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Updated: 7 min 23 sec ago

Reducing ‘stress granules’ may slow Alzheimer’s

7 hours 24 min ago

Reducing “stress granules,” gritty blobs of RNA that form when things like heat, viruses, or toxins stress a cell, may be a new way to fight Alzheimer’s disease.

A slice of brain riddled with Alzheimer’s disease holds two unmistakable hallmarks: balled-up beta-amyloid plaques, clustered outside damaged nerve cells, and spaghetti-like tangles of tau protein sprawling inside.

For decades, researchers have tackled Alzheimer’s by attacking these plaques and tangles; clear them from the brain, they reason, and we can treat this disease. But so far, it hasn’t worked.

In a paper in Nature Neuroscience, Wolozin and his team report that reducing the level of stress granules in mice changed the type and amount of tau clumping in their brains and produced significant benefits in life span and memory.

The findings offer a new understanding of the biology of Alzheimer’s disease and may eventually offer new targets for drug treatments.

‘A new chapter’

“This is a pretty big new chapter in the study of Alzheimer’s disease,” says senior author Benjamin Wolozin, a professor of pharmacology and experimental therapeutics and neurology at the Boston University School of Medicine.

“The cell says, ‘uh-oh, I’m not going to worry about being a great person right now. I’m just going to deal with this stress.'”

“Amyloid is still toxic. Tau is still toxic. Those are still important targets. But there’s this whole other pathway that you can really go in and start drugging.”

When a cell gets stressed out, Wolozin explains, it can act just like a person—hunkering down, stopping all unnecessary activities, and waiting for the storm to pass.

“The cell says, ‘uh-oh, I’m not going to worry about being a great person right now,'” he says. “‘I’m just going to deal with this stress.'”

For a cell, this means blocking RNA segments that are busily doing the non-essential, daily work of the cell. Molecules called RNA-binding proteins scurry out of the nucleus, round up the RNA into stress granules for safekeeping, and then, when the stress ends, release them to get back to business.

At least, that’s how it’s supposed to work. In neurological diseases like ALS and Alzheimer’s, the stress granules overstay their welcome.

“Something that is supposed to be transient ends up being chronic,” says Peter Ash, a postdoctoral fellow in Wolozin’s lab and second author of the paper.

The first surprise

A few years ago, Wolozin’s team discovered these persistent stress granules in the tau tangles of Alzheimer’s patients. Their finding, published in Cell Reports in 2016, zeroed in on a specific RNA-binding protein called TIA1, which is almost always found in stress granules.

What would happen, wondered Wolozin, if they could reduce the amount of TIA1 in a mouse? Would it lower the production of stress granules and somehow protect against dementia? They decided to find out.

The team started with mice that were genetically engineered to express a mutation in the tau gene. In humans, this mutation causes toxic tau to build up in the brain, leading to withering of the frontal and temporal lobes, as well as dementia.

“The mice start to accumulate tau in their brains after about three months,” says Ash. “After about six months, they start to show severe behavioral problems; and by nine months, they nearly all die.”

One gene can both cause and prevent Alzheimer’s damage

The scientists then bred a group of these mice to be born with only one copy of the gene for TIA1, instead of the normal two. They watched all the mice grow, and what happened next was striking.

On schedule, the tau mice started to show signs of brain atrophy: limb weakness, hunched posture, and worsening performance on behavior and memory tests. By contrast, the mice with one copy of the TIA1 gene knocked out showed no signs of mental or physical decline at six months and lived 21.5 percent longer than their counterparts.

“These mice still are affected by disease and die prematurely,” says Dan Apicco, first author of the Nature Neuroscience paper and now a postdoctoral scientist at Biogen. “The process just happens much less rapidly.”

Another surprise

When the scientists autopsied the mouse brains, they found another surprise. The brains showed protected nerve cells and a healthy cortex, a far cry from the atrophied brains of their counterparts. But weirdly, the healthy brains showed far more tangles of tau.

“It’s pretty unheard of to create more tangles and show mice getting better.”

“This mouse model makes five times as much tau protein; in our experiment, we’re not getting rid of it, and yet we’re still getting protection,” says Wolozin, who is the cofounder and chief scientific officer of Aquinnah Pharmaceuticals, which is currently developing drug therapies that target activity of the TIA1 gene as a way to treat Alzheimer’s. “And we said, ‘that’s weird.'”

“It’s pretty unheard of to create more tangles and show mice getting better,” adds Apicco. “It was so much of a surprise that I initially assumed that I had mixed up my samples.”

He hadn’t. Investigating further, the scientists found that the big tangles of tau were made up of very long strands, or fibrils, of protein, which are thought to be less toxic to the brain than shorter segments. Nobody knows why the long strands seem to be better for your brain; the scientists guess that many little segments of tau have more opportunity to wreak havoc in a cell, rather than longer segments all clumped together.

Protein worsens brain damage from Alzheimer’s ‘toxic tangles’

While the scientists note that mouse models of Alzheimer’s have been historically bad at predicting what’s going to work in the clinic, they remain hopeful that this research offers a new way of attacking the disease.

