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Updated: 7 min 17 sec ago

Why U.S. Supreme Court rejected deportation provision

Fri, 2018-04-20 11:33

On April 17, the Supreme Court of the United States struck down a part of the Immigration and Nationality Act that authorizes the government to deport some immigrants, including lawful permanent residents, who have been convicted of “aggravated felonies.”

Jayashri Srikantiah, director of the Immigrants’ Rights Clinic at Stanford University, discusses why the decision in Sessions v. Dimaya is so important.

The post Why U.S. Supreme Court rejected deportation provision appeared first on Futurity.

Enter your info to calculate poverty risk

Fri, 2018-04-20 11:12

What are your odds of experiencing poverty? This online tool can predict.

The poverty calculator determines an American’s expected risk of poverty based on their race, education level, gender, marital status, and age.

“Many Americans will now be able to estimate the sizable amount of economic insecurity that they will face in the future,” says Mark Rank, professor of social welfare at the Brown School at Washington University in St. Louis, who developed the tool.

This video explains how it works:

Poverty has moved from US cities to the suburbs These 6 elements redefine poverty

Source: Washington University in St. Louis

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DNA to store Massive Attack album for near eternity

Fri, 2018-04-20 09:56

An album by trip hop pioneers Massive Attack is headed for near-eternal storage in DNA molecules within tiny glass beads.

It’s been 20 years since the release of Mezzanine, the British band’s most successful project to date. To mark the album’s 20th anniversary, the band is having it stored in DNA molecules.

“This method allows us to archive the music for hundreds to thousands of years,” says Robert Grass, professor at ETH Zurich’s Functional Materials Laboratory.

Listen to a clip from Massive Attack’s “Teardrop” in the same audio quality as on the DNA:


Grass and his colleague Reinhard Heckel, a former ETH scientist now at Rice University, translated the album’s digital audio into genetic code. “While the information stored on a CD or hard disk is a sequence of zeros and ones, biology stores genetic information in a sequence of the four building blocks of DNA: A, C, G, and T,” explains Grass.

In order to keep data volumes manageable, Grass and his colleagues worked on the project using a music file that he had compressed to 15 megabytes using the Opus coding format. Opus is a compression software for audio data that is qualitatively superior to the well-known MP3.

A US company is now in the process of producing 920,000 short DNA strands, which taken together contain all of Mezzanine’s information. TurboBeads, an ETH spin-off, will then pour these molecules into 5,000 tiny (nanometer-sized) glass spheres, each of which contains part of the information. Grass expects the project to be complete in a month or two.

Mezzanine’s “genetic code.” This section corresponds to 1/27,000 of the information of the whole album. (Credit: Robert Grass/ETH Zurich)

Grass and Heckel developed this technology at ETH Zurich three years ago, and stored the text of the Swiss Federal Charter of 1291 in one of these small glass spheres for a technical feasibility study.

“What is new about the project with Massive Attack is that this technology is now also being used commercially,” says Grass. The 15-megabyte music album is the second-largest file ever stored in DNA. Microsoft reported a few months ago that it had stored a collection of files totaling more than 200 megabytes, the only known DNA storage project that is bigger.

The 5,000 glass beads of the Massive Attack album are invisible to the naked eye. They will sit in a tiny bottle of water, with a practically eternal shelf life. The DNA can be removed from the glass beads at any time, allowing the use of DNA sequencing to read the stored music file and play it back on a computer.

“Compared to traditional data-storage systems, it is quite complex and expensive to store information on DNA,” says Grass. “However, once information is stored on DNA, we can make millions of copies quickly and cost-effectively with minimal effort.”

Source: ETH Zurich

The post DNA to store Massive Attack album for near eternity appeared first on Futurity.

Drug dials down intense opioid-related itching

Fri, 2018-04-20 09:48

Chronic itching is a common side effect of opioids—a problem for some people who need the drugs for pain relief and for others fighting addiction.

A new study with mice finds a drug delivers itch relief by targeting particular opioid receptors on neurons in the spinal cord. Nalfurafine hydrochloride (brand name Remitch) is approved in Japan to alleviate itching in dialysis patients with chronic kidney disease and in patients with severe liver disease.

The drug is also being tested for its anti-itch effects in the United States, but until now scientists didn’t understood how it works.

As reported in Cell Reports, the drug targets what’s known as kappa opioid receptors on neurons in the spinal cord and may be effective against many types of chronic itching that don’t respond to conventional drugs such as antihistamines.

While other opioid receptors on the same neurons can ramp up itching, this study shows that activating the kappa receptor significantly dials it down.

“The kappa opioid receptors activate a pathway that tamps down the activity of GRPR, which our lab previously identified as the first itch gene,” says senior investigator Zhou-Feng Chen, professor of anesthesiology and director of the Center for the Study of Itch at Washington University School of Medicine in St. Louis. “This gene relays itch signals from the spine to the brain.”

Chen and colleagues studied mice treated with a substance to make them feel itchy. Others had been genetically engineered to develop chronic itching. When the drug was injected directly into the spinal cords of the animals, their scratching was markedly reduced.

About half of the neurons in the spinal cord that transmit itch signals were found to have kappa opioid receptors, and when those receptors are activated, they inhibit GRPR.

Rheumatoid arthritis drug eases mysterious itch

It may not be practical to administer spinal cord injections of drugs to patients with chronic itch—whatever the cause—but now that a way to alleviate such itching has been identified, researchers can try to activate the same receptor in other ways.

Or, Chen says, they may target some of the downstream molecules that are activated when the kappa receptor is targeted.

“Some molecules downstream from the kappa receptor may still be able to tamp down itching without causing any unwanted side effects that may occur when drugs activate the kappa receptor in parts of the body outside of the spinal cord,” says Chen, who also is a professor of psychiatry and of developmental biology.

‘Orphan’ receptor makes taking opioids so itchy

His team is now working to learn whether those strategies will work in mice, with the hope that the same molecules eventually may become therapeutic targets in people with chronic itch.

The National Institutes of Health and the National Natural Science Foundation of China funded the work.

Source: Washington University in St. Louis

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Activating these ‘keyhole’ receptors stops hunger

Fri, 2018-04-20 08:49

Researchers have characterized a complex, little-understood receptor type that, when activated, shuts off hunger. The findings may open up opportunities to fight obesity at the cellular level.

Jens Meiler, a professor of chemistry and pharmacology at Vanderbilt University, says pharmaceutical companies have long attempted to develop a small-molecule drug that can do just that. But until now, nobody knew exactly what the receptor looked like, making it nearly impossible to design the key to activate it.

“Before, it was like trying to design a key without knowing the shape of the keyhole.”

The researchers determined the first crystal structure for a neuropeptide Y receptor, deciphering the thousands of carbon, oxygen, nitrogen, and other atoms involved with it and how they bind to one another. Meiler and a PhD student in his laboratory, Brian J. Bender, translated the inherently low-quality data about the atoms’ coordinates to build accurate computer models of both the inactive receptor and what it looks like when activated.

“This is a very important milestone in the drug discovery process,” Meiler says. “The big contribution of this paper is to list the atoms with all the specific coordinates of where they are sitting in space and where they are bound to each other. We’ve actually found where there are little pockets in the structure where we can build a small molecule to bind.

“Before, it was like trying to design a key without knowing the shape of the keyhole.”

The next step in this molecular-level research is target validation: proving that the receptor really does control hunger. Past studies revealed that when the receptor is blocked from functioning in mice, they become obese.

“Once you eat, you produce this peptide, it activates the receptor, and then you don’t feel hungry anymore and you stop eating,” Meiler says. “The idea here is that we could upregulate this receptor with a small molecule and create this feeling of not being hungry, so that you eat less.”

Meiler says the new paper is part of a much larger, ongoing study that has already produced starting points for the development of potential small-molecule therapeutics.

Obesity may make ignoring ‘food cues’ even harder

Their findings are published in the journal Nature. Other authors include researchers from the Chinese Academy of Sciences in Shanghai and Leipzig University in Germany.

The Max Kade Foundation and the National Science Foundation support a student exchange that contributed to the work. The National Institute of Health and the National Science Foundation support the research at Vanderbilt.

Source: Vanderbilt University

The post Activating these ‘keyhole’ receptors stops hunger appeared first on Futurity.

