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Dinosaurs couldn’t stick out their tongues

Fri, 2018-06-22 16:02

Dinosaurs often appear as fierce creatures, baring their teeth, with tongues wildly stretching from their mouths. But a new study reveals a major problem with this classic image: Dinosaurs couldn’t stick out their tongues.

Instead of having tongues similar to lizards, dinosaur tongues were probably rooted to the bottoms of their mouths in a manner akin to those of alligators, researchers say.

“Tongues are often overlooked. But, they offer key insights into the lifestyles of extinct animals.”

Researchers made the discovery by comparing the hyoid bones—the bones that support and ground the tongue—of modern birds and crocodiles with those of their extinct dinosaur relatives.

Further, the findings also propose a connection on the origin of flight and an increase in tongue diversity and mobility.

“Tongues are often overlooked. But, they offer key insights into the lifestyles of extinct animals,” says Zhiheng Li, an associate professor at the Key Laboratory of Vertebrate Evolution and Human Origins of the Chinese Academy of Sciences. He conducted the work while earning his PhD at the University of Texas Jackson School of Geosciences.

Researchers compared the hyoid bones of extinct dinosaurs, pterosaurs, and alligators to the hyoid bones and muscles of modern birds and alligator specimens. Hyoid bones act as anchors for the tongue in most animals, but in birds these bones can extend to the tip.

Because extinct dinosaurs are related to crocodiles, pterosaurs, and modern birds, comparing anatomy across these groups can help scientists understand the similarities and differences in tongue anatomy and how traits evolved through time and across different lineages.

The comparison process involved taking high-resolution images of hyoid muscles and bones from 15 modern specimens, including three alligators and 13 bird species as diverse as ostriches and ducks, at the Jackson School’s High-Resolution X-Ray Computed Tomography Facility (UTCT).

The fossil specimens, most from northeastern China, were scrutinized for preservation of the delicate tongue bones and included small bird-like dinosaurs, as well as pterosaurs and a Tyrannosaurus rex.

The results, which appear in PLOS ONE, indicate that hyoid bones of most dinosaurs were like those of alligators and crocodiles—short, simple, and connected to a tongue that was not very mobile.

“If you can’t use a hand to manipulate prey, the tongue may become much more important to manipulate food.”

These findings mean that dramatic reconstructions that show dinosaurs with tongues stretching out from between their jaws are wrong, says coauthor and Jackson School professor Julia Clarke.

“They’ve been reconstructed the wrong way for a long time,” Clarke says. “In most extinct dinosaurs their tongue bones are very short. And in crocodilians with similarly short hyoid bones, the tongue is totally fixed to the floor of the mouth.”

For an earlier study on dinosaur vocalizations, Clarke found evidence that large dinosaurs might make booming or cooing sounds, similar to the sounds made by crocodiles and ostriches.

In contrast to the short hyoid bones of crocodiles, pterosaurs, bird-like dinosaurs, and living birds have a great diversity in hyoid bone shapes, researchers say.

The range of shapes could be related to flight ability, or in the case of flightless birds such as ostriches and emus, evolved from an ancestor that could fly. Taking to the skies could have led to new ways of feeding that could be tied to diversity and mobility in tongues, the researchers propose.

“Birds, in general, elaborate their tongue structure in remarkable ways,” Clarke says. “They are shocking.”

That elaboration could be related to the loss of dexterity that accompanied the transformation of hands into wings, Li says.

“If you can’t use a hand to manipulate prey, the tongue may become much more important to manipulate food. That is one of the hypotheses that we put forward.”

Dinosaurs may have mumbled with their mouths shut

The scientists note one exception linking tongue diversity to flight. Ornithischian dinosaurs—a group that includes triceratops, anklyosaurus, and other plant-eating dinosaurs that chewed their food—had hyoid bones that were highly complex and more mobile, though they were structurally different from those of flying dinosaurs and pterosaurs.

Further research on other anatomical changes that occurred with shifts in tongue function could help improve our knowledge of the evolution of birds, Clarke says. For example, changes in the tongues of living birds are associated with changes in the position of the opening of the windpipe. These changes could in turn affect how birds breathe and vocalize, she explains.

Tiny dino may have used rainbow feathers to wow mates

However, the fossil record as yet can’t pin down when these changes to the windpipe occurred, Li says. “There is more work to be done.”

The Chinese Academy of Sciences, the University of Texas at Austin, the Smithsonian Institution, and the Gordon and Betty Moore Foundation funded the work.

Source: University of Texas at Austin

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Will Trump’s executive order change things at Mexican border?

Fri, 2018-06-22 10:47

US Attorney General Jeff Sessions recently announced changes to asylum requirements, leading to thousands of asylum seekers being charged with federal crimes and imprisoned—their children detained separately.

Here, Jayashri Srikantiah, a professor of law and director of the Immigrants’ Rights Clinic at Stanford University, and Lisa Weismann-Ward, clinical supervising attorney and lecturer in law at the university, discuss the evolving policies and President Trump’s new executive order.

The post Will Trump’s executive order change things at Mexican border? appeared first on Futurity.

Tiny device forces us to rethink ‘What is a computer’?

Fri, 2018-06-22 10:21

Researchers have developed a computer device that measures just 0.3 mm to a side—dwarfed by a grain of rice.

IBM’s announcement that they had produced the world’s smallest computer back in March raised a few eyebrows at the University of Michigan, home of the previous champion of tiny computing.

“We are not sure if they should be called computers or not. It’s more of a matter of opinion whether they have the minimum functionality required…”

The reason for the curiosity is that IBM’s claim calls for a re-examination of what constitutes a computer. Previous systems, including the 2x2x4mm Michigan Micro Mote, retain their programming and data even when they are not externally powered.

Unplug a desktop computer, and its program and data are still there when it boots itself up once the power is back. These new microdevices, from IBM and now U. Michigan, lose all prior programming and data as soon as they lose power.

“We are not sure if they should be called computers or not. It’s more of a matter of opinion whether they have the minimum functionality required,” says David Blaauw, a professor of electrical and computer engineering at U. Michigan who led the development of the new system

In addition to the RAM and photovoltaics, the new computing devices have processors and wireless transmitters and receivers. Because they are too small to have conventional radio antennae, they receive and transmit data with visible light. A base station provides light for power and programming, and it receives the data.

One of the big challenges in making a computer about 1/10th the size of IBM’s was how to run at very low power when the system packaging had to be transparent. The light from the base station—and from the device’s own transmission LED—can induce currents in its tiny circuits.

“We basically had to invent new ways of approaching circuit design that would be equally low power but could also tolerate light,” Blaauw says.

For example, that meant exchanging diodes, which can act like tiny solar cells, for switched capacitors.

Another challenge was achieving high accuracy while running on low power, which makes many of the usual electrical signals (like charge, current, and voltage) noisier.

Designed as a precision temperature sensor, the new device converts temperatures into time intervals, defined with electronic pulses. The intervals are measured on-chip against a steady time interval sent by the base station and then converted into a temperature. As a result, the computer can report temperatures in minuscule regions—such as a cluster of cells—with an error of about 0.1 degrees Celsius.

The system is very flexible and could be reimagined for a variety of purposes, but the team chose precision temperature measurements because of a need in oncology. Their longstanding collaborator, Gary Luker, a professor of radiology and biomedical engineering, wants to answer questions about temperature in tumors.

Some studies suggest that tumors run hotter than normal tissue, but the data isn’t solid enough for confidence on the issue. Temperature may also help in evaluating cancer treatments.

“Since the temperature sensor is small and biocompatible, we can implant it into a mouse and cancer cells grow around it,” Luker says. “We are using this temperature sensor to investigate variations in temperature within a tumor versus normal tissue and if we can use changes in temperature to determine success or failure of therapy.”

Tiny robotic fly gets power from laser beam

Even as Luker’s experiments run, the researchers look forward to what purposes others will find for their latest microcomputing device.

“When we first made our millimeter system, we actually didn’t know exactly all the things it would be useful for. But once we published it, we started receiving dozens and dozens and dozens of inquiries,” Blaauw says.

And that device, the Michigan Micro Mote, may turn out to be the world’s smallest computer even still—depending on what the community decides are a computer’s minimum requirements.

What good is a tiny computer? Applications for the Michigan Micro Mote include:

  • Pressure sensing inside the eye for glaucoma diagnosis
  • Cancer studies
  • Oil reservoir monitoring
  • Biochemical process monitoring
  • Surveillance: audio and visual
  • Tiny snail studies

The researchers presented their study on June 21 at the 2018 Symposia on VLSI Technology and Circuits.

The work was done in collaboration with Mie Fujitsu Semiconductor Ltd. Japan and Fujitsu Electronics America Inc.

