually plan this, but that is just how science works sometimes: you start researching one thing and end up somewhere else," says ETH Professor Dimos Poulikakos. Together with scientists from his group and from the National University of Singapore, they developed and tested various superhydrophobic materials - which are, like Teflon, extremely good at repelling liquids such as water and blood. The goal was to find coatings for devices that come into contact with blood, for example heart-lung machines or artificial heart devices.

One of the materials tested demonstrated some unexpected properties: not only did it repel blood, but it also aided the clotting process. Although this made the material unsuitable for use as a coating for blood pumps and related devices, the researchers quickly realised that it would work ideally as a bandage.

Repelling blood and achieving fast clotting are two different properties are both beneficial in bandages: blood-repellent bandages do not get soaked with blood and do not adhere to the wound, so they can be later removed easily, avoiding secondary bleeding. Substances and materials that promote clotting, on the other hand, are used in medicine to stop bleeding as quickly as possible. However, to date, no materials that simultaneously repel blood and also promote clotting have been available - this is the first time that scientists have managed to combine both these properties in one material.

Antibacterial effect

The researchers took a conventional cotton gauze and coated it with their new material - a mix of silicone and carbon nanofibres. They were able to show in laboratory tests that blood in contact with the coated gauze clotted in only a few minutes. Exactly why the new material triggers blood clotting is still unclear and requires further research, but the team suspects that it is due to the interaction with the carbon nanofibres.

They were also able to show that the coated gauze has an antibacterial effect, as bacteria have trouble adhering to its surface. In addition, animal tests with rats demonstrated the effectiveness of the new bandage.

Reducing the risk of infection

"With the new superhydrophobic material, we can avoid reopening the wound when changing the bandage," explains Athanasios Milionis, a postdoctoral researcher in Poulikakos's group. "Reopening wounds is a major problem," he continues, "primarily because of the risk of infection, including from dangerous hospital germs - a risk that is especially high when changing bandages."

The potential areas of application are huge: They range from emergency medicine and surgery for avoiding major blood loss, to plasters for use in the home and on the go.

ETH Zurich and the National University of Singapore have applied for a patent for the new material. In the meantime, the researchers need to refine and optimise the material before it can be used on humans. They also say they need to conduct further testing, first on larger animals and then on humans, to prove its effectiveness and harmlessness.

An interdisciplinary team of scientists from KU Leuven, the University of Bremen, the Leibniz Institute of Materials Engineering, and the University of Ioannina has succeeded in killing tumour cells in mice using nano-sized copper compounds together with immunotherapy. After the therapy, the cancer did not return.

Recent advances in cancer therapy use one's own immunity to fight the cancer. However, in some cases, immunotherapy has proven unsuccessful. The team of biomedical researchers, physicists, and chemical engineers found that tumours are sensitive to copper oxide nanoparticles- a compound composed of copper and oxygen. Once inside a living organism, these nanoparticles dissolve and become toxic. By creating the nanoparticles using iron oxide, the researchers were able to control this process to eliminate cancer cells, while healthy cells were not affected.

"Any material that you create at a nanoscale has slightly different characteristics than its normal-sized counterpart," explain Professor Stefaan Soenen and Dr Bella B. Manshian from the Department of Imaging and Pathology, who worked together on the study. "If we would ingest metal oxides in large quantities, they can be dangerous, but at a nanoscale and at controlled, safe, concentrations, they can actually be beneficial."

As the researchers expected, the cancer returned after treating with only the nanoparticles. Therefore, they combined the nanoparticles with immunotherapy. "We noticed that the copper compounds not only could kill the tumour cells directly, they also could assist those cells in the immune system that fight foreign substances, like tumours," says Dr Manshian.

The combination of the nanoparticles and immunotherapy made the tumours disappear entirely and, as a result, works as a vaccine for lung and colon cancer - the two types that were investigated in the study. To confirm their finding, the researchers injected tumour cells back into the mice. These cells were immediately eliminated by the immune system, which was on the lookout for any new, similar, cells invading the body.

The authors state that the novel technique can be used for about sixty per cent of all cancers, given that the cancer cells stem from a mutation in the p53 gene. Examples include lung, breast, ovarian, and colon cancer.

A crucial element is that the tumours disappeared without the use of chemotherapy, which typically comes with major side-effects. Chemotherapeutic drugs not only attack cancer cells, they often damage healthy cells along the way. For example, some of these drugs wipe out white blood cells, abolishing the immune system.

"As far as I'm aware, this is the first time that metal oxides are used to efficiently fight cancer cells with long-lasting immune effects in live models," Professor Soenen says. "As a next step, we want to create other metal nanoparticles, and identify which particles affect which types of cancer. This should result in a comprehensive database."

The team also plans to test tumour cells derived from cancer patient tissue. If the results remain the same, Professor Soenen plans to set up a clinical trial. For that to happen, however, there are still some hurdles along the way. He explains: "Nanomedicine is on the rise in the USA and Asia, but Europe is lagging behind. It's a challenge to advance in this field, because doctors and engineers often speak a different language. We need more interdisciplinary collaboration, so that we can understand each other better and build upon each other's knowledge."