‘Sea Monkeys’ show how tiny critters churn ocean

Fri, 2018-04-20 08:23

Swarms of tiny ocean organisms known collectively as zooplankton may have an outsize influence on their environment.

These clusters of centimeter-long individuals, each beating tiny feathered legs, can, in aggregate, create powerful currents that may mix water over hundreds of meters in depth.

Although the work was carried out in the lab, the research is the first to show that migrating zooplankton—or any organism—can create turbulence at a scale large enough to mix the ocean’s waters. The findings could alter the way scientists think about global nutrient cycles like carbon, phosphate, and oxygen, or even currents themselves.

“Ocean dynamics are directly connected to global climate through interactions with the atmosphere,” says John Dabiri, professor of civil and environmental engineering and of mechanical engineering at Stanford University and senior author of the paper in Nature.

“The fact that swimming animals could play a significant role in ocean mixing—an idea that has been almost heretical in oceanography—could therefore have consequences far beyond the immediate waters where the animals reside.”

Deep mixing

The findings could also help scientists understand how the ocean sequesters carbon dioxide from the atmosphere and lead to updates in ocean climate models.

“Right now a lot of our ocean climate models don’t include the effect of animals or if they do, it’s as passive participants in the process,” Dabiri says.

One of the most common zooplankton, krill are among the most abundant marine organisms and migrate daily in giant swarms, heading hundreds of meters deep by day and up to the ocean’s surface by night to feed.

Dabiri knew that in terms of forces that drive the mixing of oceans, wind, and tidal currents are thought to play the largest role. But he wondered if giant zooplankton migrations could also be involved—an idea first proposed by oceanographer Walter Munk in 1966, and since then debated but never systematically explored.

Dabiri and graduate student Isabel Houghton tried to answer that question not in the ocean but in the relatively controlled environment of large water tanks in the lab. The pair worked with Jeffrey Koseff and Stephen Monismith, professors of civil and environmental engineering, to create flow environments that mimic the ocean with saltier water on the bottom of the tank and less salty water on the top. The resulting gradient mirrors ocean conditions that any organism would need to disrupt in order to cycle nutrients between the ocean’s surface and water deep below.

“There’s no appreciable deep mixing of oxygen or carbon dioxide in the ocean if you can’t overcome the stabilizing influence of salinity and temperature gradients,” Koseff says.

Water eddies

In the lab, the group was looking to see whether the tiny organisms they studied—mostly brine shrimp (also known as sea monkeys) as a stand-in for less lab-hardy krill—are simply churning water locally, leaving the gradient intact, or redistributing salt into a more uniform mixture. If they can mix layers in the lab, chances are they can do the same in the ocean.

To carry out the study, Houghton placed brine shrimp in the tank and activated laser or LED lights from either above or below. Because brine shrimp are attracted to light, they migrated toward the source. When she reversed the lights the tiny creatures scurried to the other end in a migration that lasted about 10 minutes.

With cameras closely recording the animals’ movements, researchers were able to measure the individual water eddies surrounding each brine shrimp and the larger currents in the tank. From these, they showed that turbulence from individual organisms aggregates into a much larger turbulent jet in the wake of the migration. What’s more, those flows were powerful enough to mix the tank’s salt gradient.

“They weren’t just displacing fluid that then returned to its original location,” Houghton says. “Everything mixed irreversibly.”

Ocean ‘bathtub drains’ pull flotsam together

Before the current study, scientists thought that krill and other zooplankton could only create turbulence in their own size range—on the order of centimeters. That’s hardly enough to move nutrients on a meaningful scale.

Now it appears that zooplankton have the capacity to mix ocean waters, at least regionally. Furthermore, the findings might not just apply to organisms like krill in the upper kilometer of the ocean, but also to jellyfish, squid, fish, and mammals that swim even deeper, potentially churning the entire water column.

Little diatoms have big influence on ocean nutrients

The findings need to be verified in the ocean, Dabiri says, which will involve finding and following swarms of krill in locations as diverse as the California coast and frigid Antarctic waters.

But if they continue to see mixing at the scales the lab work suggests, the findings could change the way ocean scientists think about the role of animals in influencing their watery environment—and potentially our climate on land.

Source: Stanford University

The post ‘Sea Monkeys’ show how tiny critters churn ocean appeared first on Futurity.

Wireless camera streams HD video with way less power

Thu, 2018-04-19 19:49

Engineers have created a new way to stream HD video from a wireless camera with far less power than current technology.

Wearable cameras offer incredible promise, but because these cameras must use smaller batteries to stay lightweight and functional, these devices can’t perform high-definition video streaming.

The new prototype, however, skips the power-hungry parts and has something else, like a smartphone, process the video instead.

Backscatter breakthrough

The researchers achieve this with a technique called backscatter, through which a device can share information by reflecting signals that have been transmitted to it.

“The fundamental assumption people have made so far is that backscatter can be used only for low-data rate sensors such as temperature sensors,” says paper coauthor Shyam Gollakota, an associate professor in the University of Washington’s Paul G. Allen School of Computer Science & Engineering. “This work breaks that assumption and shows that backscatter can indeed support even full HD video.”

“There could be tiny HD cameras everywhere recording the action: stuck on players’ helmets, everywhere across the stadium. And you don’t have to ever worry about changing their batteries.”

In today’s streaming cameras, the camera first processes and compresses the video before it is transmitted via Wi-Fi. These processing and communication components eat a lot of power, especially with HD videos. As a result, a lightweight streaming camera that doesn’t need large batteries or a power source has been out of reach.

The team developed a new system that eliminates all of these components. Instead, the pixels in the camera directly connect to the antenna, which sends intensity values via backscatter to a nearby smartphone. The phone, which doesn’t have the same size and weight restrictions as a small streaming camera, processes the video instead.

For the video transmission, the system translates the pixel information from each frame into a series of pulses where the width of each pulse represents a pixel value. The time duration of the pulse is proportional to the brightness of the pixel.

“It’s sort of similar to how the cells in the brain communicate with each other,” says coauthor Joshua Smith, a professor in the Allen School and the University of Washington’s electrical engineering department. “Neurons are either signaling or they’re not, so the information is encoded in the timing of their action potentials.”

The team tested their idea using a prototype that converted HD YouTube videos into raw pixel data. Then they fed the pixels into their backscatter system. Their design could stream 720p HD videos at 10 frames per second to a device up to 14 feet away.

“That’s like a camera recording a scene and sending the video to a device in the next room,” says coauthor and computer science and engineering doctoral student Mehrdad Hessar.

Seeing the future in HD

The group’s system uses 1,000 to 10,000 times less power than current streaming technology. But it still has a small battery that supports continuous operation. The next step is to make wireless video cameras that are completely battery-free, says Smith.

The team has also created a low-resolution, low-power security camera, which can stream at 13 frames per second. This falls in line with the range of functions the group predicts for this technology.

The research team also created a low-resolution, low-power security camera, shown here on a stand. It can stream at 13 frames per second to another device, such as a smartphone. (Credit: Dennis Wise/U. Washington)

“There are many applications,” says coauthor and recent electrical engineering alum Saman Naderiparizi. “Right now home security cameras have to be plugged in all the time. But with our technology, we can effectively cut the cord for wireless streaming cameras.”

The group also envisions a world where these cameras are smart enough to only turn on when they are needed for their specific purpose, which could save even more energy.

“This video technology has the potential to transform the industry as we know it. Cameras are critical for a number of internet-connected applications, but so far they have been constrained by their power consumption,” he says.

Why consumers may regret all this free streaming

“Just imagine you go to a football game five years from now,” Smith adds. “There could be tiny HD cameras everywhere recording the action: stuck on players’ helmets, everywhere across the stadium. And you don’t have to ever worry about changing their batteries.”

The team presented their findings April 10 at the Advanced Computing Systems Association’s Symposium on Networked Systems Design and Implementation.

The researchers have licensed the technology to Jeeva Wireless, a Seattle-based startup a team of university researchers founded, including Gollakota, Smith, and Vamsi Talla, a recent alum and coauthor of this paper.

The National Science Foundation, the Alfred P. Sloan Foundation, and Google Faculty Research Awards funded the research.

Source: Sarah McQuate for University of Washington

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Survey finds reasons to worry about U.S. democracy

Thu, 2018-04-19 19:00

A new survey of political science scholars and the general public finds reasons to be concerned about American democracy.