Source: University of Michigan

The post Tiny device forces us to rethink ‘What is a computer’? appeared first on Futurity.

Whirlpools are hot spots for great white sharks

Fri, 2018-06-22 09:02

Marine biologists studying the movements of adult female white sharks in the Gulf Stream and North Atlantic Ocean have discovered, to their surprise, that they prefer warm-water eddies—ocean whirlpools that spin clockwise north of the equator.

“We’ve decimated some open-ocean shark populations to a fraction of what they were 100 years ago. And yet we don’t know the basics of their biology,” says lead author Peter Gaube, a senior oceanographer at the University of Washington’s Applied Physics Laboratory.

“If we know where those sharks, or turtles, or whales might be in the open ocean, then the fisheries can avoid them, and limit their bycatch.”

Gaube investigates how ocean eddies, or whirlpools, influence the behavior of marine animals. A previous study found that loggerhead sea turtles also prefer the anticyclonic, or clockwise-spinning in the Northern Hemisphere, eddies. These features trap large amounts of water at the ocean’s surface and are most often warm, clear, and low in nutrients.

Tagged females

The new study analyzed movements of two female great white sharks tagged in September 2012 off Cape Cod and in March 2013 off Jacksonville, Florida. OCEARCH, a nonprofit group that focuses on tagging and tracking sharks, did the tricky job of tagging the animals.

In March 2013, OCEARCH caught, tagged, and released a 14.5-foot shark that was given the name Lydia. It was one of two animals that provided position data for the study. Credit: R. Snow/OCEARCH)

One shark just had a position tag, while the other had a second tag that also recorded temperature and depth. The group tracked the sharks for nearly 6 years, with one still reporting its position regularly, as they swim north with the Gulf Stream and then out into the open ocean.

Early shark-tagging projects could only offer rough ideas of where sharks were swimming, Gaube says, but since precise satellite position networks became available to the public, and with improvements in computing and batteries, the tags can now collect detailed information as sharks travel throughout the marine environment.

Coauthor Chris Fischer uses a putty knife to protect the shark’s fin while attaching the tagging. Mary Lee, tagged off Cape Cod in September 2012, was one of two sharks analyzed in the study. (Credit: R. Snow/OCEARCH)

Researchers took the data from the two sharks and compared their position in the ocean with sea-surface height data from satellites showing where the huge, swirling warm- and cold-water eddies were located at that time.

Size of Massachusetts

“These eddies are everywhere, they cover 30 percent of the ocean’s surface,” Gaube says. “It’s like what you see if you’re walking along a river, and these eddies form behind rocks, but it happens on a different scale in the ocean: Instead of being a little thing that disappears after a few seconds, they can be the size of the state of Massachusetts, and can persist for months to years. You could be in the middle of an eddy in a ship and you’d probably never know it. The water may be a little warmer, and it could be a little clearer, but otherwise you wouldn’t know.”

The satellite tags, built by Wildlife Computers in Redmond, Washington, transmit the animal’s location as soon as it surfaces. (Credit: OCEARCH)

Analysis shows that the two sharks spent significantly more time in warm-water eddies than the cold-water eddies that spin the other way. Sharks lounged the longest at about 450 meters (about a quarter of a mile) deep inside the warm-water eddies, especially during the daytime, likely feeding on the abundant fish and squid at these depths. They were more likely to come to the surface at night.

This preference goes against common wisdom, because it’s the cold-water eddies that generally bring nutrient-rich water up from the depths of the ocean, and satellite images show that cold-water eddies are rich in marine plant life.

The new study, which appears in Nature Scientific Reports, is the first to show that sharks gravitate toward eddies, and that they prefer the warmer variety, researchers say.

Twilight zone

“White sharks are effectively warm-blooded,” Gaube says. “They have to keep their body temperature elevated. We believe that these warm eddies allow white sharks to forage longer at depth, where most of the biomass in the open ocean is found. One reason that the sharks might prefer them is by diving in these warm eddies, they can spend more time in the deeper water.”

Further, recent studies suggest that the “twilight zone,” below the depths that satellites can see, contains many more fish than previously believed—and much more than at the surface. Those patterns might be different than the ones we can easily detect from space.

“Could these ‘ocean deserts’ actually be super productive at depth? That’s what we think might be happening,” Gaube says.

Some recent deep-sea net surveys have found larger, toothy fish like pomfret below the surface in anticyclonic eddies, which could provide a motivation for the sharks to dive there.

How shark poo keeps coral reefs healthy

“These sharks are 2,800 pounds. It’s hard to imagine that they’re just eating krill and small fish all of the time they’re in the open ocean,” Gaube says. “If they can find pomfret and lots of squid in these eddies, then sharks can really get a meal out of that.”

Data sharks collected could help to protect this “twilight zone” as it’s just beginning to be targeted by major fisheries, Gaube says. And information about where great white sharks like to hang out could help conserve this vulnerable species.

“Maybe if we understand the biology of these animals, how they use these features, we could say, ‘OK, do not fish anticyclonic eddies during this time of year, because you’re more likely to catch white sharks,'” Gaube says.

2017 was ‘just an average year’ for shark attacks

“Instead of cordoning off a particular area, we could say there’s this feature, it moves every day, let’s make a ‘mobile marine protected area’ and not touch it because we know it’s a hot spot for great white sharks.”

See real-time tracks of all sharks OCEARCH has tagged.

Wildlife Computers in Redmond, Washington made the tags. Other coauthors are from the University of Washington, the Woods Hole Oceanographic Institution; the Massachusetts Division of Marine Fisheries; and OCEARCH. The National Science Foundation, NASA, and the Woods Hole Oceanographic Institution’s Ocean Life Institute funded the work.

Source: University of Washington

The post Whirlpools are hot spots for great white sharks appeared first on Futurity.

How managers can spark, not squelch, our motivation

Fri, 2018-06-22 08:27

Does your boss empower you to make your own decisions? Or are you stuck with a micro-manager?

New research from Gavin R. Slemp and Lara H. Mossman at the University of Melbourne identifies the best ways for bosses to foster motivation—and it’s not through overseeing every little thing.

Here, Slemp and Mossman offer practical tips resulting from their study in the journal Motivation and Emotion:

“Intrinsic motivation, in contrast, is driven by inner experiences, such as enjoyment, satisfaction, or growth.”

Have you ever had a conversation with your staff about why they turn up to work? If so, you’ve probably noticed that employees bring different motivations to work each day. Some are just going through the motions and are completely indifferent about their work.

Others might be motivated by a desire for material rewards or approval, or to avoid punishments or criticism. Some might use their job as a form of self-esteem maintenance: by working, they avoid guilt and feel secure and productive.

And yet others may turn up because they value their work activities, see work as part of “who they are,” or simply love their work and enjoy the experiences it brings them. This “intrinsic motivation” is the key to a productive, satisfied workforce, and our recently published meta-analysis of more than 30,000 employees worldwide has identified how leaders can foster it in the workplace.

Why do we work?

The varied forms of work motivation sit along a spectrum—from a complete lack of motivation, to highly extrinsic forms of motivation, to intrinsic motivation.

Highly extrinsic forms are contingent on external events, like rewards or approval. Intrinsic motivation, in contrast, is driven by inner experiences, such as enjoyment, satisfaction, or growth. It involves participating in an activity simply because it is interesting or enjoyable.

Intrinsic motivation is regarded as the highest quality form of work motivation because it tends to foster greater workplace wellbeing, proactivity, engagement, and performance. It is also more sustainable because when employees are intrinsically motivated, they are self-motivated.

So, how do leaders foster intrinsically motivated employees?

According to our study they can use particular practices to have a positive influence on employee work motivation, performance, and psychological functioning.

These include:

  • providing opportunities for employees to make their own choices and have inputs into decisions
  • encouraging self-initiated behaviors within structured guidance and boundaries
  • showing an interest in the perspective of employees, demonstrating empathic concern
  • encouraging ownership over goals, and interest and value in work tasks by clearly articulating a rationale about why those tasks are important
  • avoiding the use of controls that restrain autonomy, like overtly controlling behavior (e.g. micro-management), or tangible sanctions or rewards to prompt desired job behaviors.
Control vs. autonomy

These autonomy supportive behaviors contrast with an opposing style of leadership, which employees experience as controlling.

“A controlling leadership style is restraining and suffocating, whereas an autonomy supportive style is empowering…”

The evolution of cars might help clarify how these two leadership styles differ. Early cars had manual gearshifts. At every point the driver was in control of the gears, speed, and direction. A manual car is fully “controlled” by the driver. Yet as automotive technology has developed, cars have become more autonomous and it is the car—not the person in the driving seat—that is in control. The driver becomes a guide, making small corrections, but generally leaving the car in control.