“What makes me personally excited about this finding is that we’re not just reducing tau in these animals; we’re changing the way that tau aggregates,” says Apicco. “This is adding a completely new target that might be successful in humans. It’s definitely a new approach, which is always exciting.”

The National Institutes of Health, the Alzheimer’s Association, the Cure Alzheimer’s Fund, and others fund Wolozin’s work.

Source: Boston University

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Wheat genome comes together like jigsaw puzzle

7 hours 44 min ago

Researchers have sequenced the genome of the species of wheat most commonly grown for making bread, Triticum aestivum.

“After many years of trying, we’ve finally been able to produce a high-quality assembly of this very challenging genome,” says Steven Salzberg, professor of biomedical engineering and genetic medicine at Johns Hopkins University and author of the paper in the journal GigaScience outlining the near-complete DNA sequencing of the wheat.

“It’s like trying to put together a jigsaw puzzle of a landscape scene with a huge blue sky.”

The same research team was also involved in sequencing the bread wheat’s “ancestor,” Aegilops tauschii. The journal Nature published a separate report on that achievement.

Together, the wheat genome sequences can help biologists better understand the evolutionary history of wheat, and may also advance the quest for hardier, more pest- and drought-resistant wheat types to help feed the world’s growing population, the scientists say.

Bread wheat has one of the most complex genomes known to science, containing an estimated 16 billion base pairs of DNA and six copies each of seven chromosomes, the scientists say. The human genome is roughly one-fifth that size, with about 3 billion base pairs and two copies of 23 chromosomes.

Previously published versions of the bread wheat genome have contained large gaps in its highly repetitive DNA sequence.

“The repetitive nature of this genome makes it difficult to fully sequence,” Salzberg says. “It’s like trying to put together a jigsaw puzzle of a landscape scene with a huge blue sky. There are lots of very similar small pieces to assemble.”

It took a year for the team to assemble 1.5 trillion bases of raw data into a final assembly of 15.34 billion base pairs.

To do it, the team used two types of genome sequencing technology: high throughput and nanopore sequencing.

Mapping firefly genomes is beautiful work

As its name implies, high throughput sequencing generates massive amounts of DNA base pairs very quickly and cheaply, although the fragments are very short—just 150 base pairs long for this project.

To help assemble the repetitive areas, the team used nanopore sequencing, which forces DNA through tiny pores with an electric current running through them. The technology enables scientists to read up to 20,000 base pairs at a time by measuring changes in the flow of the current as a strand of DNA passes through the pore.

Salzberg says that sequencing a genome of this size requires not only genetic expertise, but also very large computing resources available at relatively few research institutions around the world. The team used approximately 100 CPU years to put this genome together.

Salzberg and his team also participated in the collaborative effort to sequence Aegilops tauschii, commonly referred to as goatgrass and still found in parts of Asia and Europe. Its genome is approximately one-third the size of the bread wheat genome, but has similar levels of repetition. The work took about four years.

Salzberg’s colleagues on the bread wheat study are from Johns Hopkins University; Pacific Biosciences in Menlo Park, California; and the Earlham Institute in the United Kingdom. The National Science Foundation and National Human Genome Research Institute helped to fund the project.

Cactus genomes reveal complex family tree

Salzberg worked with researchers from the University of California, Davis and the University of Georgia for the Aegilops tauschii research.

Source: Johns Hopkins University

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Method demystifies the center of our chromosomes

Mon, 2017-11-20 19:30

A new technique could give scientists access to the “final frontier” of our DNA—the centromere.

It’s in nearly every one of our cells, at the center of every X-shaped chromosome, and it plays a crucial role in the everyday cell division that keeps us healthy. Which also makes it a key suspect in birth defects, cancers, and other diseases that arise from cell division problems.

“With this technique, we and others can study their genetics, and epigenetics, in a real-time, user-friendly way.”

Already, the first test of the approach has yielded clues about the role of centromeres in Down syndrome, which arises when a child inherits an extra copy of chromosome 21.

Soon, the technique’s developers at the University of Michigan Medical School hope it will accelerate research on other conditions that may have roots in centromere-related problems.

“We now have the opportunity to understand the dynamics of centromeres, and how these sequences expand or contract during evolution and/or disease processes,” says Rafael Contreras-Galindo, lead author of the new paper and an assistant professor of internal medicine.

“We can now understand at which centromeres in specific chromosomes key centromere proteins sit and form the kinetochores that are vital to cell division. With these studies, we can begin to understand how centromere DNA instability could affect centromere function, as we appear to see in Down syndrome.”

Faster genetic analysis

In a new paper in Genome Research, the researchers describe the technique they developed and its first test. In essence, it changes the analysis of centromere DNA from a long, labor-intensive task to a fast and relatively easy one that can accelerate research on centromere-related diseases.

“Centromeres are important for cell division, but poorly understood from a genetic standpoint…”

Their approach is based on the discovery of unique DNA repetition patterns found in the centromere of nearly every chromosome. Their new catalog of these chromosome-specific patterns makes it possible to use a DNA-amplifying tool called polymerase chain reaction, or PCR.