“One of the greatest threats to democracy is the idea that it is unassailable,” is the tagline of Bright Line Watch. Made up of four political scientists, the non-partisan initiative aims to monitor democratic practices in the United States and potential threats to those practices.

The group focuses on democratic institutions such as free and fair elections, checks and balances, and freedom of the press. Born in late 2016, Bright Line Watch found its raison d’être in the widespread concern over the possible erosion of those institutions in this country, says Gretchen Helmke of the University of Rochester.

Listen to Helmke and Mitch Sanders discuss the findings:
 Slow erosion

There are several factors that the scholarship indicates would protect American democracy, says Helmke, adding that the chances of a complete breakdown of democracy in the US—the kind that occurred in the 20th century in parts of Latin America, for example—are slim.

“A military coup-style breakdown is highly unlikely,” she notes. Scholars who have studied the statistical likelihood of that type of breakdown look at such factors as the relationship between levels of wealth in the US—where wealth is comparatively high—and also the age of this country’s democracy. Research shows that the age of a given democracy serves to protect it.

Basically, the longer—the stronger.

But don’t exhale quite yet, cautions Helmke who notes the group’s concern about the gradual and slow erosion of democracy in this country. “That process—where it’s a slow kind of piecemeal challenging of different institutions that support democracy—is something that we see in several parts of the world, and something that we are now seeing in the United States today. It’s very early on so I don’t know what the long-term prospects are, but yes, I think there are reasons to be concerned,” she says.

Explaining their impetus to be watchful, the scholars write that “at a time of potential danger to American democratic norms and institutions, it is more urgent than ever for scholars to highlight the risks to our system of government.” That’s why together they compile quarterly reports, based on careful scientific polling of more than 1,000 political experts and a nationally representative sample of 2,000 members of the public. The latest report is available online.

‘Sobering’ results

The results are “sobering,” say the researchers: Helmke, Brendan Nyhan and John Carey of Dartmouth College, and Susan Stokes of Yale University.

While the public assesses the state of American democracy more negatively than the polled experts, both groups agree that the performance of US democracy has declined since President Trump took office just over a year ago, the researchers conclude in their latest report.

“You can define democracy in a lot of different ways, but all of those involve a connection between the public and the government.”

At the core of their regular surveys is a battery of 27 measures, ranging from free speech and an unimpeded press, to constitutional limits on executive powers, to vote representation, and the independence of the judiciary. On 21 of these 27 democratic principles, the survey finds that the experts’ rating has declined over time.

For example, the latest survey finds that more than 80 percent of the polled experts rate US elections free of overt fraud. Yet, fewer than 15 percent of the experts believe that political leaders generally share a common understanding of relevant facts, or think that elected official try to compromise with their political opponents.

The only principle on which the team saw substantial improvement is that “law enforcement investigations of public officials or their associates are free from political influence or interference.” That statement was first included in Bright Line Watch’s May 2017 survey, which took place soon after President Trump had fired FBI director James Comey—prompting a very low initial rating on the principle, the group reasons.

However, the evaluations improved in the third survey. The team ascribes the rising evaluation to the appointment of Special Counsel Robert Mueller, before again declining somewhat to the present level in the fourth survey. The quartet writes that the survival and independence of the Mueller investigation remains precarious, citing President Trump’s attempted firing of Mueller in June 2017.

Can democracy survive without a middle class?

Overall, the political experts rated 13 democratic principles significantly lower, all of them related to institutional checks and balances. Bright Line Watch found that the expert judgment in the ability of Congress, the courts, or the Constitution to reign in the power of the executive all eroded by 8 to 10 percentage points. The polled experts’ confidence in judicial independence from the elected branches plummeted by 16 percentage points. Results from the general public survey were even more consistently negative.

The public knows

Why does it matter what the public believes about the state of our democracy?

While experts may have a more acute understanding of certain violations, and conversely, of built-in checks and balances, the public’s view remains essential.


“You can define democracy in a lot of different ways, but all of those involve a connection between the public and the government,” says Mitch Sanders, a political scientist with a PhD from the University of Rochester who manages survey methodology for Bright Line Watch. “So, understanding what the public sees as important for democracy, understanding what the public perceives as the extent to which the United States is fulfilling or not fulfilling certain standards—I think that’s a vital part of understanding democracy today.”

Does custom political news hurt democracy?

The public, Sanders argues, would recognize the weakening of democracy.

Helmke says her work made her think of a sentence uttered by President Abraham Lincoln in one of his first speeches, given roughly thirty years before the Civil War. At the time, the 16th President talked about threats to the rule of law and political institutions in the US: “We hope all dangers may be overcome, but to conclude that no danger may ever arise would itself be extremely dangerous.'”

Source: University of Rochester

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Here’s how effective the next flu shot will be

Thu, 2018-04-19 18:45

This fall’s flu shot, a new H3N2 formulation for the first time since 2015, won’t be any more effective than the vaccine given in 2016 and 2017, experts warn.

Researchers say that’s due to viral mutations related to vaccine production in eggs.

Scientists created a method, known as pEpitope (pronounced PEE-epih-tope), more than 10 years ago as a fast, inexpensive way of gauging the effectiveness of proposed flu vaccine formulations.

A new study, which appears in Clinical Infectious Diseases, suggests the pEpitope method is a more accurate predictor of vaccine efficacy than long-relied-upon ferret tests, particularly for data researchers gathered in the past decade. The pEpitope method accounts for 77 percent of what affects the efficacy of the vaccine in humans.

Predicting vaccine efficacy

pEpitope is a computational method that measures critical differences in the genetic sequences of flu strains. In the new study, the method accurately predicted vaccine efficacy rates for more than 40 years of flu records. These included the past two flu seasons in which vaccines offered only limited protection against the most widely circulating strain of influenza A.

“The vaccine has been changed for 2018-19, but unfortunately it still contains two critical mutations that arise from the egg-based vaccine production process,” says Michael Deem, professor in biochemical and genetic engineering and professor of physics and astronomy at Rice University.

“Our study found that these same mutations halved the efficacy of flu vaccines in the past two seasons, and we expect they will lower the efficacy of the next vaccine in a similar manner.”

Full efficacy data for the 2017-2018 flu season are still being compiled, but pEpitope predicted it will be around 19 percent against H3N2, the type of influenza A that infected most people in the US in each of the past two years.

The Food and Drug Administration chose the same vaccine formulation in 2017 and 2016, in part because the dominant circulating strain stayed the same. In 2016, the vaccine had an efficacy of 20 percent, almost identical to the efficacy of 19 percent predicted by pEpitope.

Efficacy is the measure of how effective a vaccine is at protecting the overall population. A 20 percent efficacy means that in a population, 20 percent fewer vaccinated people will get the flu compared to the unvaccinated people.

Making the flu vaccine

Scientists formulate annual flu vaccines to protect against one type of influenza B and two strains of influenza A, one H3N2 strain and one H1N1 strain. The H and N refer to hemagglutinin and neuraminidase, two proteins that cover the outside of invading flu particles that can cause infection when we inhale them. The human immune system targets these particles for destruction based on their H and N sequences, and flu viruses constantly evolve the sequence of amino acids in these proteins to evade detection.

Vaccine makers still produce most flu vaccines with a decades-old process that involves culturing viruses in hundreds of millions of chicken eggs. Because the strain of flu that infects people is often difficult to grow in eggs, vaccine producers must make compromises to produce enough egg-based vaccine in time for fall flu shots. Unintended effects of this process have reduced vaccine efficacy against H3N2 the past two years, Deem says.

How the flu virus makes us sick

“Very often there are egg adaptations,” he says. “There were a couple of these in the vaccine strain the past two seasons that wound up making it a little bit different from the actual circulating virus strain.”

While other papers have examined these mutations using expensive and time-consuming experiments on live ferrets and laboratory cell cultures, Deem and Melia Bonomo used the pEpitope method to rapidly calculate how much the egg-passage mutations would decrease vaccine efficacy in humans.

“In fact, it’s pretty substantial,” says Bonomo, a doctoral student in applied physics. “The original strain used as a reference for the vaccine was basically a perfect match to the dominant circulating strain, and the predicted efficacy would have been around 47 percent. We found that the mutations in two amino acids out of more than 300 in one key region of the hemagglutinin protein were enough to lower efficacy to 19 percent against all circulating strains.”