Just like the driver of a manual car, leaders can be very controlling, governing every aspect of their employees’ working lives. Or they can be like the driver of an autonomous car and let their employees take control of their own work, guiding them only when necessary and appropriate—an autonomy supportive style.

A controlling leadership style is restraining and suffocating, whereas an autonomy supportive style is empowering, treating the employee like a self-directed agent who can think and act for themselves. Leaders may not entirely conform to one style over the other, but the more autonomy supportive a leader can be, the better the outcomes for their employees.

Give up on ‘finding your passion’ and do this instead

Our study drew on data from people who’ve experienced autonomy-supportive leadership to varying degrees and found it supports greater intrinsic motivation, workplace well-being, job satisfaction, committed and loyal employees, and higher work engagement. Employees are also less likely to suffer from burnout.

Interestingly, the study also showed that autonomy supportive approaches benefit employees irrespective of national culture—it is not just the way we like things to be in the West.

But perhaps the most important aspect of the study was that it showed how autonomy support leads to positive outcomes in employees. The study suggests it helps employees satisfy three basic psychological needs—for autonomy, competence, and relatedness.

The right kind of motivation comes from you

When employees work for an autonomy supportive leader they naturally feel more autonomous. Yet they also tend to behave in ways that support their competence and relatedness needs. For instance, they might seek out new challenges and learning opportunities, or take steps to develop relationships with peers. Decades of research document the positive effects of satisfying these three needs and autonomy support is an important contributor.

Given the demonstrated benefits stemming from employee autonomy, it may be worth joining the growing number of organizations proactively adopting strategies to nurture the autonomy of their employees. At Netflix, for example, leaders are encouraged to assume that employees work at their best when they don’t have to ask for approval at every turn. Instead, employees are trusted to think and act volitionally on behalf of the organization.

How do things look from your driving seat?

Source: University of Melbourne

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These brains cells don’t die, but they do move

Fri, 2018-06-22 07:48

Scientists have thought for decades that one area of the brain simply disappears during human development. Now, genetic similarities between cells in the subplate and neurons linked to autism suggest a different scenario.

In a new paper, researchers demonstrate that subplate neurons survive, and in fact become part of the adult cerebral cortex, a brain area involved in complex cognitive functions.

Researchers outline a connection between subplate neurons and certain brain disorders, and further identifies a strategy for treating such disorders via innovative stem cell techniques.

In the developing brain, the subplate sits below the cortical plate, a precursor to the cortex. During some stages of development, it’s the largest layer of the brain—making its ultimate disappearance all the more confounding.

This movie, captured over 17 hours, shows subplate neurons migrating away from their original position—a clue that these cells don’t die, but rather relocate. (Credit: Rockefeller U.) Nurturing site

“When we think about cellular-replacement therapy, we need to think about how these cells are made in the first place. The understanding about the subplate was that it expands and then the cells of the subplate just die out,” says Ali H. Brivanlou, professor at Rockefeller University. “But we hypothesized: What if these subplate cells are not dying? What if they’re just moving to a different level of the cortex—becoming part of the cortex?”

Brivanlou and colleagues found ample support for this idea. In samples of brain tissue from various developmental stages, they detected PRDM8, a protein expressed in migrating neurons that helps cells move into the cortical plate. They also detected PRDM8 in subplate-like neurons that they generated from stem cells; and experiments showed that these laboratory-grown subplate neurons wandered away from their original location. All of these findings pointed not to cell death, but to cell movement, they say.

Far from a site of demise, the subplate seems to nurture the development of functional and diverse cells.  Brivanlou observed that subplate neurons mature into various types of deep projection neurons—cells found in the deepest layers of the cortex.

Preventing disorders

In other experiments, the researchers modulated the levels of WNT signaling, a pathway known to guide many developmental processes and found that the level of WNT signaling determined the fate of subplate neurons: low levels yielded projection neurons that extend within the cortex, and high levels yielded neurons that project to other brain areas, according to the study.

The findings, which appear in Cell Stem Cell, have significant implications for understanding brain disorders, the researchers say.

Projection neuron abnormalities have been linked to several neurodevelopmental conditions, including autism; and the new research suggests that these abnormalities manifest very early in development.

Tool gives scientists a glimpse of real-time brain activity

“A lot of the genes associated with autism are first expressed in the subplate,” says postdoctoral associate Zeeshan Ozair. “And if subplate neurons don’t die but instead become part of the cortex, they will carry those mutations with them.”

In addition to shedding light on the early stages of brain disorders, the research presents new hope for preventing or treating such disorders through stem-cell therapy. For example, the scientists hope that their findings will one day make it possible to treat neurodegenerative disease using techniques to generate scarce neuronal subtypes from subplate-like stem cells.

Turning skin cells into brain cells sheds light on Huntington’s

“The deep layers of the cortex are involved in many diseases: Alzheimer’s, Lou Gehrig’s, and Huntington’s disease all kill off specific types of deep-projection neurons,” says Ozair. “When we think about cellular-replacement therapy, we need to think about how these cells are made in the first place.”

“This research shows us how to generate these neurons directly, because we know the signaling mechanism that is necessary for their fate to be unveiled,” Brivanlou says.

Source: Rockefeller University

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Blood test may offer better heart attack prediction

Thu, 2018-06-21 19:30

A new blood test improves the prediction of the long-term risk of heart attack in people with severe coronary artery disease.

In coronary artery disease, the arteries carrying oxygen-rich blood away from the heart become clogged with fatty plaque. The enzyme ACE2 has been associated with cardiovascular disease for a decade, but researchers have recently found that the higher the level of circulating ACE2, the greater the risk.

As reported in PLOS ONE, scientists followed 79 patients (men and women) with coronary artery disease over ten years, and found 46 percent of them experienced heart attacks, heart failure, or death in that time. But in those with the highest levels of ACE2, the risk was increased 2.5-fold compared to those with lower levels of ACE2.

“While our study was small, we saw the risk of heart attack, heart failure, or death was significantly increased in those with higher levels of ACE2,” says lead author and University of Melbourne professor Louise Burrell.

“Our study included only people with severe coronary artery disease diagnosed by a coronary angiogram.”

“We found that ACE2 was elevated in all patients with coronary artery disease compared to healthy subjects. Patients with coronary artery disease are already known to be at increased risk, and it was only when we followed the patients for three to four years that the adverse impact of having very high ACE2 levels on top of coronary artery disease were seen,” says Burrell.

“Seeing such a difference after a few years is very significant. If that was a result from a trial of a new drug, we’d be looking at a new treatment for coronary disease.

“The next step is to see if this result can be replicated with a bigger cohort.”

ACE2 in the bloodstream

Burrell was part of the team that first discovered a method to measure ACE2 in human blood. The enzyme plays a role in breaking down a peptide called angiotensin II, which causes inflammation and constriction in the blood vessels, contributing to the development of cardiovascular disease.

Heart disease and high blood pressure are associated with the angiotensin system being activated, but it is only in the last ten years that researchers have understood how the body attempts to balance this using ACE2.

Healthy people have undetectable to very low levels of ACE2 circulating in their bloodstream. But the enzyme’s levels start to go up with the onset of cardiovascular risk factors like hypertension and high lipids (fats and oils)—further increases have been seen in heart failure and abnormal heart rhythms.

“When people develop heart disease, we see balance between angiotensin and ACE2 go out of whack, and rather than remaining in the heart tissue and blood vessels where it’s needed, ACE2 sheds into the bloodstream. That’s when we can detect high levels,” explains Burrell.

Improving prognosis

Understanding the processes underpinning this is still an area of active research, but it is emerging as an increasingly promising avenue for researchers looking to understand who is at the greatest risk of dying from coronary artery disease.

Coronary artery disease is well understood and its prognosis is improving all the time. Management strategies include lifestyles changes like quitting smoking, a healthier diet and exercise, medications with proven cardio-protective benefits (like aspirin, statins, beta-blockers, and angiotensin enzyme inhibitors/angiotensin receptor blockers), and surgical interventions (like coronary artery bypass and stents).

Watch: Probe zooms through artery of living heart

But some people with coronary artery disease remain at higher risk of heart attack or death than others, and we need new approaches to identify these patients.

Burrell and her team have now recruited nearly 400 patients with coronary artery disease from Austin Health in Melbourne for the next step in the research, which will seek to confirm their findings in a larger cohort. They also plan to investigate the genetics underpinning ACE2.

“We shall look at both genetic material and blood in this next cohort to try to understand what outcomes having a particular ACE2 genotype will lead to,” says Burrell.