Researchers at the University of Basel have succeeded in developing molecular factories that mimic nature. To achieve this they loaded artificial organelles inside micrometer-sized natural blisters (vesicles) produced by cells. These molecular factories remain intact even after injection into an animal model and demonstrate no toxicity, as the team report in the scientific journal Advanced Science.

Within the cells, the actual biological factories, the molecules of life are assembled. The assembly lines of cells are small compartments called organelles, where a large variety of chemical reactions take place either inside or between them. For medical applications, molecular factories acting as artificial cells would ideally beused - to produce missing or required molecules or drugs.

Soft, synthetic capsules

Collaboration between the Department of Chemistry at the University of Basel, the Swiss Nanoscience Institute, and the NCCR Molecular Systems Engineering made the successful development of such molecular factories possible. First, researchers led by Professor Cornelia Palivan and Professor Wolfgang Meier designed artificial organelles, that is distinct compartments of cells. They loaded these soft, synthetic capsules with enzymes and equipped them with membrane proteins that act like "gates". These gates allow molecules involved in the enzymatic reaction to enter and leave the capsule.

Subsequently, the natural cells were feed with these artificial organelles. After stimulation, the cells produced natural micrometer-size vesicles. These possess a natural cell membrane and cytoplasm, enclose the artificial organelles and can therefore function as a molecular factory.

Zebra fish embryos as an animal model

The molecular factories were injected into zebra fish embryos by researchers from the group led by Professor Jörg Huwyler (Pharmazentrum of the University of Basel). In this animal model, they produced the desired compound, which was catalyzed by the enzyme in the artificial organelle. The viability of the animal was not compromised by the injection.

"This combination of natural vesicles and small synthetic organelles is what makes the molecular factory: Reactions that take place inside produce an end product, as also happens inside cells," explain Dr. Tomaz Einfalt and Dr. Martina Garni, first authors of the paper.

Within the molecular factories, multiple components can be made and assembled into the end product. The biosynthetic vesicles can also transfer components from one cell to the other. Different molecular factories can be combined so that complex structures with high functionality can be created - the first step toward producing artificial cells in the laboratory or in living organisms.

(Philadelphia, PA) - Like security screening to make sure nothing harmful makes its way into a crowded area, cells in the human body use checkpoints to control their growth and prevent harmful mutations from making their way into new cell populations and causing trouble. Every cell that divides and replicates its DNA must clear at least three checkpoints - all of which call on specialized genes known as tumor suppressors.

Tumor suppressor genes encode proteins that work with other molecules in cells to put the brakes on cell division when DNA damage or other defects are detected. This process prevents mutations that harm cells or that lead to uncontrolled cell growth and cancer from being passed along to new cells. Fortunately, tumor suppressors are fairly robust. Under normal circumstances, they stop working only when mutations affect both of the tumor suppressor gene's alleles, which are the different forms of a gene inherited from each parent.

But in the case of prostate cancer, researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) and Fox Chase Cancer Center recently discovered an important exception to this two mutation rule. Working in human cells and animal models, they found that a mutation leading to the loss of just one allele of a tumor suppressor gene known as PPP2R2A is enough to make a tumor caused by other mutations worse.

In a study published in the journal Oncogenesis, the team, led by Xavier Graña, PhD, Professor of Medical Genetics and Molecular Biochemistry, and in the Fels Institute for Cancer Research and Molecular Biology at LKSOM, found that patients whose prostate tumors carry only one copy of PPP2R2A do not survive as long as those whose tumors have two copies of the gene. They also showed that in cells deficient in PPP2R2A, reconstitution of the PP2A protein encoded by the gene ultimately kills prostate cancer cells.

The study is the first to show that reactivating PP2A in affected cells can slow or stop the advance of prostate cancer in an animal model.

"The majority of prostate tumors have only one functional copy of the PPP2R2A gene," Dr. Graña explained. "Because this alteration occurs so frequently, many patients could benefit from treatments that restore the gene's activity."

Dr. Graña's team mapped out specifically what happens when cells lose a copy of PPP2R2A, and what happens when PP2A is reconstituted. When lost, they found that cells were more likely to divide and replicate, thereby generating more cells - a process that fuels cancer progression. This occurred because cells just breezed through the so-called mitotic checkpoint, which normally ensures that a cell's chromosomes are organized properly for cell division. PP2A reactivation, on the other hand, resulted in sustained activation of the mitotic checkpoint - to the point that the cellular machinery responsible for separating replicated chromosomes for division collapsed, killing the cells.

"Restoring PP2A to normal levels in these cancer cells caused a weakening of their centrosome, which is the organizer of the cell machinery in charge of faithfully separating chromosomes," Dr. Graña explained. "The combination of a sustained checkpoint and a weakened centrosome results in collapse of the mitotic apparatus, with chromosomes not knowing where they have to go."

"Our findings indicate that prostate tumors often kick off a copy of the PPP2R2A gene to facilitate their growth and that bringing PP2A levels back to normal results in abnormal chromosome sorting and cell death."

Small molecules that activate PP2A and that have the potential to be developed into drugs have already been identified. Whether they specifically activate PP2A in prostate cancer remains unclear, however.

"More work is needed to find a specific drug for this complex, but we have a promising start," Dr. Graña added.