‘A really bad job’

Deem says egg adaptations like those that reduced the efficacy of vaccines in 2016 and 2017 are unavoidable as long as flu vaccines are produced in eggs. He and Bonomo compared the efficacy of the egg-based vaccine with an experimental vaccine produced from insect cells via reverse genetics.

The cell-based vaccine, which did not have the egg-passage mutations, had a predicted efficacy of 47 percent, the average value of a perfectly matched H3N2 vaccine, Deem says.

For decades, scientists have relied upon ferret models to gauge how flu viruses and flu vaccines will behave in people. But Deem says ferret studies over the past 10 years have been considerably less predictive of human effects than they were in the preceding three decades, and it is unclear why.

“It’s been apparent over the last 10 years that egg adaptations have affected the efficacy of flu vaccines,” he says. “It’s also been apparent that the ferrets have done a really bad job of predicting the reduction of the efficacy due to the egg adaptations. Additionally, it’s been difficult to get data from ferrets because the ferrets’ immune systems have not recognized the vaccines particularly well over the past 10 years.”

Why the flu shot doesn’t always work

Deem says the ferret-based measures are one-third as predictive as the pEpitope method that has consistent performance over decades of flu data.

“When we look at our model over all data and over the last 10 years, we get the same answer,” Deem says. “Whether we use the last 10 years of data or the last 50 years, our theory is very robust.”

The National Science Foundation, via Rice’s Center for Theoretical Biological Physics, and the Welch Foundation funded the research.

Source: Rice University

The post Here’s how effective the next flu shot will be appeared first on Futurity.

Growing liver cancer in the lab may speed up drug testing

Thu, 2018-04-19 11:01

Researchers have developed a method for growing liver cancer cells in the lab.

Liver cancer (hepatocellular carcinoma or HCC) is the fourth leading cause of cancer death worldwide.

A major challenge in developing effective drugs for liver cancer is the inability of current pre-clinical tumor models to accurately replicate features of the cancer and the environment in the human body in which the tumor is located. This has led to many potential drugs to fail in clinical testing.

Seeking to more accurately mimic the tumor environment to grow liver cancer cells, researchers developed models of these kinds of cancerous growths, called patient-derived xenografts (PDX). Although these models provide a more accurate picture of how effective potential cancer drugs would be in humans, they’re also expensive and time-consuming for drug screening.

HCC organoids in culture (Credit: NUS)

Growing these PDX cancer cells in the laboratory (in vitro) would be a more cost effective and faster way to test for drug efficacy. However, attempts to culture these cells robustly have been largely unsuccessful, until now.

The research team managed to grow cancer cells derived from 14 liver cancer PDX on a synthetic 3D scaffold made of a plant-based porous hydrogel.

The researchers engineered the spongy scaffold with optimized biochemical and mechanical properties, to help liver cancer cells maintain their proper shape and function and grow as organoids. By effectively recreating the tumor environment in the liver, researchers can now grow cancer cells from PDX in a petri dish for drug testing.

After growing the cells as organoids for one to three weeks, the team verified that the liver cancer cells in the organoids were alive and reproducing. Additionally, liver cancer cells usually contain specific genetic changes that are absent in healthy liver cells. Most of the organoids retained the same key genetic changes that were in the source PDX cells.

They also maintained an important feature of liver tumors—intra-tumoral heterogeneity. Not all cancer cells within a tumor are the same; distinct populations of liver cancer cells exist within the same tumor and may affect its response to treatment.

The presence of this feature is another advantage that the organoids have over traditional cell culture methods as a pre-clinical model for drug screening. In the latter’s case, all cells are identical.

Another attractive feature of the 3D organoids in scaffold is their small size—a mere 100 microns. These organoids in scaffold can easily fit inside the well of a 96-well microtiter plate (a flat plate with numerous “wells” that function as small test tubes). The microplate has become a standard tool in analytical research and clinical diagnostic testing laboratories. This is a standard platform used for high-throughput drug screening, and enables researchers to test many drugs at the same time.

Through this technology, researchers can use one PDX to produce tens to hundreds of such scaffolds containing organoids. Combined with their ability to recapitulate the genetic features and heterogeneity of the original liver tumors, these tumor avatars have the potential to revolutionize the screening and development of liver cancer drugs for patients.

“The spongy scaffolds were developed to keep normal liver cells happy and also preserve the important properties of liver cancer for drug testing. This could one day allow patients to choose the best treatment based on the drug testing results of their own liver cancer cells,” says Hanry Yu, group leader at the Institute of Bioengineering and Nanotechnology, A*STAR, and the physiology department at the National University of Singapore.

“As a bioengineer, this study truly epitomizes the positive synergy we can achieve in growing patient tumors outside the body by marrying advances in tissue engineering with cancer biology,” research co-leader Eliza Fong adds.

Nanodiamond ‘dye’ offers better look at liver cancer

And the availability of a reliable platform to grow liver cancer patient-derived cells is a major step in personalized medicine, says Toh Tan Boon, who led the research alongside Fong. “We can now use them for increased throughput drug sensitivity testing,” he says.

“Liver cancer is the second most lethal cancer in the world with few chemotherapy options,” says Dan Yock Young, associate professor and head of medicine department at the Yong Loo Lin School of Medicine and the National University Hospital. “This is in part due to our inability to customize effective therapy for individual HCC. The ability to grow cancer cells in vitro affords us the ability to conduct high throughput drug testing to validate drug efficacy before they are used on patients. This is a key step in guiding the use of effective chemotherapy and minimizing treatment futility.”

The researchers report their findings in the journal Biomaterials.

Researchers from National University of Singapore’s physiology and biomedical engineering departments, the Cancer Science Institute of Singapore, the Institute of Bioengineering and Nanotechnology, A*STAR, and the National Cancer Centre Singapore contributed to the work.

Source: National University of Singapore

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Weight might not be why obesity damages knees

Thu, 2018-04-19 10:39

The gut microbiome could be the culprit behind arthritis and joint pain that plagues people who are obese, according to a new study.

Osteoarthritis, a common side effect of obesity, is the greatest cause of disability in the US, affecting 31 million people. Sometimes called “wear and tear” arthritis, osteoarthritis in people who are obese was long assumed to simply be a consequence of undue stress on joints. But researchers now provide the first evidence that bacteria in the gut—governed by diet—could be the key driving force behind osteoarthritis.

As reported in JCI Insight, scientists found that obese mice had more harmful bacteria in their guts compared to lean mice, which caused inflammation throughout their bodies, leading to very rapid joint deterioration. While a common prebiotic supplement did not help the mice shed weight, it completely reversed the other symptoms, making the guts and joints of obese mice indistinguishable from those of lean mice.

The research team, which Michael Zuscik, associate professor of orthopedics in the Center for Musculoskeletal Research, Robert Mooney, professor of pathology and laboratory medicine, and Steven Gill, associate professor of microbiology and immunology, led, fed mice a high fat diet akin to a Western “cheeseburger and milkshake” diet.

“Cartilage is both a cushion and lubricant, supporting friction-free joint movements. When you lose that, it’s bone on bone, rock on rock.”

Just 12 weeks of the high fat diet made mice obese and diabetic, nearly doubling their body fat percentage compared to mice fed a low-fat, healthy diet. Pro-inflammatory bacteria dominated their colons, which almost completely lacked certain beneficial, probiotic bacteria, like the common yogurt additive Bifidobacteria.

The changes in the gut microbiomes of the mice coincided with signs of body-wide inflammation, including in their knees where the researchers induced osteoarthritis with a meniscal tear, a common athletic injury known to cause osteoarthritis. Compared to lean mice, osteoarthritis progressed much more quickly in the obese mice, with nearly all of their cartilage disappearing within 12 weeks of the tear.

“Cartilage is both a cushion and lubricant, supporting friction-free joint movements,” says Zuscik. “When you lose that, it’s bone on bone, rock on rock. It’s the end of the line and you have to replace the whole joint. Preventing that from happening is what we, as osteoarthritis researchers, strive to do—to keep that cartilage.”