Ultimately, confirming their findings will mean the researchers can update clinical guidelines for doctors treating patients with coronary artery disease. And, ideally, they will be able to add high ACE2 levels to the range of risk factors and biomarkers already considered.

“Being able to add a blood test for ACE2 levels to the risk assessment for people with coronary artery disease can only serve to make sure the right people get the right treatments for this disease—which remains such a big killer.”

Source: University of Melbourne

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How setbacks make us rethink our goals

Thu, 2018-06-21 19:20

New research digs into how setbacks affect the pursuit of our goals, such as weight loss.

Setbacks are to be expected when pursuing a goal, whether you’re trying to lose weight or save money. The challenge is getting back on track and not giving up after a difficulty or crisis, says José Rosa, marketing professor in Iowa State University’s Ivy College of Business.

“We know it’s hard to get back on once people take the off ramp.”

Rosa is part of a research team working on practical ways to help people stick to health-related goals—specifically, prescribed regimens for medical ailments that require significant lifestyle changes. The work is personal for Rosa. His diabetic sister nearly died when her blood sugar hit dangerously high levels, and she struggles with poor vision and health, he says.

Staying committed to a long-term health goal is challenging, because it may feel as if there is no light at the end of the tunnel, Rosa says. If your goal is to lose 20 pounds, there is a defined timeframe and a point to celebrate achieving your goal. However, if you are diabetic and need to cut certain foods from your diet or change your daily routine to exercise more, the goal has a different feel, Rosa says.

“These are some of the most difficult goals we face, because the effort has to become a way of life. If you’re a diabetic, you have to be thinking about your diet every time you eat,” Rosa says. “In many ways, it is sacrificial. You must endure this cost and the reward is health.”

Unfortunately, the reward is not immediate and often difficult to realize with certain ailments, such as diabetes or high blood pressure. As we age, other health issues can complicate the outcome of the initial goal and appear as if our efforts aren’t paying off. This makes it harder to stick to the goal, Rosa says, even though we know giving up can have serious consequences.

In the new study, researchers conducted five experiments to understand how crisis influences motivation and commitment to the goal. The researchers found that a setback or difficulty often prompts people to reassess the cost-benefits of their goal and consider quitting.

The experiments simulated a series of situations in which some participants faced an action crisis. They then answered several questions to determine how they would react. Rosa says an action crisis may be related or unrelated to the goal, but it is a point during goal pursuit when circumstances change, causing us to question whether the goal really matters.

Once that questioning begins, we shift our mindset from implementation to evaluation. We renegotiate the importance of the outcomes and may determine it is no longer worth it, Rosa says.

The researchers refer to that decision to quit as “taking the off ramp,” which can snowball into other problems.

“We know it’s hard to get back on once people take the off ramp. This causes some people to feel like failures and stop trying all together. In some situations, the off ramp leads to behaviors that cause another crisis or a significant decline,” he says.

For example, Rosa says a man with high blood pressure stops taking his medication and suffers a heart attack, or a diabetic woman has an insulin reaction causing her to black out and crash her car.

Little treats aren’t a vice. They get us to our goals

Researchers are now using data from the experiments to develop and test interventions for patients on prescribed health regimens. Rosa says the goal is to provide specific instructions for patients to follow and help shift their mindset from renegotiation or evaluation back to implementation.

The potential benefit of such an intervention extends beyond the individual patient, Rosa says. From a marketing perspective, it is an issue of consumption and making health care more effective for patients. Rosa says the right intervention will help patients stay on track, lessening the risk for additional health issues and lowering health care costs.

The results are published online in the journal Psychology & Marketing.

Researchers from Penn State and the University of Wyoming also contributed to the work.

Source: Iowa State University

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Team finds hidden state of matter in superconductive alloy

Thu, 2018-06-21 19:15

Using the physics equivalent of strobe photography, researchers have used ultrafast spectroscopy to visualize electrons interacting as a hidden state of matter in a superconductive alloy.

It takes intense, single-cycle pulses of photons—flashes—hitting the cooled alloy at terahertz speed—trillions of cycles per second—to switch on this hidden state of matter by modifying quantum interactions down at the atomic and subatomic levels.

“We are creating and controlling a new quantum matter that can’t be achieved by any other means.”

And then it takes a second terahertz light to trigger an ultrafast camera to take images of the state of matter that, when fully understood and tuned, could one day have implications for faster and heat-free quantum computing, information storage, and communication.

The discovery of this new switching scheme and hidden quantum phase was full of conceptual and technical challenges.

To find new, emergent electron states of matter beyond solids, liquids, and gases, today’s condensed matter physicists can no longer fully rely on traditional, slow, thermodynamic tuning methods such as changing temperatures, pressures, chemical compositions, or magnetic fields, says Jigang Wang, professor of physics and astronomy at Iowa State University and a faculty scientist at the US Department of Energy’s Ames Laboratory.

“The grand, open question of what state is hidden underneath superconductivity is universal, but poorly understood,” Wang says. “Some hidden states appear to be inaccessible with any thermodynamic tuning methods.”

The new quantum switching scheme developed by the researchers (they call it terahertz light-quantum-tuning) uses short pulses of trillionths of a second at terahertz frequency to selectively bombard, without heating, superconducting niobium-tin, which at ultracold temperatures can conduct electricity without resistance. The flashes suddenly switch the model compound to a hidden state of matter.

In most cases, exotic states of matter such as the one described in this research paper are unstable and short-lived. In this case, the state of matter is metastable, meaning it doesn’t decay to a stable state for an order of magnitude longer than other, more typical transient states of matter.

The fast speed of the switch to a hidden quantum state likely has something to do with that.

“Here, the quantum quench (change) is so fast, the system is trapped in a strange ‘plateau’ and doesn’t know how to go back,” says Wang, corresponding author of the paper in Nature Materials. “With this fast-quench, yet non-thermal system, there’s no normal place to go.”

A remaining challenge for the researchers is to figure out how to control and further stabilize the hidden state and determine if it is suitable for quantum logic operations, Wang says. That could allow researchers to harness the hidden state for practical functions such as quantum computing and for fundamental tests of bizarre quantum mechanics.

It all starts with the researchers’ discovery of a new quantum switching scheme that gives them access to new and hidden states of matter.

“We are creating and controlling a new quantum matter that can’t be achieved by any other means,” says Wang.

Source: Iowa State University

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Sodium-based batteries could be great alternative to lithium

Thu, 2018-06-21 19:13

New evidence suggests batteries based on sodium and potassium hold promise as a potential alternative to lithium-based batteries.

The growth in battery technology has led to concerns that the world’s supply of lithium, the metal at the heart of many of the new rechargeable batteries, may eventually be depleted.

“One of the biggest obstacles for sodium- and potassium-ion batteries has been that they tend to decay and degrade faster and hold less energy than alternatives,” says Matthew McDowell, an assistant professor in the George W. Woodruff School of Mechanical Engineering and the School of Materials Science and Engineering at Georgia Tech.

“But we’ve found that’s not always the case,” he adds.

For the study, which appears in the journal Joule, the research team looked at how three different ions—lithium, sodium, and potassium—reacted with particles of iron sulfide, also called pyrite and fool’s gold.

As batteries charge and discharge, ions are constantly reacting with and penetrating the particles that make up the battery electrode. This reaction process causes large volume changes in the electrode’s particles, often breaking them up into small pieces. Because sodium and potassium ions are larger than lithium, it’s traditionally been thought that they cause more significant degradation when reacting with particles.

In their experiments, the reactions that occur inside a battery were directly observed inside an electron microscope, with the iron sulfide particles playing the role of a battery electrode. The researchers found that iron sulfide was more stable during reaction with sodium and potassium than with lithium, indicating that such a battery based on sodium or potassium could have a much longer life than expected.

The difference between how the different ions reacted was stark visually. When exposed to lithium, iron sulfide particles appeared to almost explode under the electron microscope. On the contrary, the iron sulfide expanded like a balloon when exposed to the sodium and potassium.

“We saw a very robust reaction with no fracture—something that suggests that this material and other materials like it could be used in these novel batteries with greater stability over time,” says graduate student Matthew Boebinger.

The study also casts doubt on the notion that large volume changes that occur during the electrochemical reaction are always a precursor to particle fracture, which causes electrode failure leading to battery degradation.

The researchers suggest that one possible reason for the difference in how the different ions reacted with the iron sulfide is that the lithium was more likely to concentrate its reaction along the particle’s sharp cube-like edges, whereas the reaction with sodium and potassium was more diffuse along all of the surface of the iron sulfide particle.

As a result, the iron sulfide particle when reacting with sodium and potassium developed a more oval shape with rounded edges.

While there’s still more work to be done, the new research findings could help scientists design battery systems that use these types of novel materials.

