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2015-05-01

Engineering a better solar cell: Defects in popular perovskites pinpointed -- ScienceDaily

These superefficient crystal structures have taken the scientific community by storm in the past few years because they can be processed very inexpensively and can be used in applications ranging from solar cells to light-emitting diodes (LEDs) found in phones and computer monitors.

A new study published online April 30 in the journal Science by University of Washington and University of Oxford researchers demonstrates that perovskite materials, generally believed to be uniform in composition, actually contain flaws that can be engineered to improve solar devices even further.

"Perovskites are the fastest-growing class of photovoltaic material over the past four years," said lead author Dane deQuilettes, a UW doctoral student working with David Ginger, professor of chemistry and associate director of the UW's Clean Energy Institute.

"In that short amount of time, the ability of these materials to convert sunlight directly into electricity is approaching that of today's silicon-based solar cells, rivaling technology that took 50 years to develop," deQuilettes said. "But we also suspect there is room for improvement."

The research team used high-powered imaging techniques to find defects in the perovskite films that limit the movement of charges and, therefore, limit the efficiency of the devices. Perovskite solar cells have so far have achieved efficiencies of roughly 20 percent, compared to about 25 percent for silicon-based solar cells.

In a collaboration made possible by the Clean Energy Institute, the team used a technique called confocal optical microscopy, which is more often used in biology, and applied it to semiconductor technology. They used fluorescent images and correlated them with electron microscopy images to find "dark" or poorly performing regions of the perovskite material at intersections of the crystals. In addition, they discovered that they could "turn on" some of the dark areas by using a simple chemical treatment.

The images offered several surprises but also will lead to accelerated improvements in the materials' uniformity, stability and efficiency, according to corresponding author Ginger, the Alvin L. and Verla R. Kwiram Endowed Professor of Chemistry and Washington Research Foundation Distinguished Scholar.

"Surprisingly, this result shows that even what are being called good, or highly-efficient perovskite films today still are 'bad' compared to what they could be. This provides a clear target for future researchers seeking to improve and grow the materials," Ginger said.

The imaging technique developed by the UW team also offers an easy way to identify previously undiscovered flaws in perovskite materials and to pinpoint areas where their composition can be chemically altered to boost performance, Ginger said.

deQuilettes, who spearheaded the project as a Clean Energy Institute graduate fellow, estimates there are more than a thousand laboratories around the world currently researching the semiconducting properties of perovskite materials. Yet there is more work to be done to understand how to consistently make a material that is stable, has uniform brightness and can stand up to moisture without degrading. The UW research offers new ways for people to think strategically about how to improve the materials and how to extend their applications to high performance light-emitting devices such as LEDs and lasers.

"There are so many of us focusing on perovskites, so hopefully this technique will offer some new direction and steer us toward the places we can look to optimize their energy-capturing and emitting potential," deQuilettes said.

Co-authors of the study are Sarah M. Vorpahl, Hirokazu Nagaoka and Mark E. Ziffer of the UW and Samuel D. Stranks, Giles E. Eperon and Henry J. Snaith at Oxford.

Funding for the research was provided by the state of Washington through the UW Clean Energy Institute.

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Pesticides alter bees' brains, making them unable to live and reproduce adequately -- ScienceDaily

To make their discovery, Connolly and colleagues fed bees a sugar solution with very low neonicotinoid pesticide levels typically found in flowers (2.5 parts per billion) and tracked the toxins to the bee brain. They found that pesticide levels in the bees' brains were sufficient to cause the learning cells to run out of energy. Additionally, the brain cells were even vulnerable to this effect at just one tenth of the level present. When the ability of the bee's brain to learn is limited, the bee is unable to master key skills such as recognizing the presence of nectar and pollen from the smell emitted from flowers. In addition, scientists fed bumblebee colonies this same very low level of pesticide in a remote site in the Scottish Highlands where they were unlikely to be exposed to any other pesticides. They found that just a few of the exposed colonies performed well, colonies were smaller, and nests were in poor condition with fungus taking over. This further suggests that bumblebees exposed to this type of pesticide become poor learners, become unable to properly gather food, and become unable to properly nurture the next generation of bees.

"It is ironic that neonicotinoids, pesticides developed to preserve the health of plants, ultimately inflict tremendous damage on plant life," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "These chemicals destroy the insect communities required by plants for their own reproduction."