Supplementing high-fat diets

Surprisingly, the effects of obesity on gut bacteria, inflammation, and osteoarthritis were completely prevented when researchers added a common prebiotic, called oligofructose, to the high fat diet of obese mice. The knee cartilage of obese mice that ate the oligofructose supplement was indistinguishable from that of the lean mice.

Oligofructose made obese mice less diabetic, but not thinner.

Although rodents and humans can’t digest prebiotics like oligofructose, they are welcome treats for certain types of beneficial gut bacteria, like Bifidobacteria. Colonies of those bacteria chowed down and grew, taking over the guts of obese mice and crowding out bad actors like pro-inflammatory bacteria. This, in turn, decreased systemic inflammation and slowed cartilage breakdown in the mice’s osteoarthritic knees.

Oligofructose even made the obese mice less diabetic, but there was one thing the dietary supplement didn’t change: body weight.

Obese mice that received oligofructose remained obese, bearing the same load on their joints, yet their joints were healthier. Just reducing inflammation was enough to protect joint cartilage from degeneration, supporting the idea that inflammation—not biomechanical forces—drive osteoarthritis and joint degeneration.

“That reinforces the idea that osteoarthritis is another secondary complication of obesity—just like diabetes, heart disease, and stroke, which all have inflammation as part of their cause,” says Mooney. “Perhaps, they all share a similar root, and the microbiome might be that common root.”

Don’t buy a prebiotic just yet

Though there are parallels between mouse and human microbiomes, the bacteria that protected mice from obesity-related osteoarthritis may differ from the bacteria that could help humans. Zuscik, Mooney, and Gill aim to collaborate with researchers in the Military and Veteran Microbiome: Consortium for Research and Education at the US Department of Veteran’s Affairs to move this research into humans.

The team hopes to compare veterans who have obesity-related osteoarthritis to those who don’t to further identify the connections between gut microbes and joint health. They also hope to test whether prebiotic or probiotic supplements that shape the gut microbiome can have similar effects in vets suffering from osteoarthritis as they did in mice.

“There are no treatments that can slow progression of osteoarthritis—and definitely nothing reverses it,” says first author Eric Schott, postdoctoral fellow in the CMSR and soon-to-be clinical research scientist at Solarea Bio, Inc. “But this study sets the stage to develop therapies that target the microbiome and actually treat the disease.”

Source: University of Rochester

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Implant would put a mole on your skin to warn of tumor

Thu, 2018-04-19 10:25

A prototype early warning system for the four most common types of cancer makes a visible mole appear on the skin when calcium levels indicate a tumor has developed.

Many cancer patients only receive a diagnosis after a tumor has developed extensively. This often significantly reduces the chance of recovery: the cure rate for prostate cancer is 32 percent and only 11 percent for colon cancer. The ability to detect such tumors reliably and early would not only save lives, but also reduce the need for expensive, stressful treatment.

Researchers working with Martin Fussenegger, professor at the department of biosystems science and engineering at ETH Zurich in Basel, created a synthetic gene network that serves as an early warning system. It recognizes prostate, lung, colon, and breast cancer at a very early stage.

“The mole does not mean that the person is likely to die soon.”

The early warning system comprises a genetic network that biotechnologists integrate into human body cells, which go into an implant. This encapsulated gene network sits under the skin where it constantly monitors the blood calcium level.

As soon as the calcium level exceeds a particular threshold value over a longer period of time, a signal cascade initiates production of the body’s tanning pigment melanin in the genetically modified cells. The skin then forms a brown mole that is visible to the naked eye.

The mole appears long before the cancer becomes detectable through conventional diagnosis. “An implant carrier should then see a doctor for further evaluation after the mole appears,” explains Fussenegger. It is no reason to panic. “The mole does not mean that the person is likely to die soon,” he stresses. It simply means that clarification and possibly treatment are needed.

Early detection

The researchers used calcium as the indicator of the development of the four types of cancer, as it is regulated strongly in the body. Bones serve as a buffer that can balance out concentration differences. However, too much calcium in the blood may serve as a sign for one of the four cancers.

“Early detection increases the chance of survival significantly,” says Fussenegger. For example, if breast cancer is detected early, the chance of recovery is 98 percent; however, if the tumor is diagnosed too late, only one in four women has a good chance of recovery. “Nowadays, people generally go to the doctor only when the tumor begins to cause problems. Unfortunately, by that point it is often too late.”

The implant also has an additional advantage: “It is intended primarily for self-monitoring, making it very cost effective,” he explains. However, for those who would prefer not to deal with the constant stress, an implant that develops a mark visible only under a red light is also an option. “This regular check could be carried out by their doctor.”

3D printing could make medical implants in hours

The disadvantage is that the service life of such an implant is limited, as Fussenegger has learned from other studies. “Encapsulated living cells last for about a year, according to other studies. After that, they must be inactivated and replaced.”

Next steps

So far, this early warning implant is a prototype; the associated work recently published in the journal Science Translational Medicine is a feasibility study. The researchers have tested their early warning system in a mouse model and on pig skin. It functioned reliably during these tests. Moles developed only when the calcium concentration reached a high level.

Should couples learn to check each other’s moles?

The scientists still have a long way to go before human testing can begin. “Continued development and clinical trials in particular are laborious and expensive, which we as a research group cannot afford,” says Fussenegger. However, he would like to promote the translation of his developments, so that one day they will lead to applicable products. He estimates that bringing such a cancer diagnosis implant to market maturity will take at least ten years of research and development.

The concept of the “biomedical tattoo,” as Fussenegger describes this new finding, would also be applicable to other gradually developing illnesses, such as neurodegenerative diseases and hormonal disorders. In principle, the researchers could replace the molecular sensor to measure biomarkers other than calcium.

Source: ETH Zurich

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Devices ease limitations for doctors with disabilities

Thu, 2018-04-19 09:26

A new device could help doctors with disabilities overcome the challenges of performing standard patient examinations.

Instead of using a traditional stethoscope or otoscope to examine a patient, Molly Fausone, a physician-in-training at the University of Michigan, uses a long, flexible wire with a camera at its tip. A live video feed plays diagnostic information back on her cell phone.

After a swimming accident at age 15 left Fausone paralyzed from the chest down with limited use of her hands, she wanted to stay away from hospitals as much as she could. She spent the first half of her college career at Stanford University exploring her options, thinking maybe she would become an engineer.

The image Molly Fausone sees on her mobile device as she examines patients with the device. (Credit: David Lorch/U. Michigan)

“I wanted to find something I was excited about, and when I took a course in human biology I knew that was what I wanted to do,” she says.

She thought about a career in biological research but medicine was still in the back of her mind. After graduation, she taught biology for a year at Stanford and enjoyed working closely with students.

“I slowly made my way back to medicine after my injury, working in a free clinic in Chicago for two years after teaching at Stanford. I had reached the conclusion that medicine was a good combination of research, interpersonal interactions, and teaching, too,” she says.

Fausone is now a third-year medical student and is determined to become a doctor despite the physical limitations of her disability.

Few doctors with disabilities

Though doctors treat patients with all kinds of disabilities, illnesses, or injuries, doctors themselves rarely have disabilities. While more than 20 percent of Americans live with disabilities, under 2 percent of practicing physicians do.

“Very few universities accept first year medical students who are paraplegic or quadriplegic,” says David Burke, professor and interim chair of the human genetics department. “Historically, certain people have been dissuaded from areas of medicine.

“Most of the imaging systems that doctors use require the doctor to be up against the patient’s ear or mouth, or nose. The physician’s eye has to be collinear with the object being examined. If the patient is lying down, going to the other side of the patient isn’t always possible, as some examination rooms aren’t big enough to take a wheelchair around both sides,” Burke says.

Recognizing that even a straightforward patient examination can pose a major challenge, Burke and David Lorch, program director for the Global Challenges for the Third Century Initiative on Deep Monitoring, started brainstorming, eventually creating a device that allows doctors with disabilities to examine a patient’s skin, eyes, ears, nose, throat, and mouth from a distance.

“Being able to align my eye with a patient’s ear or nose isn’t the critical component of being a doctor,” Fausone says. “The crux of it is finding a problem, interpreting it, and treating it.”

The device has a long, flexible wire and a camera in its speculum, which is the cone-shaped piece at the end of a standard medical otoscope used to examine a patient’s ears. The system displays images on any mobile device.