Sugar cubes solve big problem with lithium metal batteries

“Lithium batteries are still the most attractive right now because they have the most energy density—you can pack a lot of energy in that space,” McDowell says.

“Sodium and potassium batteries at this point don’t have more density, but they are based on elements a thousand times more abundant in the earth’s crust than lithium. So they could be much cheaper in the future, which is important for large scale energy storage—backup power for homes or the energy grid of the future.”

The National Science Foundation and the US Department of Energy funded the research. Any opinions, findings, and conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of the sponsors.

Source: Georgia Tech

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How 1 ‘super tumor suppressor gene’ shields us from cancer

Thu, 2018-06-21 18:50

New research reveals how a so-called “super tumor suppressor gene” known as p53 prevents cancer.

In our bodies, we all have genes working hard to prevent cancer. If they don’t do their job properly, rogue cells can mutate and develop into the life-threatening disease.

The malfunction of p53 causes at least half of all cancers. When it works, p53 regulates how a cell reacts to various stresses and can instruct a rogue cell to die or stop multiplying.

Researchers have known about the significance of p53 in protecting us from cancer for about 30 years, but until now no one has explained how it prevents cancer development.

Now, scientists have discovered that a special group of genes that function in the body’s normal DNA repair process are critical to p53’s effectiveness in preventing the development of cancer.

The team found that the DNA repair gene MLH1 and as well as other related genes are critical to p53’s ability to prevent the development of B-cell lymphomas.

This new information could help doctors better identify patients with an increased risk of certain cancers. It could also lead to safer, more effective treatments.

A big deal

Ana Janic, a researcher at University of Melbourne, says that while the results will take several years to translate into clinical practice, the discovery is ground-breaking.

She says it paves the way for researchers to investigate whether the DNA repair process is as important in cancers other than lymphoma, like pancreatic and colon cancer.

“It is defects (mutations) in this gene that’s actually causing 50 percent of human cancers,” Janic says. “It’s really exciting because we’ve kind of opened the window for many new discoveries in this area.”

Janic says that knowing MLH1 (and related DNA repair factors) functions as a powerful weapon for p53 should eventually help doctors diagnose patients earlier and prescribe safer, more targeted cancer treatments.

“For instance, if a patient has lymphoma with a mutation that disables the DNA repair mechanism, doctors will now know to avoid certain DNA-damaging treatments, like chemotherapy, that may only make the cancer more aggressive,” she says.

The discovery could help many people with cancer but particularly those with a condition called Li-Fraumeni Syndrome, a familial predisposition to a range of cancers that is caused by inherited mutations in—you guessed it—p53.

According to Janic, p53 is mutated in close to 70 percent of colon and pancreatic cancers, so this discovery could also have a significant impact on understanding and treating these diseases.

“We are keen to test whether genes involved in the DNA repair process might also play a role in helping p53 to prevent the development of these highly prevalent and, in the case of pancreatic cancer, highly deadly cancers,” she says.

A ‘holy grail’

The next step is to investigate how human cells react to cancer inducing stresses in tissue culture and eventually develop more personalized treatments for individual patients.

Andreas Strasser, a professor from Melbourne, says understanding how p53 works is a “holy grail” for cancer researchers.

“We are planning to continue our studies into the genes that are regulated by p53, digging deeper into understanding other potential processes that might impact its function,” he says.

Just 1 missing atom may lead to colon cancer

Marco Herold, an associate professor also from Melbourne, says their findings stemmed from a screen of more than 300 genes directly regulated by p53 to identify which ones were critical for its tumor-suppressing function, demonstrating the importance of detailed functional analyses.

“It was amazing to find that the loss of the DNA repair gene MLH1 prevented p53 from functioning properly, causing the development of lymphoma,” he says. “And when MLH1 was put back into the equation, tumor development was significantly stalled.

“This led us to explore other DNA repair genes and it has become clear just how important the whole DNA repair machinery is to p53’s ability to prevent cancer development.”

Like many discoveries at this level, Janic says the results were a surprise as researchers had no idea that p53 worked in this way. But, it also means there’s a lot of potential for further exploration.

“We actually found that the DNA repair (MLH1) is one of the most critical processes for this,” she says. “This was an absolutely novel discovery for us and for the field. The field is very excited about our work and where this will lead in the near future.”

How breast cancer hijacks immune cells to weaken our defense

The Australian National Health and Medical Research Council, Cancer Council Victoria, Australian Phenomics Network, Cancer Australia, the Leukemia & Lymphoma Society of America, Marie Curie Actions and Beatriu de Pinos, and the Lady Tata Memorial Trust supported the research.

The research appears in Nature Medicine.

Source: Cheryl Critchley for University of Melbourne

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Endometriosis isn’t just a ‘thin women’s disease’

Thu, 2018-06-21 10:59

New research debunks the myth that endometriosis is a ‘skinny woman’s disease.’

Painful, stressful, and all-too-common, endometriosis—abnormal tissue growth affecting a woman’s reproductive and pelvic organs—can be devastating, in some cases leaving women infertile and vulnerable to complications elsewhere in the body.

Despite affecting one in 10 women of reproductive age, the condition is relatively under-researched and remains difficult to diagnose and treat. Now, new research seeks to open the way for tailored treatments, screening for complications, and shedding light on its genetic underpinning.

The study of 500 women with surgically confirmed endometriosis, found that, contrary to popular belief, endometriosis is not associated with thin body types, instead the majority of patients have a body-mass index (BMI) in the healthy range.

And although the study, which appears in the Journal of Endometriosis and Pelvic Pain Disorders, confirms that obese women are less likely to have the disease, it finds that when they do get it they are much more likely to have a severe form.

The research is the first to feature women with surgically confirmed cases of endometriosis. Previous studies have relied on self-reported cases.

What is endometriosis?

Endometriosis occurs when tissues similar to the endometrium, which lines the uterus, grow in other places. Instead of shedding the lining with menstruation, the blood and tissues can travel upwards and out through the fallopian tubes, surviving anywhere in the pelvic cavity like the ovaries, outside the fallopian tubes or on the internal surface of the abdomen.

While ultrasounds and MRI scans can be used to investigate the condition, laparoscopic (or “keyhole”) surgery is the only way to reach a definite diagnosis.

“When a surgeon goes in to investigate endometriosis, they are looking for things like abnormal blisters and lesions of various sizes,” says lead author Sarah Holdsworth-Carson, a postdoctoral research fellow in the Gynaecology Research Centre at the Royal Women’s Hospital and the University of Melbourne.

“The severity of the condition is based on what the surgeon sees. The more lesions there are, the bigger they are, and the deeper they have invaded the tissue, the more severe the case. Lesions on the ovaries also increase the severity.”

Often the surgeon will remove the endometriosis during the same laparoscopic surgery, reducing the number of surgeries the patient experiences. This can be an effective treatment in the majority of cases.

When the condition is severe, however, they may not be able to remove everything, meaning the patient might need to return for more surgery. It is also common for endometriosis to return, even if the surgeon has removed all the lesions in the previous surgery.

“Our findings provide really vital information that clinicians need when planning surgery,” says Holdsworth-Carson. “If the patient is obese, they now know the chances are she will have a more severe form of the disease, meaning they can plan accordingly. This should hopefully reduce the number of surgeries women are experiencing.”

For the study, which has now attracted over 800 participants, researchers are recording lifestyle information, body shape, medical histories, pathology reports, genetic information, and tissue samples, with the aim of understanding as much as possible about the disease.

Researchers also follow up with patients 12 months after their surgeries with a second questionnaire—the goal being to gather as much information as possible so that women can be given more tailored interventions and therapies.

Looking forward

“Endometriosis can strike any time from a woman’s first period until menopause, often causing considerable pelvic pain and sometimes fertility problems,” says Holdsworth-Carson. “It can be really devastating. We need to understand it in more detail so we can offer women better treatments.”

Doctors will often try hormone therapies like the pill, particularly with teenagers, to suppress the patient’s periods and stop lesions forming.

“But when it comes time for them to have a family, they obviously need to stop their treatments—it’s a horrible situation for many women.”

For some women the condition is asymptomatic, and they only discover they have it when they find themselves unable to fall pregnant.

Researchers are exploring two genes with no known role in uterine biology or reproductive biology and are hopeful they will be able to decipher the genetic factors underlying the disease.

This drug-testing device has a vagina, cervix, and uterus

Further, Holdsworth-Carson also has a growing interest in the link between endometriosis and metabolism.

“We are getting lots of clues about the link between endometriosis and poor cardiovascular health and poor metabolism. For example, we already know that women with endometriosis are more likely to have high cholesterol. That’s why we wanted to look at BMI with this latest study.