"Our study shows that the neonicotinoid pesticides are a risk to our bees and we should stop using them on plants that bees visit," said Christopher N. Connolly, Ph.D., a researcher involved in the work from the Medical Research Institute at the Ninewells Medical School at the University of Dundee in Dundee, UK. "Neonicotinoids are just a few examples of hundreds of pesticides we use on our crops and in our gardens. Stop using all pesticides in your garden and see insect damage as a success. You are providing for your native wildlife. Nasty caterpillars grow into beautiful butterflies."

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New tool can switch behavior -- such as voracious eating -- 'on' and 'off' -- ScienceDaily

When this complex signaling system goes awry, the results can lead to a plethora of diseases, including schizophrenia, depression, Alzheimer's Disease, Parkinson's Disease, eating disorders, and epilepsy. Cell surface receptors also play roles in cancers, diabetes, digestive conditions, and other diseases. This new technique could be modified to study them, as well.

This is the first technology to stem from the initial set of NIH BRAIN Initiative grants to create new cutting-edge research tools to improve our understanding of the brain.

"This new chemogenetic tool will show us how brain circuits can be more effectively targeted to treat human disease, " said Bryan L. Roth, MD, PhD, the Michael Hooker Distinguished Professor of Protein Therapeutics and Translational Proteomics at the UNC School of Medicine. "The problem facing medical science is that although most approved drugs target these brain receptors, it remains unclear how to selectively modulate specific kinds of receptors to effectively treat disease."

Roth addressed this problem by inventing a technology he dubbed "DREADDs" -- Designer Receptor Exclusively Activated by a Designer Drug.

The first-generation DREADD technology was developed in 2007.

Essentially, in lab experiments, Roth's team altered the chemical structure of G protein-coupled receptors so that the receptors expressed synthetic proteins when reintroduced into a mouse. This way, the mutated receptor could only be activated or inhibited by a specific synthesized drug-like compound. The receptor became like a lock; the synthetic drug became the only key that fit the lock. Depending on what Roth's team wanted to study, they could lock or unlock the specific brain circuits and behaviors associated with that one receptor.

This DREADD technology -- also known as chemogenetics -- is now used by hundreds of labs worldwide. It helped revolutionize our understanding of how brain circuits control normal and abnormal behavior, emotions, perception, pain sensation, memory, and many other processes. DREADDs have been used to improve the function of insulin-producing cells in mice as a way of treating diabetes. DREADD technology has also helped scientists treat epileptic seizures in mice.

But scientists could use this first DREADD to only manipulate a single receptor in one direction -- excite the receptor or inhibit it.

Last year, Roth and UNC colleagues Thomas Kash, PhD, and Jian Jin, PhD, received a $2.84-million NIH BRAIN Initiative grant to develop the next generation of DREADDs.

Today in the journal Neuron, UNC and NIH researchers revealed the first fruit of that grant -- a new chemogenetic technology they have named KORD (k-opioid receptor DREADD). This new tool, co-invented by Roth and Eyal Vardy, PhD, a former UNC postdoctoral fellow, can target two different kinds of receptors on the same neuron sequentially. This allowed them to study the function of two kinds of receptors as they relate to each other.

In the Neuron paper, Roth's team explain how they modified the receptors in the lab, packaged the receptors in an viral vector, and injected them into mice so that the synthetic receptors were expressed only in certain kinds of neurons in specific parts of the brain.

Then they administered the synthetic drug-like compound to demonstrate how neuronal signaling could be manipulated to turn the same neurons 'on' and 'off' and thereby turning 'on' and 'off' specific behaviors in mice.

In one type of experiment, the NIH lab of Michael Krashes, PhD, was able to turn 'on' and 'off' voracious feeding behavior in mice. In another type of experiment, UNC researchers were able to turn 'on' and 'off' behaviors similar to those induced by drugs such as cocaine and amphetamines.

Elliot Robinson, an MD/PhD student at UNC and co-first author of the Neuron paper, said, "These experiments have validated KORD as a new tool for researchers interested in controlling the function of specific populations of cells while also highlighting their therapeutic potential."

Reid Johnson, UNC graduate student and paper co-author, said, "Using genetically modified mice, we can now tease apart the interactions between seemingly disparate neuronal systems in a logical fashion."

Roth added, "We are now sharing KORD and other DREADD technology freely with other scientists, and it is likely that new uses for these technologies will appear in the near future."