Other features on the way

Burke and Lorch are working on adding other features. Adding video recording, for example, would provide a variety of opportunities for all doctors, such as looking back at older recordings to see if a condition has changed, sending the recording to a specialist, or using it to teach medical students.

“We now have a set of low-cost technologies that make it easier to build machines that can capture high-quality information from patients and then send it, rather than the physician and the patient needing to physically be in the same place at the same time,” Burke says.

“I think this will be particularly important for remote and underserved populations, places where there are a low density of physicians, especially specialists.”

The live video stream can enhance and zoom in on images to facilitate the physician’s examination. The device has its own WiFi network to ensure recordings are sent safely.

Body feedback could make assisted walking easier

Another challenge Fausone faces is standard neurological examinations that require the physician to exert significant force, such as when the examiner asks the patient to press against his or her hand with the same amount of force.

“We’re using three dimensional tracking technologies so that we can find a way for her to measure a person’s strength and mobility without her having to make direct contact with the patient,” Lorch says.

The device would capture the amount of force a patient exerted, allowing for more accurate measurement compared to a physician’s subjective assessment of the neurological examination. Both Burke and Lorch also note this device could help create more standardization in the medical field.

The goal is for all physicians to use these devices, regardless of whether they have a physical limitation or disability. The option to use them could broaden the opportunities of a medical career for many who otherwise would not be able to meet its demands.

“When we think about disability, we typically think about physical disabilities,” says Donna Omichinski, center coordinator for the University of Michigan Rehabilitation and Engineering Research Center, Technology Increasing Knowledge: Technology Optimizing Choice (TIKTOC RERC).

“There are also invisible disabilities such as hearing impairment or neurodevelopmental disability. Finding ways to adapt and accommodate training within medical professions is not just an issue for doctors with disabilities.

Clothes are more than a hassle for people with disabilities

“This can be an issue for nurses, physical therapists, physician’s assistants, etc. Oftentimes, the environment becomes the factor that limits a person’s function and accessibility, and technology can serve as a bridge to these barriers.”

A grant program from Third Century Initiative Global Challenges funded the force and movement assessing device. The device for examining a patient’s skin, eyes, ears, nose, throat, and mouth is primarily funded by the TIKTOC RERC small grant program.

Source: University of Michigan

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These interruptions slow down E.R. nurses

Thu, 2018-04-19 06:23

Workflow interruptions in the emergency department are most likely to occur as nurses document electronic medical records and while they directly care for patients, research finds.

A new paper in International Journal of Human-Computer Interaction suggests that changes could increase efficiency and help patients.

“Our analysis showed that when emergency department nurses were interrupted in patient care activities, their workload was about two times higher,” says Jung Hyup Kim, assistant professor in the industrial and manufacturing systems engineering department at the University of Missouri.

“When electronic medical documentation was added to those tasks, the workload was about four times higher than in a non-interruption scenario.”

Kim and a team of graduate and undergraduate students traveled to the Mayo Clinic in Rochester, Minnesota, to study how brief interruptions affected nurses in the emergency department.

The “time and motion” study was completed over the course of a week, during which Kim and his team observed a group of experienced nurses and studied their tasks.

For better patient care, prevent nurse burnout

After noting the ED nurses’ most frequent tasks, they broke them down into eight basic categories, such as direct care, documentation, social breaks, and other tasks including supervision and education. They also noted the five most common interruptions to the nurses’ work included phone calls, colleagues, residents, doctors, and relatives of the patient.

The researchers then used the information to create two simulation models—one illustrating how efficient the workflow was without interruption and another to illustrate the potential effects of interruptions on tasks. The model was used to reach the conclusions regarding the higher workloads after interruptions during EMR documentation and patient care.

Tough cases scar nurses, but this program can help

“Our study showed that ED nurses should be trained to avoid answering questions or non-emergency phone calls while delivering direct care to patients and while engaged in EMR documentation,” Kim says. “Also, relatives of patients should allow the health care worker to perform critical duties without interruption.”

Source: University of Missouri

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How volcanic rock traps CO2 and turns it inert

Wed, 2018-04-18 19:16

New research shows how effective injecting carbon dioxide (CO2) into the volcanic rock basalt could be for fighting carbon emissions.

Burning fossil fuels produces carbon dioxide. As the gas rises and the atmosphere traps it, it retains heat as part of a process called the greenhouse effect. The increased temperatures associated with the greenhouse effect can cause melting ice caps, higher sea levels, and a loss of natural habitat for plant and animal species.

Environmental scientists trying to mitigate the effects of CO2 have experimented with injecting it deep underground, trapping it. These trials have mainly taken place in sandstone aquifers, however, the CO2 primarily remains present as a bubble that can return to the surface if is there are fracture in the capping formation.

A different approach using basalt flows as injection sites—chiefly at the CarbFix site in Iceland and in Washington state—has yielded dramatic results. Metals in basalt have the ability to transform CO2 into a solid inert mineral in a matter of months.

While the new method holds promise, the underground injections can be imprecise, difficult to track and measure. The new research sheds light on what happens underground after injecting CO2 into basalt.

“In a field site, you inject the carbon dioxide in, and it’s a very open system,” says Daniel Giammar, professor of environmental engineering in the School of Engineering & Applied Science at Washington University in St. Louis. “You can’t get a good constraint in terms of a capacity estimate. You know you made some carbonate from the CO2, but you don’t really know how much. In the lab, we have well-defined boundaries.”

To obtain a clearer, quantifiable look at carbon trapping rates in basalt, Giammar collected samples of the rock from Washington state, where researchers previously injected a thousand tons of CO2 gas deep underground into a basalt flow. He placed the rocks in small reactors that resemble slow cookers to simulate underground conditions, and then injected CO2 to test the variables involved in the carbonization process.

“We reacted it at similar pressure and temperature conditions to what they had in the field, except we do all of ours in a small sealed vessel,” Giammar says. “So we know how much carbon dioxide went in and we know exactly where all of it went. We can look at the entire rock afterwards and see how much carbonate was formed in that rock.”

Watch: Greater animal diversity means more trapped carbon

The lab kept the basalt in the pressurizers and followed up, using 3D imaging to analyze their pore spaces at six weeks, 20 weeks, and 40 weeks. They watched moment to moment the CO2 turned into mineral, saw the exact voids within the basalt it filled, and observed the precise spots in the rock where the carbonization process began.

Once they collected and analyzed all of the data, Giammar and his team predicted that one cubic meter of basalt could convert 47 kilograms of CO2 into mineral. Researchers can use this estimate as a baseline to scale up, quantifying how much CO2 entire areas of basalt flow can effectively convert.

“People have done surveys of available basalt flows,” Giammar says. “This data will help us determine which ones could actually be receptive to having CO2 injected into them, and then also help us to determine capacity. It’s big. It’s years and years worth of US CO2 emissions.”

Giammar’s lab is currently sharing its results with colleagues at the University of Michigan, who will assist in developing a computational model to further help researchers to look for a solid fix for CO2 abatement. The researchers have also been invited to take part in the second phase of the US Department of Energy’s Carbon Storage Assurance Facility Enterprise, or CarbonSAFE, which investigates new technologies for CO2 abatement.

U.S. forests could be storing tons and tons more carbon

The researchers report their findings in the journal Environmental Science & Technology Letters.

The US Department of Energy funded the research. Additional collaborators are from the Pacific Northwest National Laboratory and Washington University.

Source: Washington University in St. Louis

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Tungsten in drinking water builds up in bones

Wed, 2018-04-18 19:10

New research could add to doubts over the once-universal assumption that tungsten poses little or no health risk to the general human population.

The study shows how and where tungsten accumulates in bones of mice exposed to the element through drinking water.

With the highest melting point of any metal, tungsten’s remarkably high density and hardness make it a prized ingredient in a range of industrial, military, and medical applications. Used in cutting tools, ammunition, medical devices, and even some medications, the metal has become part of our daily lives.

While many regulatory agencies have set limits on exposure to airborne tungsten dust—primarily to protect workers who mine and process the metal—there are very few officially mandated limits on water-soluble tungsten compounds, to which a broader cross-section of the community are at risk of exposure.