“It looks like endometriosis could be more than just than a gynecological condition. There could be implications for patients in the long term, 20 or 30 years down the track.”

Ultimately the aim is to improve the understanding of the condition and to develop a screening tool that could better diagnose women with endometriosis.

Further, such tools could be useful for identifying women who are at high risk of developing other diseases, so doctors can offer support to help prevent their onset.

Is human embryo research the key to treating infertility?

“Endometriosis hasn’t received much attention in the past, but this is more than a ‘little’ disease,” says Holdsworth-Carson. “I suspect we’ve only just scratched the surface of what we can learn about it.”

The National Health and Medical Research Council (NHMRC) funded the work.

Source: University of Melbourne

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Fracking exposure leads to more fat cells

Thu, 2018-06-21 10:34

Exposure to fracking chemicals and wastewater promotes fat cell development, or adipogenesis, in living cells in a laboratory, according to a new study.

Researchers observed increases in both the size and number of fat cells after exposing living mouse cells in a dish to a mixture of 23 commonly used fracking chemicals. They also observed these effects after exposing the cells to samples of wastewater from fracked oil and gas wells and surface water believed to be contaminated with the wastewater.

“We saw significant fat cell proliferation and lipid accumulation, even when wastewater samples were diluted 1,000-fold from their raw state and when wastewater-affected surface water samples were diluted 25-fold,” says Chris Kassotis, a postdoctoral research associate at Duke’s Nicholas School of the Environment, who led the study.

“Rather than needing to concentrate the samples to detect effects, we diluted them and still detected the effects,” he says.

Previous lab studies by Kassotis and his colleagues have shown that rodents exposed during gestation to the mix of 23 fracking chemicals are more likely to experience metabolic, reproductive, and developmental health impacts, including increased weight gain.

Kassotis says further research is necessary to assess whether similar effects occur in humans or animals who drink or come into physical contact with affected surface waters outside the laboratory.

Hydraulic fracturing across the United States uses more than 1,000 different chemicals, many of which have been demonstrated through laboratory testing to act as endocrine disrupting chemicals in both cell and animal models.

To conduct this study, Kassotis and colleagues collected samples of fracking wastewater and wastewater-contaminated surface water near unconventional (aka, fracked) oil and gas production sites in Garfield County, Colorado, and Fayette County, West Virginia, in 2014.

The researchers exposed laboratory cultures of mouse cells to these waters at varying concentrations or dilutions over a two-week period. The researchers measured how the waters affected fat cell development in the cultures. They performed similar tests exposing cell models to a mix of 23 fracking chemicals.

Within each experiment, researchers exposed other cells to rosiglitazone, a pharmaceutical known to be highly effective at activating fat cell differentiation and causing weight gain in humans.

The results showed that the 23-chemical mix induced about 60 percent as much fat accumulation as the potent pharmaceutical; the diluted wastewater samples induced about 80 percent as much; and the diluted surface water samples induced about 40 percent as much.

In all three cases, the number of pre-adipocytes, or precursor fat cells, that developed was much greater in cell models exposed to the chemicals or water samples than in those exposed to the rosiglitazone.

Fracking chemicals may harm developing immune system

The tests also provided insights into the mechanisms that might be driving these effects.

“Activation of the hormone receptor PPAR-gamma, often called the master regulator of fat cell differentiation, occurred in some samples, while in other samples different mechanisms such as inhibition of the thyroid or androgen receptor, seemed to be in play,” Kassotis explains.

The research appears in Science of the Total Environment.

Additional coauthors are from the University of Missouri and Duke.

Primary funding came from the National Institute for Environmental Health Sciences. Additional funding came from the University of Missouri, a crowdfunding campaign via Experiment.com, and an EPA 520 STAR Fellowship Assistance Agreement.

Source: Duke University

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‘E-skin’ lets prosthetic hands sense touch and pain

Thu, 2018-06-21 09:40

A new electronic “skin” may restore a sense of touch for amputees who use prosthetic hands.

The skin’s inventors say that when the “e-dermis” is layered on top of a prosthetic, it brings back feeling through the fingertips.

“After many years, I felt my hand, as if a hollow shell got filled with life again,” says the anonymous amputee who served as the team’s principal volunteer tester.

Made of fabric and rubber laced with sensors to mimic nerve endings, e-dermis recreates a sense of touch as well as pain by sensing stimuli and relaying the impulses back to the peripheral nerves.

“We’ve made a sensor that goes over the fingertips of a prosthetic hand and acts like your own skin would,” says lead researcher Luke Osborn, a biomedical engineering graduate student at Johns Hopkins University. “It’s inspired by what is happening in human biology, with receptors for both touch and pain.

(Credit: Larry Canner/Johns Hopkins)

“This is interesting and new,” Osborn adds, “because now we can have a prosthetic hand that is already on the market and fit it with an e-dermis that can tell the wearer whether he or she is picking up something that is round or whether it has sharp points.”

The work, which appears in Science Robotics, shows it’s possible to restore a range of natural, touch-based feelings to amputees who use prosthetic limbs. The ability to detect pain could be useful, for instance, not only in prosthetic hands but also in lower limb prostheses, alerting the user to potential damage to the device.

Bringing a more human touch to modern prosthetic designs is critical, especially when it comes to incorporating the ability to feel pain, Osborn says.

“Pain is, of course, unpleasant, but it’s also an essential, protective sense of touch that is lacking in the prostheses that are currently available to amputees. Advances in prosthesis designs and control mechanisms can aid an amputee’s ability to regain lost function, but they often lack meaningful, tactile feedback or perception.”

That is where the e-dermis comes in, conveying information to the amputee by stimulating peripheral nerves in the arm. The device does this by electrically stimulating the amputee’s nerves in a non-invasive way, through the skin, says the paper’s senior author, Nitish Thakor, professor of biomedical engineering and director of the Neuroengineering and Biomedical Instrumentation Laboratory.

“For the first time, a prosthesis can provide a range of perceptions, from fine touch to noxious to an amputee, making it more like a human hand,” says Thakor, cofounder of Infinite Biomedical Technologies, the Baltimore-based company that provided the prosthetic hardware used in the study.

The researchers connected the e-dermis output to the volunteer by using a noninvasive method known as transcutaneous electrical nerve stimulation, or TENS. In a pain-detection task, the team determined that the test subject and the prosthesis were able to experience a natural, reflexive reaction to both pain while touching a pointed object and non-pain when touching a round object.

This artificial skin can sense ladybug footsteps

The e-dermis is not sensitive to temperature—for this study, the team focused only on detecting object curvature (for touch and shape perception) and sharpness (for pain perception).

The e-dermis technology could make robotic systems more human, and it could also expand or extend to astronaut gloves and space suits, Osborn says.

‘Skin’ sensor gives robots better sense of touch

The researchers plan to further develop the technology and better understand how to provide meaningful sensory information to amputees in the hopes of making the system ready for widespread patient use.

Other researchers from the Johns Hopkins departments of biomedical engineering, electrical and computer engineering, and neurology, and from the Singapore Institute of Neurotechnology contributed to the work. Space@Hopkins, the Applied Physics Laboratory, and the National Institute of Biomedical Imaging and Bioengineering funded the work.

Source: Johns Hopkins University

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People in Nairobi’s slums face ‘double jeopardy’

Thu, 2018-06-21 08:49

Tenants in the slums of Nairobi, Kenya, receive drastically inferior household services and pay more rent compared to those in its formal settlements, a new study shows.

“Around a billion people worldwide currently reside in urban slums under deplorable conditions.”

The study found that households in Nairobi’s slum areas face significant gaps in public services. For example, in the case of water, toilet, and public sewage disposal, the gaps are as high as 40 to 50 percent.

Further, these residents pay about 16 percent more than their formal area counterparts, when adjusted for housing quality conditions.

“Around a billion people worldwide currently reside in urban slums under deplorable conditions,” says Debabrata Talukdar, professor of marketing in the School of Management at the University at Buffalo and author of the paper, which appears in World Development.

“People living in Kenyan slums face depraved living conditions and a rental housing market that is highly exploitative of its tenants.”

Talukdar analyzed nearly 1,200 responses from households in the slums and formal areas of Nairobi to conduct a systematic empirical analysis of the market conditions faced by residents in both areas.

Why rising temps pose deadlier risk in Nairobi slums

The double jeopardy situation could be solved with significant public financing to increase the amount of housing and improve infrastructure, Talukdar says, but that solution is impractical based on the current capabilities of a developing country like Kenya.

“The more pragmatic approach relies on combined public and private investments for policy initiatives that would be beneficial to both parties,” he says. “Specific initiatives could include formalizing tenancy rights, slum upgrading or redevelopment, or regulatory liberalizations in the housing sector.”