Vardy, co-first author of the Neuron paper, is now a senior scientist at Merck Pharmaceuticals. Robinson conducted his experiments while in the lab of CJ Malanga, PhD, associate professor of neurology at the UNC School of Medicine and paper co-author. Johnson is part of the lab headed by Juan Song, assistant professor of pharmacology at UNC and paper co-author. Thomas Kash was also an author on this paper.

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Light -- not pain-killing drugs -- used to activate brain's opioid receptors -- ScienceDaily

In a test tube, the scientists melded the light-sensing protein rhodopsin to key parts of opioid receptors to activate receptor pathways using light. They also influenced the behavior of mice by injecting the receptors into the brain, using light instead of drugs to stimulate a reward response.

Their findings are published online April 30 in the journal Neuron.

The eventual hope is to develop ways to use light to relieve pain, a line of discovery that also could lead to better pain-killing drugs with fewer side effects.

"It's conceivable that with much more research we could develop ways to use light to relieve pain without a patient needing to take a pain-killing drug with side effects," said first author Edward R. Siuda, a graduate student in the laboratory of Michael R. Bruchas, PhD, an assistant professor of anesthesiology and of neurobiology.

But before that's possible, the researchers are attempting to learn the most effective ways to activate and deactivate the opioid receptor's pathways in brain cells. Bruchas, the study's principal investigator, explained that working with light rather than pain-killing drugs makes it much easier to understand how the receptors function within the complex array of cells and circuits in the brain and spinal cord.

"It's been difficult to determine exactly how opioid receptors work because they have multiple functions in the body," Bruchas explained. "These receptors interact with pain-killing drugs called opiates, but they also are involved in breathing, are found in the gastrointestinal tract and play a role in the reward response."

So the researchers sought a way to limit opioid receptors to performing a single task at a time, and it turned out to be almost as easy as flipping on a light switch, according to Bruchas, Siuda and their collaborators, including co-first author Bryan A. Copits, PhD, a postdoctoral research scholar in the laboratory of Robert W. Gereau, IV, PhD, the Dr. Seymour and Rose T. Brown Professor of Anesthesiology.

By combining the rhodopsin protein, which senses light in the eye's retina, with a specific type of opioid receptor called a Mu opioid receptor, the researchers were able to build a receptor that responds to light in exactly the same way that standard opioid receptors respond to pain-killing drugs.

When an opioid receptor is exposed to a pain-killing drug, it initiates activity in specific chemical pathways in the brain and spinal cord. And when the researchers shone light on the receptors that contained rhodopsin, the same cellular pathways were activated.

In a test tube and in cells, Siuda exposed the receptors to light and then watched as they released the same chemicals that standard opioid receptors release. Then, in mice, the researchers implanted a light-emitting diode (LED) device the size of a human hair into a brain region linked to the reward response. They injected the light-sensing receptors they had genetically manufactured into the same brain region. Neurons in that part of the brain release chemicals such as dopamine that create feelings of euphoria.

In decades of past opioid studies, researchers have observed mice and rats to press a lever to receive a dose of morphine, for example. The morphine would activate opioid receptors and the release of dopamine, and the animals would enjoy the response and press the lever again to continue feeling that reward sensation. This is one of the reasons opiates are so often abused in patients being treated for pain -- people like the way the drugs make them feel as much as the pain relief they provide -- and rates of abuse have skyrocketed over the past ten years.

Working to deliver a similar reward sensation using light, the researchers put the mice into an enclosed chamber. In one part of the chamber, the lighted laser fiber-optic device stimulated the release of dopamine in the brain. When the animals left that part of the chamber, the light in the brain turned off. Soon after, the mice returned to the part of the chamber that activated the fiber-optic device so that the brain could receive more light stimulation.

"By activating the receptors with light, we are presumably causing the brain to release more dopamine," Bruchas explained. "Rather than a drug such as morphine activating an opioid receptor, the light provides the reward."

The researchers were able to vary the animals' response depending on the amount and type of light emitted by the LED. Different colors of light, longer and shorter exposure to light, and whether the light pulsed or was constant all produced slightly different effects.

When a person takes an opioid drug such as Vicodin or OxyContin to relieve pain, such drugs interact with receptors in the brain to blunt pain sensations. But over time, patients develop tolerance and sometimes addiction. Opioids also can dramatically slow a person's breathing, too, and typically cause constipation.