Tungsten in the water

The issue came to prominence in the early 2000s when scientists investigated a possible link between a cluster of childhood leukemia cases in Fallon, Nevada, and high levels of tungsten in the groundwater from which the town drew its supply. The case prompted the US Centers for Disease Control and Prevention to nominate tungsten for toxicology and carcinogenesis studies.

To date, research into tungsten’s toxicity and possible role as a carcinogen has produced mixed results. Some studies have shown that other communities exposed to tungsten levels comparable to those in Fallon were not affected by a higher-than-normal incidence of cancer—a finding that appeared to exonerate tungsten. But subsequent research has revealed that in subjects exposed to both tungsten and cobalt, tungsten appears to augment the toxicity of the other substance.

These findings pointed to a need to better understand how tungsten accumulates in the body and in what form, and to what extent the body is capable of eliminating tungsten following exposure.

Chronic exposure from within

The new study on tungsten exposure in mice, published in Communications Chemistry, used powerful x-ray spectroscopy techniques to find answers to these questions. The results raise a number of concerns.

With the body unable to clear tungsten from the cortex, the bone effectively becomes a source of chronic exposure.

While researchers have previously shown that tungsten accumulates in bone, McGill University researchers have discovered that the element didn’t accumulate uniformly across bones; rather, it was concentrated in certain hot spots.

“We found that tungsten, once thought to be non-toxic and inert, does in fact accumulate heterogeneously in bone,” says Cassidy VanderSchee, lead author of the study and doctoral student in the chemistry department at McGill. “Not only that, we found that it accumulated in a chemically different form to that in which it was administered, which confirmed that tungsten is chemically active in the body.”

The study shows that in mice exposed to high levels of tungsten through drinking water, the element accumulated in specific regions—bone marrow and porous (or “cancellous”) bone tissue—to a degree 10 times greater than background levels. The deposition of tungsten in cancellous bone suggests the element is incorporated during bone growth and remodeling, indicating that young, growing individuals are particularly susceptible.

The researchers also found that the bone’s hard outer layer—the cortex—retained tungsten even after the mice were given tungsten-free water for a period of eight weeks after initial exposure. With the body unable to clear tungsten from this tissue, the bone effectively becomes a source of chronic exposure.

Of even greater concern was the finding that tungsten was changing form in the body. The results show that the element was accumulating in a form resembling phosphotungstate, a known chemical catalyst with significant potential to intervene in the biological processes that occur in bone marrow and cancellous bone—immune cell formation and bone growth among them.

“We believe that many of the biological effects of tungsten we’ve been investigating will be traced back to changes in the bone,” says Koren Mann, associate professor of oncology and a coauthor of the study. “This includes the effects on the immune system, stem cells, and cancer.”

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“While research continues into the health risks posed by human exposure to tungsten, our study provides important insights into how the element accumulates in the body—findings that are crucial to developing effective therapies for removing it,” says chemistry professor and senior author Scott Bohle.

The research took place in collaboration with scientists at the Canadian Light Source synchrotron in Saskatoon, Saskatchewan, and the US Department of Energy’s National Synchrotron Light Source II facility at Brookhaven National Laboratory in Upton, NY.

Funding for the research came from the Natural Sciences and Engineering Research Council of Canada, Canadian Institutes of Health Research, and the Canada Research Chairs Program.

Source: McGill University

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ALS-linked protein clusters may actually protect neurons

Wed, 2018-04-18 19:05

Protein clusters thought to be tied to amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, may actually protect—not harm—neurons.

Autopsy studies of ALS patients often reveal the accumulation of large, fibrous aggregates of a protein called SOD1 in disease-affected motor neurons. Researchers have hypothesized that these fibrils are what kill neurons and cause ALS in some people, but the new study, which appears in the Proceedings of the National Academy of Sciences, contradicts that.

“This is potentially an important finding not only for ALS research but for neurodegenerative disease research in general, because the formation of fibril aggregates is so common in these diseases,” says senior author Nikolay Dokholyan, a professor of biochemistry and biophysics at the University of North Carolina at Chapel Hill.

This suggests SOD1 fibrils aren’t the problem in SOD1-linked ALS; they might be a solution.

Large, often fibril-type protein aggregates are in fact the most obvious pathological features of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, ALS, and other major neurodegenerative diseases. Scientists designed many of the candidate drugs developed in recent years to clear these protein aggregates. But none of these fibril-targeting strategies have proven effective in large clinical trials. Laboratory studies have also largely failed to prove that large SOD1 fibrils are harmful to neurons.

At the same time, researchers have found that much smaller protein clusters called oligomers—made of only a few copies of these proteins—can be highly toxic to motor neuron-like cells grown in the lab and thus are more likely to be the chief causes of brain-cell death in these diseases.

In a 2016 study, for example, Dokholyan’s lab found evidence that “trimer” structures made of just three copies of the SOD1 protein are toxic to the type of neuron affected in ALS.

For the new study, Dokholyan’s team, including lead author Cheng Zhu, a postdoctoral researcher in his lab, conducted complicated experiments to compare how trimers affect neurons to how larger fibrils affect neurons.

“One challenge is that the smaller structures such as trimers tend to exist only transiently on the way to forming larger structures,” Zhu says. “But we were able to find an SOD1 mutation that stabilizes the trimer structure and another mutation that promotes the creation of the larger fibrils at the expense of smaller structures. So, we were able to separate the effects of these two species of the protein.”

The researchers expressed the mutant SOD1 proteins in test cells that closely resemble the muscle-controlling neurons killed in ALS. They found—as they did in the 2016 study—that when these cells expressed SOD1 mutants that predominantly form trimers, the cells died much more quickly than control cells containing normal SOD1. The trimer-expressing cells even died more quickly than cells expressing mutant forms of SOD1 that are found in severe hereditary ALS cases.

“Looking at various SOD1 mutants, we observed that the degree of toxicity correlated with the extent of trimer formation,” Zhu says.

On the other hand, the viability of cells containing mutant SOD1 that strongly forms fibrils but suppresses trimers tended to be similar as wild-type SOD1, suggesting that the fibrils are protective, not merely less toxic.

This suggests SOD1 fibrils aren’t the problem in SOD1-linked ALS; they might be a solution.

“Taking a drug to promote fibril formation could be one way to reduce toxicity in SOD1-ALS,” Dokholyan says.

ALS shares genetic links with rare dementia

An alternative strategy, he notes, would be to limit the formation of trimers or other small, toxic SOD1 oligomers. SOD1 normally works in cells as a two-copy structure, a dimer. Trimers and other abnormal structures appear to originate when the dimers fall apart. So Dokholyan and colleagues are looking for potential drug molecules that can stabilize the dimers.

SOD1 is linked to a significant proportion of ALS cases. Mutations in the SOD1 gene account for about 12 percent of ALS cases that run in families. All of these mutations destabilize the protein’s normal structure and promote abnormal SOD1 structures. SOD1 mutations also appear to account for about 1.5 percent of cases that do not obviously run in families.

“Although SOD1-associated ALS represents a small fraction of all ALS cases, uncovering the origins of neurotoxicity in SOD1 aggregation may shed light on the underlying causes of an entire class of neurodegenerative diseases,” Dokholyan says.

The next steps for Dokholyan’s lab is to pinpoint downstream cellular mechanisms of toxicity of pathological trimeric SOD1 and find drugs that mitigate the formation of trimers.

Additional study authors are from UNC at Chapel Hill. The National Institutes of Health funded this work.

Source: University of North Carolina at Chapel Hill

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Stressed out cells stash RNA to keep it safe

Wed, 2018-04-18 18:45

When stress strikes, our cells focus on socking away the important stuff—free-floating material that relays genetic information and helps them grow and divide.

The speed and accuracy of this activity may have a lot to do with development of diseases like cancer and nerve-killing conditions such as Alzheimer’s and Lou Gehrig’s diseases, researchers say.

Stress granules as safe harbors

To store the material safely, cells use something called a “stress granule.”

These tiny bundles of protein and genetic material have fascinated cell biologists for years. They show up as dark, dense areas in electron microscope images of cells that have been stressed by heat, chemicals, or a buildup of imperfect cell products.

Researchers have probed the many proteins that can make up stress granules by carefully picking them apart.

But the genetic material inside them—in the form of messenger RNA, or mRNA—has resisted the same level of analysis. Each mRNA strand acts as the intermediate step between the instructions encoded in a gene and the protein that the cell can make from those instructions.