Source: University at Buffalo

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Ancient primates had extra claws just for grooming

Thu, 2018-06-21 08:45

Fossil evidence shows that ancient primates—including one of the oldest known, Teilhardina brandti—had specialized grooming claws as well as nails, according to a new study.

Humans and other primates are outliers among mammals for having nails instead of claws. But how, when, and why we transitioned from claws to nails has been an evolutionary head-scratcher.

The findings overturn the prevailing assumption that the earliest primates had nails on all their digits and suggest the transition from claws to nails was more complex than previously thought.

(Credit: U. Florida)

“We had just assumed nails all evolved once from a common ancestor, and in fact, it’s much more complicated than that,” says Jonathan Bloch, study coauthor and Florida Museum of Natural History curator of vertebrate paleontology at the University of Florida.

Grooming claws

Grooming in mammals is not just about looking good. Thick body hair is a haven for ticks, lice, and other parasites—possible health threats, as well as nuisances. Having a specialized claw for removing pests would be an evolutionary advantage, says Doug Boyer, an associate professor in the department of evolutionary anthropology at Duke University and the study’s lead author.

It’s one that has been retained in many primates. Lemurs, lorises, galagoes, and tarsiers have nails on most of their digits and grooming claws on their second—and in tarsiers, second and third—toes.

So, why did the ancestors of monkeys, apes, and humans lose their grooming claws? One possible answer: because we have each other.

“The loss of grooming claws is probably a reflection of more complex social networks and increased social grooming,” Boyer says. “You’re less reliant on yourself.”

This could explain why more solitary monkey species, such as titi and owl monkeys, have re-evolved a grooming claw, he says.

Researchers had thought grooming claws likely developed independently several times along the lines that gave rise to living primates. But these fossils suggest grooming claws were hallmark features of the earliest primates, dating back at least 56 million years.

They also come from five different genera of ancient primates that belonged to the omomyoids, the ancestors of monkeys, apes, humans, and tarsiers—not the branch of primates that gave rise to lemurs, lorises, and galagoes.

‘Nail in the coffin’

In 2013, Boyer was at the University of California Museum of Paleontology, sifting through sediment collected in Wyoming several decades earlier, when he found several curious primate fossils. They were distal phalanges, the bones at the tips of fingers and toes, from omomyoids.

The shape of these bones reveals whether they support a claw or nail. Bones topped with a claw mimic its narrow, tapered structure while bones undergirding a nail are flat and wide. The distal phalanges that Boyer discovered looked like they belonged to animals with grooming claws.

These images created from CT scans show side and top views of a bone that supported a grooming claw, left, and a nail, right. Researchers attribute these fossils to Teilhardina brandti, one of the earliest primates, based on their size and similarity to existing primates. The fossils were found in Bighorn Basin, Wyoming, which was home to this ancient primate 56 million years ago. (Credit: Boyer et al. in the Journal of Human Evolution)

“Prior to this study, no one knew whether omomyoids had grooming claws,” Boyer says. “Most recent papers came down on the side of nails.”

Meanwhile, Bloch, picking through collections recently recovered from Bighorn Basin, Wyoming, came across what looked like a “strange, narrow nail” bone. But when he compared it to modern primates, “it looked just like a tarsier grooming claw.” Smaller than a grain of rice, it matched the proportions of Teilhardina brandti, a mouse-sized, tree-dwelling primate.

Bloch and Boyer had coauthored a 2011 study describing the first fossil evidence of nails in Teilhardina. At the time, they believed the primate had nails on all its digits. Now, fossils were making them reevaluate their assumptions, not only about Teilhardina, but other omomyoids.

On the off-chance that they could add one more ancient primate to the growing list of claw-bearers, the pair drove out to Omomys Quarry, Wyoming, once inhabited by another genus of omomyoid, Omomys.

“We spent a day combing that site, never expecting to find something as tiny and delicate as a grooming claw,” Boyer says.

The team picked one right off the surface. They had found grooming claws at three independent sites from omomyoids spanning about 10 million years in the fossil record.

“That was the last nail in the coffin,” Boyer says.

‘Our evolutionary story’

Why did primates develop nails at all? The question is a contentious one, but Bloch and Boyer think the transition away from claws could have mirrored changes in primate movement. As we ramped up climbing, leaping, and grasping, nails might have proven more practical than claws, which could snag or get in the way.

Grooming claws might seem insignificant, but they can provide crucial insights into ancient primates, many of which are known only from fossil teeth, Bloch says. These tiny claws offer clues about how our earliest ancestors moved through their environment, whether they were social or solitary and what their daily behavior was like.

“We see a bit of ourselves in the hands and feet of living primates,” Bloch says. “How they got this way is a profoundly important part of our evolutionary story.”

The findings appear in the Journal of Human Evolution. Additional coauthors are from Stony Brook University, the University of California Museum of Paleontology at Berkeley, and the University of Florida.

The National Science Foundation and the Institute of Museum and Library Services provided funding for the research.

Models of the fossils are available on Morphosource, an open-access repository of 3D data that Boyer directs.

Source: University of Florida

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Enzyme from our bodies could spawn Zika drug

Wed, 2018-06-20 19:20

New research suggests future antiviral drugs could take advantage of viperin, a naturally occurring enzyme in humans and other mammals that has antiviral effects on a wide variety of viruses, including West Nile, hepatitis C, rabies, and HIV.

The enzyme facilitates a reaction that produces the molecule ddhCTP, which prevents viruses from copying their genetic material and thus from multiplying. This discovery could allow researchers to develop a drug that induces the human body to produce this molecule and could act as a broad-spectrum therapy for a range of viruses. A paper describing the study appears in Nature.

“We knew viperin had broad antiviral effects through some sort of enzymatic activity, but other antivirals use a different method to stop viruses,” says Craig Cameron, professor of biochemistry and molecular biology at Penn State and an author of the study.

We “showed the effects of ddhCTP on a virus’s ability to replicate its genetic material. Surprisingly, the molecule acts in a similar manner to drugs that were developed to treat viruses like HIV and hepatitis C. With a better understanding of how viperin prevents viruses from replicating, we hope to be able to design better antivirals.”

A virus typically co-opts the host’s genetic building blocks to copy its own genetic material, incorporating molecules called nucleotides into new strands of RNA. The molecule ddhCTP mimics these nucleotide building blocks and becomes incorporated into the virus’s genome. Once incorporated into a new strand of the virus’s RNA, these “nucleotide analogs” prevent an enzyme called RNA polymerase from adding more nucleotides to the strand, thus preventing the virus from making new copies of its genetic material.

“Long ago, the paradigm was that in order to kill a virus, you had to kill the infected cell,” says Cameron. “Such a paradigm is of no use when the virus infects an essential cell type with limited capacity for replenishment. The development of nucleotide analogs that function without actually killing the infected cell changed everything.”

Most nucleotide analogs on the market are synthetic, but often come with complications. Because many proteins and enzymes of the cell use nucleotides, numerous opportunities exist for analogs to interfere with normal cellular function.

Unintended targets

“The major obstacle to developing therapeutically useful antiviral nucleotides is unintended targets,” says Jamie Arnold, associate research professor of biochemistry and molecular biology at Penn State and an author of the paper.

“For example, a few years ago we discovered that a nucleotide analog under development for treatment of hepatitis C could interfere with the production of RNA in mitochondria, subcellular organelles important for energy production in the patient’s own cells. That meant people with mitochondrial dysfunction are predisposed to any negative effects of this unintended interference.”

The molecule ddhCTP, however, does not appear to have any unintended targets. The research team suspects that the natural origin of the compound within the human body necessitates that it be nontoxic.

“Unlike many of our current drugs, ddhCTP is encoded by the cells of humans and other mammals,” says Cameron. “We have been synthesizing nucleotide analogs for years, but here we see that nature beat us to the punch and created a nucleotide analog that can deal with a virus in living cells and does not exhibit any toxicity to date. If there’s something out there that’s going to work, nature has probably thought of it first. We just have to find it.”

To verify the effectiveness of ddhCTP, the research team showed that the molecule inhibited the RNA polymerases of dengue virus, West Nile virus, and Zika virus, which are all in a group of viruses called flaviviruses. Then they investigated whether the molecule halted replication of Zika virus in living cells.

“The molecule directly inhibited replication of three different strains of Zika virus,” says Joyce Jose, assistant professor of biochemistry and molecular biology at Penn State and an author of the paper. “It was equally effective against the original strain from 1947 as it was against two strains from the recent 2016 outbreak. This is particularly exciting because there are no known treatments for Zika. This study highlights a new avenue of research into natural compounds like ddhCTP that could be used in future treatments.”