In theory, receptors tuned to light may not present the same danger. Siuda said it someday may be possible to activate, or deactivate, nerve cells without affecting any of the other receptors that pain-killing drugs trigger, although achieving that goal will be difficult.

Bruchas' team is planning future studies that will use these receptors to test ways to control the brain cells that mediate pain and reward behavior with light rather than drugs.

The research was supported by a EUREKA award from the National Institute on Drug Abuse, the National Institute of Mental Health and the National Institute of General Medical Sciences of the National Institutes of Health (NIH); grant numbers R01 DA037152, F31 MH101956, K99 DA038725, TR32 GM108539 and NSTR01 NS081707. Additional funding from a W.M. Keck Fellowship in Molecular Medicine; and the Howard Hughes Medical Institute.

Siuda ER, Copits BA, Schmidt MJ, Baird MA, Al-Hasani R, Planer WJ, Funderburk SC, McCall JG, Gereau RW, Bruchas M. Spatiotemporal control of opioid signaling and behavior. Neuron, published online April 30, 2015.

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Wild bearded capuchin monkeys really know how to crack a nut -- ScienceDaily

The monkeys are known to use stone "hammers" to crack nuts. The new study shows that the monkeys are quite careful about the amount of force delivered to those nuts. They adjust the force applied with each strike based on the condition of the nutshell, making it less likely that they'll end up smashing the tasty kernel inside.

"Wild bearded capuchin monkeys dynamically modulate their strikes based on the outcome of the preceding strike while using stone hammers to crack nuts," says Madhur Mangalam of the University of Georgia at Athens. "Until now, this level of dexterity was not suspected of any monkey."

Mangalam's graduate advisor, Dorothy Fragaszy, and her colleagues have studied nut-cracking in wild bearded capuchin monkeys since 2005, when they established the EthoCebus research project. They were especially curious how the monkeys managed to crack such hard nuts. They also wondered whether the monkeys might change their nut-cracking approach with nuts that are softer.

In the new study, the researchers videotaped 14 capuchin moneys cracking nuts. They carefully analyzed the tapes to determine the height and velocity of each and every strike. It typically takes several strikes with a stone to reach the nut inside.

And what they discovered came as quite a surprise.

"It was a 'eureka' moment when we realized that the monkeys modulated the strikes systematically according to the condition of the nut following the preceding strike," Mangalam says.

They had expected the monkeys to maintain the force of their strikes within a certain range, or possibly to increase it until the nuts cracked. It never crossed their minds that the monkeys might show such a sophisticated ability to match their action to the physical state of the nut. But that's exactly what they did.

"Our finding opens our eyes to the fact that non-human primates modulate their actions with a tool to accommodate the rapidly changing requirements of the task, which is a cognitive accomplishment," Mangalam says.

The researchers now plan to examine whether other species make adjustments in tool use on the fly. They'll also explore how this kind of dexterity influences each species' tool-use repertoire.

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Keen sense of touch allows bats to fly with breathtaking precision -- ScienceDaily

Scientists from Johns Hopkins University, as well as Columbia University and the University of Maryland, determined how the sense of touch plays a key role in powered flight. In a paper published April 30 in the journal Cell Reports, they show how sensory receptors in bat wings send information about airflow to neurons in the brain, enabling the bat to make split-second flight control adjustments.

"Until now no one had investigated the sensors on the bat's wing, which allow it to serve as more than a propeller, a flipper, an airplane wing or any simple airfoil," said Johns Hopkins neuroscientist Cynthia F. Moss, one of the senior authors and a professor in the Department of Psychological and Brain Sciences in the Krieger School of Arts and Sciences. "These findings can inform more broadly how organisms use touch to guide movement."

Moss and the team studied the big brown bat, a common species found throughout North America. Bats are the only mammals capable of true powered flight, able to reach speeds of 7 to 20 mph with the sort of aerial maneuverability humans only wish they could engineer.

The team found that the evolutionary process that allowed bats to form wings resulted in unusual tactile circuitry that not only enhances control during flight, but also allows bats to use their wings to climb, cradle their young and capture insects.

First, they discovered an array of sensory receptors in bat wings -- a significant number of which are clustered at the base of tiny hairs that cover the appendages. That placement of these touch cells, both lanceolate endings and Merkel cells, allows the bat, while flying, to sense changes in airflow as air ruffles the hairs.