Generally, scientists have assumed that cells bind up whatever snippets of RNA happen to be floating in the cell’s cytoplasm when stress strikes, snatching them indiscriminately to protect them from harm.

The new research, however, suggests that cells act much more strategically.

Preferential treatment

In a new paper in Molecular Cell, researchers show that cells focus on squirreling away the mRNA sequences that have the most to do with cell growth and proliferation.

The study gives the first side-by-side look of the impacts of different stresses on stress granule mRNA composition.

The reactions vary by circumstance. For instance, when the cell’s own product-packaging machinery (the endoplasmic reticulum) gets bogged down with misfolded proteins, certain mRNAs get pulled into stress granules, the team finds.

Meanwhile, when a chemical- or heat-based stress is applied, cells might stash away other mRNAs.

No matter what, the researchers found, stress granules generally bind up longer bits of mRNA and ones that contain certain sequences called AREs (adenylate-uridylate-rich elements). Those AREs appear to play a key role in attracting the specific mRNAs that will be bundled into granules.

“We know that RNA complexed with protein is in there—and, in fact, that RNA is the major component of stress granules,” says Jun Hee Lee, professor of molecular and integrative physiology at University of Michigan. “But only recently have we analyzed their function, how they localize to the stress granule and how that affects cell physiology.”

Lee and colleagues isolated all the messenger RNA in cells that they had subjected to stress and ones that they hadn’t. The team used next-generation sequencing to spell out the mRNA sequences and figure out which genes they corresponded to.

“Not all RNAs get sequestered, and ones that are essential for cell survival and growth were preferentially sequestered into granules,” says Lee. “It’s as if the cells are putting the brakes on their own growth.”

Protecting valuable assets

One of the key types of mRNA that Lee and his colleagues found in stress granules was the type generated by proto-oncogenes. In their normal form, such genes are crucial to regular cell growth. But a mutation in them can lead to out-of-control growth and development—in other words, cancer.

A little bit of stress keeps aging cells robust

The fact that cells preferentially sequestered proto-oncogene products into stress granules indicates their importance, but also reinforces previous findings that stress granule dysregulation is closely linked to cancer.

Lee and his team are now working on further studies to find out how cancer throws off the granulation process.

They’re also looking at the mix of mRNA found in stress granules in nerve cells—the kind of cells that die out in amyotrophic lateral sclerosis (also called Lou Gehrig’s disease) and Alzheimer’s disease. Other research has shown that stress granules accumulate in such cells, and hinted that the granules themselves may be defective.

Still, there is much more to learn.

“Stress granule formation can be a universal mechanism for cells to deal with stresses of all kinds, but we still don’t understand how cells form these granules, nor what happens to the mRNA inside them once the stress eases and conditions become more favorable,” says Lee. “Perhaps the proteins involved in granulation are also involved in unwinding the mRNA and allowing it to continue toward its intended use to drive protein production.”

Just as most stockbrokers go back to normal trading after the adverse financial conditions have eased, Lee suspects that cells may become less conservative in their mRNA traffic after stress has passed. And whether it’s money or living cells at stake, the goal is the same: preserve precious assets, and grow them.

Source: University of Michigan

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Longer lives mean more people will have dementia

Wed, 2018-04-18 11:08

The rate of older Americans with dementia is on the decline, but the growing number of people 85 or older will roughly double in the next 20 years. That means the actual number of people will increase substantially, a new study warns.

More than 45 million people worldwide have the condition and the impact on both them and the people who care for them is significant.

Its economic impact, including unpaid care provided by families, is estimated to be about $800 billion annually, says Robert Schoeni, a professor at the University of Michigan Institute for Social Research, Gerald R. Ford School of Public Policy, and department of economics.

Schoeni and colleagues Vicki Freedman and Ken Langa led a special supplement to the Journals of Gerontology, Series B: Psychological Sciences and Social Sciences that examines trends in dementia across the United States.

“The overall favorable trend seems to be linked to higher education levels among today’s older Americans,” says Freedman. “But substantial gaps remain between more and less educated groups.”

The supplement stems from a May 2017 workshop that aimed to broaden the understanding of dementia trends, including a study that examines how education levels influence life expectancy.

Other studies look at the impact of cardiovascular disease. Reducing cardiovascular diseases and other chronic diseases is critical for the health of individuals and families, but because such advantages allow people to live to older ages when dementia is more common, the number of cases may not decrease.

“By far the most powerful way to lower both the proportion and number of people with dementia is to develop prevention strategies and treatments that would directly delay the onset…,” says Langa, a research professor at the Institute for Social Research and Institute for Healthcare Policy and Innovation, professor of internal medicine, and research scientist at the Veterans Affairs Ann Arbor Center for Clinical Management Research.

Exercise may be #1 way to prevent dementia

In addition to the overall decline in dementia prevalence, the supplement’s studies show the following:

  • Some groups of older adults in the United States are living fewer years with dementia.
  • Racial and socioeconomic disparities are large and not diminishing.
  • Rising levels of education partially account for the decline, but more research is needed to understand the role cardiovascular risk factors.
  • Reducing the incidence of diabetes and hypertension in midlife will increase the future number of cases of dementia because people will live longer.Therefore, postponing the onset of dementia directly is the most effective way to further reduce the size of the population living with dementia.

Source: University of Michigan

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Know-it-alls are more ignorant than they’ll admit

Wed, 2018-04-18 11:07

People who think their knowledge and beliefs are superior to others are especially prone to overestimating what they actually know, new research suggests.

Even after getting feedback showing them how much they didn’t know relevant political facts, these people still claimed that their beliefs were objectively more correct than everyone else’s. On top of that, they were more likely to seek out new information in biased ways that confirm their sense of superiority.

The study focused on people who profess “belief superiority”—or thinking their views are superior to other viewpoints—as it relates to political issues. The researchers note that people also claim belief superiority in a variety of other domains besides politics, such as the environment, religion, relationship conflicts, and even relatively trivial topics such as etiquette and personal preferences.

“Whereas more humble participants sometimes even underestimated their knowledge, the belief superior tended to think they knew a lot more than they actually did…”

The research used several studies to answer two key questions about political belief superiority: Do people who think that their beliefs are superior have more knowledge about the issues they feel superior about? And do belief-superior people use superior strategies when seeking out new knowledge?

To answer the first question, participants reported their beliefs and feelings of belief superiority about several political topics. Researchers asked them how much they thought they knew about these topics and then had them complete quizzes testing their actual knowledge about those issues.

Across six studies and several political topics, people who were high in belief superiority thought that they knew a great deal about these topics. However, when comparing this perceived knowledge to how much people actually knew, they found that belief-superior people were consistently overestimating their own knowledge.

“Whereas more humble participants sometimes even underestimated their knowledge, the belief superior tended to think they knew a lot more than they actually did,” says Michael Hall, a psychology graduate student at the University of Michigan and the study’s lead author.

For the second question, researchers presented participants with news articles about a political topic and asked them to select which ones they would like to read. Half of the articles supported the participants’ own point of view, whereas the other half challenged their position.

Belief-superior people were significantly more likely than their modest peers to choose information that supported their beliefs. Furthermore, they were aware that they were seeking out biased information: when the researchers asked them what type of articles they had chosen, they readily admitted their bias for articles that supported their own beliefs.

“We thought that if belief-superior people showed a tendency to seek out a balanced set of information, they might be able to claim that they arrived at their belief superiority through reasoned, critical thinking about both sides of the issue,” Hall says.

Does custom political news hurt democracy?

Instead, researchers found that these individuals strongly preferred information that supported their views, indicating that they were probably missing out on opportunities to improve their knowledge.

So why do people seem to shun opposing viewpoints? Researchers suggest that while some people insist that they are always right, all of us feel good when the beliefs we think are important are confirmed.

In other words, when a belief is strongly held, is tied to one’s identity or values, or is held with a sense of moral conviction, people are more likely to distance themselves from information and people that challenge their belief.

“Having your beliefs validated feels good, whereas having your beliefs challenged creates discomfort, and this discomfort generally increases when your beliefs are strongly held and important to you,” says study coauthor Kaitlin Raimi, assistant professor of public policy.

The findings appear in the Journal of Experimental Social Psychology.

Source: University of Michigan

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