Some viruses, but not others

Together, these results demonstrate promising antiviral effects of ddhCTP on a variety of flaviviruses. However, the RNA polymerases of human rhinovirus and poliovirus, which are in a group called picornaviruses, were not sensitive to the molecule. The researchers plan to investigate the polymerase structures of these viruses to better understand why flaviviruses are sensitive to ddhCTP while the picornaviruses tested in this study are not. This investigation may also offer insights into how flaviviruses might develop resistance to the molecule.

Will bat-borne Nipah virus be the next pandemic?

“Development of resistance to an antiviral agent is always an issue,” says Cameron. “Having some idea of how resistance happens, or being able to prevent it from happening, will be critical if this is to be used as a broad-spectrum therapy.”

Additional researchers contributed from the Albert Einstein College of Medicine and the Institute for Protein Innovation. The National Institute of Allergy and Infectious Diseases and the National Institutes of General Medical Sciences of the National Institutes of Health supported the work, as did Penn State and the Price Family Foundation.

Source: Penn State

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Just 1 missing atom may lead to colon cancer

Wed, 2018-06-20 19:02

The development of an aggressive, early-onset form of colon cancer may come down to a single missing iron atom in a key DNA repair protein, according to new research.

The findings, which will appear in Nature Chemistry, reveal how a mutation in the MUTYH protein prevents it from doing its job repairing damaged DNA. The study also shows for the first time in humans that our DNA can function like an electrical wire, conveying important signals—the interruptions of which can lead to a proliferation of additional genetic errors, and thus to cancer.

While researchers have linked other mutations in the MUTYH repair protein with cancer before, this is the first time the mutation was associated with a cluster of iron and sulfur atoms in the protein. These clusters are at the heart of how the repair proteins perform DNA charge-transport chemistry—where the strands of our DNA transmit important information about faulty sections of genetic code that need to be fixed.

The research began when Stephen Gruber, a professor of medicine at the Keck School of Medicine of the University of Southern California, identified an unusual genetic mutation from a family of patients with early-onset colon cancer. Through genetic analysis, Gruber determined that the mutation was affecting MUTYH.

“This is an essential DNA-repair enzyme,” says David Sherman, research professor at University of Michigan’s Life Sciences Institute. “It scans along the DNA and, if there is a mutation, it can sense the mutation, cut out the bad base, and put in a new one. It’s pretty amazing. But there is still a longstanding question of how it scans. How does this protein know when it’s reached an incorrect base pair?”

Gruber asked Sherman to help characterize the protein biochemically and determine how the mutation might be contributing to this aggressive form of cancer. The researchers discovered that the mutation, called C306W, affects a portion of the protein that normally helps hold a critical co-factor made up of a cluster of four iron and four sulfur atoms inside the protein. The mutation causes the iron-sulfur cluster to be degraded when exposed to oxygen, resulting in a cluster with only three iron atoms.

And with that one iron atom missing, the MUTYH protein can’t do its job.

To understand why the mutant protein no longer responds to damaged DNA, the team turned to Jacqueline Barton, chair of the chemistry and chemical engineering division at the California Institute of Technology. As a pioneer in the field of DNA-mediated charge transport, Barton has demonstrated that DNA strands in bacteria can act as wires, transmitting electrical signals.

This latest research demonstrates that the same electrical signaling is also at work in human versions of DNA repair proteins—and that interruptions to this process may be linked to cancer.

“This ability of DNA to transmit electrical signals is essentially how MUTYH detects where there’s a lesion, by virtue of this cluster of iron and sulfur atoms,” Sherman says.

Normally, the iron-sulfur cluster on the protein allows electrons to pass in and out of the MUTYH protein, enabling it to receive signals about damaged DNA. With just the one iron atom missing, however, the protein is no longer able to receive and interpret the electronic signals being transmitted along the DNA strand. And without that signaling, it cannot find and repair a damaged gene.

What’s more, because this one mutation to the gene that makes the MUTYH protein disables it from repairing damaged DNA, it leads to further mutations across the genome.

“This mutation essentially allows the human genome to develop multiple mutations in other cancer repressors—proteins that actually can control the onset of malignancy,” Sherman says.

Colon cancer patients who eat nuts have lower death risk

Support for the research came from the National Institutes of Health, the American Society of Clinical Oncology, the USC Norris Comprehensive Cancer Center, the Ming Hsieh Institute for Engineering-Medicine for Cancer, Daniel and Maryann Fong, the Anton B. Burg Foundation, and the Moore Foundation.

Additional authors of the study are from USC; the University of Michigan; Caltech; the University of Texas; and Amgen.

Source: University of Michigan

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Warming oceans may spark international ‘fish wars’

Wed, 2018-06-20 19:00

Climate change is forcing fish species to shift their habitats faster than the world’s system for allocating fish stocks, a situation that could exacerbate international fishing conflicts, researchers say.

The study shows for the first time that new fisheries are likely to appear in more than 70 countries all over the world. Past studies show that newly shared fisheries often spark conflict among nations.

Conflict leads to overfishing, which reduces the food, profit, and employment fisheries can provide, and can also fracture international relations in other areas, researchers say. A future with lower greenhouse gas emissions, like the targets under the 2015 Paris climate agreement, would reduce the potential for conflict, the study says.

“Most people may not understand that the right to harvest particular species of fish is often decided by national and regional fisheries management bodies,” says Malin Pinsky, an assistant professor of ecology, evolution, and natural resources at Rutgers–New Brunswick University’s School of Environmental and Biological Sciences.

“Those bodies have made the rules based on the notion that particular fish species live in particular waters and don’t move much. Well, they’re moving now because climate change is warming ocean temperatures.”

Mackerel war

Many commercially important fish species could move their ranges hundreds of miles northward in search of colder water, Pinsky and postdoctoral associate James Morley report. This movement has already begun, and the results have been highly disruptive for fisheries.

“Consider flounder, which have already shifted their range 250 miles farther north,” Pinsky says. “Federal fisheries rules have allocated many of those fish to fishers in North Carolina, and now they have to steam hundreds of extra miles to catch their flounder.”

Pinsky and his coauthors cite other examples of the disruption of fisheries causing international disputes, including the “mackerel war” between Iceland and the European Union (EU).

Under rules agreed to by EU member nations, fishers harvest a certain number of mackerel each year. But by 2007, those mackerel had begun to move to colder waters near Iceland, which is not an EU member. Iceland began fishing the sudden abundance of mackerel, but could not agree with the EU on sustainable fishing limits.

The dispute became a trade war and is still ongoing. Lobster fishers from the United States and Canada have also come into conflict over the lobster fishery, which is also moving north from New England to the Canadian Maritime Provinces.

Avoiding conflict

Given climate change, the movement of fish to new ranges is inevitable, but the conflicts over fish stocks are not, the study says. Governing bodies such as the one overseeing the EU’s fisheries might negotiate with neighboring fisheries organizations to take account of old fisheries moving out and new ones moving in.

Pinsky and coauthors suggest, for example, that governments might allow the trading of fishing permits or quotas across international boundaries.

See an almost real-time map of global fishing

“We need international agreements for the collaborative monitoring and sharing of fisheries as they move, much as the Antarctic conservation agreement has begun to do,” he says. The Antarctic management body known as CCAMLR cooperates closely with neighboring fisheries managers to share information about shared fisheries, including those that will continue to move.

The alternative to such agreements is grim, including overfishing and conflicts over fisheries that can spill over into international tensions over trade, borders, and sovereignty.

Tool locates the best fishing spots while avoiding turtles

“We have a chance to avoid conflict over fisheries that could escalate international tensions, threaten our food supply, and reduce profit and employment worldwide,” Pinsky says. “Avoiding fisheries conflicts and overfishing ultimately provides more fish, more food and more jobs for everyone.”

The study appears in Science. Other coauthors are from the University of British Columbia, Utrecht University, Cardiff University, Stockholm University, and James Cook University who are participating in the Nippon Foundation-University of British Columbia Nereus Program.

Source: Rutgers University

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3D printing makes flexible bone grafts

Wed, 2018-06-20 18:55

Researchers have created a new way to make flexible bone grafts using 3D-printed materials.

The transplantation of bone tissue, known as bone grafting, typically involves allograft, which is bone from a deceased donor, or autograft, which comes from the patient’s own body.

Ramille Shah, a materials scientist from Northwestern University, along with materials engineer Adam Jakus, validated the commercialization potential of a new 3D-printable synthetic material they call “hyperelastic bone.”

The researchers foresee that the new technique will be a vast improvement over the current options, including other synthetic materials.

The National Science Foundation supported the research.

Source: National Science Foundation

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