When the team stimulated these hairs with brief air puffs, neurons in the bat's primary somatosensory cortex responded with precisely timed but sparse bursts of activity, suggesting this circuitry helped guide bats during fast, dynamic flight.

The team also found that the innervation of bat wings -- the distribution in and supply of nerves to the wings -- is unlike that of other mammalian forelimbs, a clue into how wings grew in bats during evolution. The researchers were surprised to discover that neurons in the wing skin connected not only to the higher parts of the spinal cord where forelimbs typically connect, but also to lower parts of the spinal cord that would normally only innervate an animal's trunk.

These findings lay the groundwork for understanding how bats use sensory information to fly with precision in the dark and catch prey midair. The information, researchers say, could eventually help people design air vehicles that better negotiate obstacles by sensing and adjusting to air turbulence.

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Brain scan reveals out-of-body illusion -- ScienceDaily

The sense of owning one's body and being located somewhere in space is so fundamental that we usually take it for granted. To the brain, however, this is an enormously complex task that requires continuous integration of information from our different senses in order to maintain an accurate sense of where the body is located with respect to the external world. Studies in rats have shown that specific regions of the brain contain GPS-like 'place cells' that signal the rat's position in the room -- a discovery that was awarded the 2014 Nobel Prize in Physiology or Medicine. To date, however, it remains unknown how the human brain shapes our perceptual experience of being a body somewhere in space, and whether the regions that have been identified in rats are involved in this process.

In a new study, published in the scientific journal Current Biology, the scientists created an out-of-body illusion in fifteen healthy participants placed inside a brain scanner. In the experiment, the participants wore head-mounted displays and viewed themselves and the brain scanner from another part of the room. From the new visual perspective, the participant observes the body of a stranger in the foreground while their physical body is visible in the background, protruding from the bore of the brain scanner. To elicit the illusion, the scientist touches the participant's body with an object in synchrony with identical touches being delivered to the stranger's body, in full view of the participant.

"In a matter of seconds, the brain merges the sensation of touch and visual input from the new perspective, resulting in the illusion of owning the stranger's body and being located in that body's position in the room, outside the participant's physical body," says Arvid Guterstam, lead author of the present study.

In the most important part of the study, the scientists used the out-of-body illusion to perceptually 'teleport' the participants between different places in the scanner room. They then employed pattern recognition techniques to analyze the brain activity and show that the perceived self-location can be decoded from activity patterns in specific areas in the temporal and parietal lobes. Furthermore, the scientists could demonstrate a systematic relationship between the information content in these patterns and the participants' perceived vividness of the illusion of being located in a specific out-of-body position.

"The sense of being a body located somewhere in space is essential for our interactions with the outside world and constitutes a fundamental aspect of human self-consciousness," says Arvid Guterstam. "Our results are important because they represent the first characterization of the brain areas that are involved in shaping the perceptual experience of the bodily self in space."

One of the brain regions from which the participants' perceived self-location could be decoded was the hippocampus -- the structure in which the Nobel Prize awarded 'place cells' have been identified.

"This finding is particularly interesting because it indicates that place cells are not only involved in navigation and memory encoding, but are also important for generating the conscious experience of one's body in space," says principal investigator Henrik Ehrsson, professor at the Department of Neuroscience.

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Scientists discover key driver of human aging: May lead to slowing or reversing aging process -- ScienceDaily

In the study, scientists at the Salk Institute and the Chinese Academy of Science found that the genetic mutations underlying Werner syndrome, a disorder that leads to premature aging and death, resulted in the deterioration of bundles of DNA known as heterochromatin.

The discovery, made possible through a combination of cutting-edge stem cell and gene-editing technologies, could lead to ways of countering age-related physiological declines by preventing or reversing damage to heterochromatin.

"Our findings show that the gene mutation that causes Werner syndrome results in the disorganization of heterochromatin, and that this disruption of normal DNA packaging is a key driver of aging," says Juan Carlos Izpisua Belmonte, a senior author on the paper. "This has implications beyond Werner syndrome, as it identifies a central mechanism of aging--heterochromatin disorganization--which has been shown to be reversible."

Werner syndrome is a genetic disorder that causes people to age more rapidly than normal. It affects around one in every 200,000 people in the United States. People with the disorder suffer age-related diseases early in life, including cataracts, type 2 diabetes, hardening of the arteries, osteoporosis and cancer, and most die in their late 40s or early 50s.

The disease is caused by a mutation to the Werner syndrome RecQ helicase-like gene, known as the WRN gene for short, which generates the WRN protein. Previous studies showed that the normal form of the protein is an enzyme that maintains the structure and integrity of a person's DNA. When the protein is mutated in Werner syndrome it disrupts the replication and repair of DNA and the expression of genes, which was thought to cause premature aging. However, it was unclear exactly how the mutated WRN protein disrupted these critical cellular processes.

In their study, the Salk scientists sought to determine precisely how the mutated WRN protein causes so much cellular mayhem. To do this, they created a cellular model of Werner syndrome by using a cutting-edge gene-editing technology to delete WRN gene in human stem cells. This stem cell model of the disease gave the scientists the unprecedented ability to study rapidly aging cells in the laboratory. The resulting cells mimicked the genetic mutation seen in actual Werner syndrome patients, so the cells began to age more rapidly than normal. On closer examination, the scientists found that the deletion of the WRN gene also led to disruptions to the structure of heterochromatin, the tightly packed DNA found in a cell's nucleus.

This bundling of DNA acts as a switchboard for controlling genes' activity and directs a cell's complex molecular machinery. On the outside of the heterochromatin bundles are chemical markers, known as epigenetic tags, which control the structure of the heterochromatin. For instance, alterations to these chemical switches can change the architecture of the heterochromatin, causing genes to be expressed or silenced.

The Salk researchers discovered that deletion of the WRN gene leads to heterochromatin disorganization, pointing to an important role for the WRN protein in maintaining heterochromatin. And, indeed, in further experiments, they showed that the protein interacts directly with molecular structures known to stabilize heterochromatin--revealing a kind of smoking gun that, for the first time, directly links mutated WRN protein to heterochromatin destabilization.

"Our study connects the dots between Werner syndrome and heterochromatin disorganization, outlining a molecular mechanism by which a genetic mutation leads to a general disruption of cellular processes by disrupting epigenetic regulation," says Izpisua Belmonte. "More broadly, it suggests that accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging. This begs the question of whether we can reverse these alterations--like remodeling an old house or car--to prevent, or even reverse, age-related declines and diseases."

Izpisua Belmonte added that more extensive studies will be needed to fully understand the role of heterochromatin disorganization in aging, including how it interacts with other cellular processes implicated in aging, such as shortening of the end of chromosomes, known as telomeres. In addition, the Izpisua Belmonte team is developing epigenetic editing technologies to reverse epigenetic alterations with a role in human aging and disease.

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'Dead zones' found in Atlantic open waters: Moving west, could lead to mass fish kills -- ScienceDaily

Dead zones are areas of the ocean depleted of oxygen. Most marine animals, like fish and crabs, cannot live within these regions, where only certain microorganisms can survive. In addition to the environmental impact, dead zones are an economic concern for commercial fishing, with very low oxygen concentrations having been linked to reduced fish yields in the Baltic Sea and other parts of the world.

"Before our study, it was thought that the open waters of the North Atlantic had minimum oxygen concentrations of about 40 micromol per litre of seawater, or about one millilitre of dissolved oxygen per litre of seawater," says lead-author Johannes Karstensen, a researcher at GEOMAR, the Helmholtz Centre for Ocean Research Kiel, in Kiel, Germany. This concentration of oxygen is low, but still allows most fish to survive. In contrast, the minimum levels of oxygen now measured are some 20 times lower than the previous minimum, making the dead zones nearly void of all oxygen and unsuitable for most marine animals.

Dead zones are most common near inhabited coastlines where rivers often carry fertilisers and other chemical nutrients into the ocean, triggering algae blooms. As the algae die, they sink to the seafloor and are decomposed by bacteria, which use up oxygen in this process. Currents in the ocean can carry these low-oxygen waters away from the coast, but a dead zone forming in the open ocean had not yet been discovered.

The newly discovered dead zones are unique in that they form within eddies, large masses of water spinning in a whirlpool pattern. "The few eddies we observed in greater detail may be thought of as rotating cylinders of 100 to 150 km in diameter and a height of several hundred metres, with the dead zone taking up the upper 100 metres or so," explains Karstensen. The area around the dead-zone eddies remains rich in oxygen.

"The fast rotation of the eddies makes it very difficult to exchange oxygen across the boundary between the rotating current and the surrounding ocean. Moreover, the circulation creates a very shallow layer -- of a few tens of meters -- on top of the swirling water that supports intense plant growth," explains Karstensen. This plant growth is similar to the algae blooms occurring in coastal areas, with bacteria in the deeper waters consuming the available oxygen as they decompose the sinking plant matter. "From our measurements, we estimated that the oxygen consumption within the eddies is some five times larger than in normal ocean conditions."

The eddies studied in the Biogeosciences article form where a current that flows along the West African coast becomes unstable. They then move slowly to the west, for many months, due to the Earth's rotation. "Depending on factors such as the [eddies'] speed of rotation and the plant growth, the initially fairly oxygenated waters get more and more depleted and the dead zones evolve within the eddies," explains Karstensen. The team reports concentrations ranging from close to no oxygen to no more than 0.3 millilitres of oxygen per litre of seawater. These values are all the more dramatic when compared to the levels of oxygen at shallow depths just outside the eddies, which can be up to 100 times higher than those within.

The researchers have been conducting observations in the region off the West African coast and around the Cape Verde Islands for the past seven years, measuring not only oxygen concentrations in the ocean but also water movements, temperature and salinity. To study the dead zones, they used several tools, including drifting floats that often got trapped within the eddies. To measure plant growth, they used satellite observations of ocean surface colour.

Their observations allowed them to measure the properties of the dead zones, as well as study their impact in the ecosystem. Zooplankton -- small animals that play an important role in marine food webs -- usually come up to the surface at night to feed on plants and hide in the deeper, dark waters during the day to escape predators. However, within the eddies, the researchers noticed that zooplankton remained at the surface, even during the day, not entering the low-oxygen environment underneath.

"Another aspect related to the ecosystem impact has a socioeconomic dimension," says Karstensen. "Given that the few dead zones we observed propagated less than 100 km north of the Cape Verde archipelago, it is not unlikely that an open-ocean dead zone will hit the islands at some point. This could cause the coast to be flooded with low-oxygen water, which may put severe stress on the coastal ecosystems and may even provoke fish kills and the die-off of other marine life."

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No Hogwarts invitation required: Invisibility cloaks move into the real-life classroom -- ScienceDaily

Real-life invisibility cloaks do exist, in a manner of speaking: researchers have engineered systems that bend light around an object, shielding it from detection. But most are very tiny and only work at very small wavelength ranges, rendering them less impressive to the average observer.

Now, a group of researchers from the Karlsruhe Institute of Technology (KIT), in Karlsruhe, Germany, has developed a portable invisibility cloak that can be taken into classrooms and used for demonstrations. It can't hide a human, but it can make small objects disappear from sight without specialized equipment.

Scientists hoping to divert light around an object to render it invisible must find a way to compensate for the increased distance the light must now travel. On a road trip, you might solve this problem by changing your speed. If you had planned to take the rutted scenic road directly over the mountain pass, but it's closed for the season, you could instead take the six-lane superhighway that goes around the mountain. The greater distance is offset by the higher speed limit.

Unfortunately, light is a bit more challenging than a station wagon. Because relativity prevents mass from traveling faster than the vacuum speed of light, there's no way to further speed up the detoured light in a vacuum or in air.

To address this challenge, the KIT team constructed their cloak from a light-scattering material. By scattering light, the material slows down the effective propagation speed of the light waves through the medium. Then the light can be sped up again to make up for the longer path length around the hidden object.

In this cloak, the object to be concealed is placed inside a hollow metal cylinder coated with acrylic paint, which diffusely reflects light. The tube is embedded within a block of polydimethylsiloxane, a commonly used organic polymer, doped with titanium dioxide nanoparticles that make it scatter light.

"Our cloak takes advantage of the much lower effective propagation speed in light-scattering media," said Robert Schittny, who led the research project. "As we seemingly slow down the light everywhere, speeding it up again in the cloak to make up for the longer path around the core is not a problem." If the average time it takes light to travel through the polydimethylsiloxane block is in just the right proportion to the average time it takes to travel through the cloak, the core will become invisible.

On the other hand, the completely solid-state cloak can be easily transported to classrooms. "It is a macroscopic cloak that you can look at with your bare eyes and hold in your hands," said Schittny. "With a reasonably strong flashlight in a not too bright room, it is very easy to demonstrate the cloaking. That means no fancy lab equipment, no microscopes, no post-processing of measurement data. The effect is just there for everyone to see."

Schittny and his colleagues hope their cloak will be used in classrooms and labs to excite and educate students about physics.

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