The massive repeated sections of DNA that make up most of every centromere have made the structures hard to sequence and study in the past because the same long stretches appear on every chromosome.

So most centromere researchers have studied the proteins and other molecules that interact with centromeres—factors referred to as epigenetics—rather than the DNA itself.

But the new approach harnesses small chromosome-specific variations and uses them as PCR primers. This makes it fast and easy for researchers to recognize the centromeres of almost every chromosome in a cell, and tell them apart, in just half an hour.

“Centromeres are important for cell division, but poorly understood from a genetic standpoint because the DNA sequences in them are very repetitive,” says David Markovitz, senior author of the new paper and a professor of internal medicine. “With this technique, we and others can study their genetics, and epigenetics, in a real-time, user-friendly way.”

Down syndrome insights

In the new paper, Contreras-Galindo, Markovitz, active emeritus professor Mark Kaplan, and a team of collaborators report results from their comparison of centromeres from individuals with and without Down syndrome.

They show a strong link between the condition and instabilities found on chromosome 21—both in the centromere and in the stretches of DNA that flank it, called pericentromeres.

Unstable centromeres and pericentromeres could help explain why people with Down syndrome inherit an extra copy of that chromosome, though much work remains to test this hypothesis.

After all, as every biology student learns, cells preparing to divide rely on centromeres to help divide up the double amount of DNA they’ve produced, and distribute it to the two “daughter” cells they will produce. To do this, the cells grow long, skinny structures called spindles that look like spider legs, and attach to one centromere of each chromosome, which is made up of two identical stretches of DNA.

Fertility fails if chromosomes don’t have time to ‘zip’

The spindles retract as the cell divides, plucking the two halves of a chromosome apart. If the plucking doesn’t happen correctly because of a centromere-related issue, that could cause both halves of the chromosome to travel together into the “daughter” cell.

In the new study, people with Down syndrome also differed from those without the condition in their levels of a key protein that binds to centromere DNA and helps form the structure that the spindles attach to. People with Down syndrome had much less of that one protein attached to their centromeres, compared to those without the condition.

Virus DNA

The researchers didn’t set out to study centromeres. They originally wanted to learn more about hidden virus DNA that has become embedded in our genome over centuries.

These human endogenous retroviruses, or HERVs, have given us stretches of DNA that get copied and handed down from generation to generation.

The team had previously found unknown HERV RNA in the blood of patients with HIV/AIDS. Over time, they discovered HERV DNA near the edges of the centromere region of certain chromosomes. They dubbed the viruses K111 and K222.

The HERV sequences weren’t in the Human Genome Project database because they’re in the centromere region. But the researchers and their colleagues showed that the same HERVs could also be found in other higher primates, including chimpanzees and Neanderthals.

But while these human relatives have a few copies, we humans have thousands of copies of the HERV DNA near our centromeres—and on many of our chromosomes. K111, for instance, could be found on 15 chromosomes’ centromeres, slightly altered in each one. This suggests that centromeres over time have had genetic material “cross over” to other chromosomes.

Using the HERV sequences as an anchor point to study centromere DNA, the team used PCR of so-called alpha-repeat sequences to more fully analyze nearly all human centromeres.

The new paper includes their results from 23 of the 24 different human chromosomes—including the X and Y. Only chromosome 19 has so far resisted the development of a diagnostic PCR assay, as the researchers search for sequences unique to it.

Funding came from the National Institutes of Health, as well as from the Concerned Parents for AIDS Research and the University of Michigan. The university has applied for a patent on the approach.

Source: University of Michigan

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This kind of alone time is linked with creativity

Mon, 2017-11-20 18:12

New research links one form of social withdrawal, called “unsociability,” with creativity.

Although everyone needs an occasional break from the social ramble, spending too much time alone can be unhealthy and there is growing evidence that the psychosocial effects of too much solitude can last a lifetime.

But the new research suggests that not all forms of social withdrawal are detrimental.

Understanding withdrawal

“Motivation matters,” says Julie Bowker, an associate professor in University at Buffalo’s psychology department and lead author of the study, the first on social withdrawal to include a positive outcome. “We have to understand why someone is withdrawing to understand the associated risks and benefits.”

“…we think unsociability may be better characterized as a potentially beneficial form of social withdrawal…”

Bowker’s study results are reminiscent of realities that surface in literature, from Thoreau’s retreat to Walden to Thomas Merton’s work as a cloistered monk, but for all the conversation and examples about the benefits of withdrawing to nature or reconnecting to the self, the pursuit has remained something that hadn’t been well investigated in the psychological literature, according to Bowker. Until now.

“When people think about the costs associated with social withdrawal, often times they adopt a developmental perspective,” she says.

“During childhood and adolescence, the idea is that if you’re removing yourself too much from your peers, then you’re missing out on positive interactions like receiving social support, developing social skills and other benefits of interacting with your peers,” Bowker explains.

“This may be why there has been such an emphasis on the negative effects of avoiding and withdrawing from peers.”

But, in recent years, Bowker says there is growing recognition for the different reasons why youth withdraw from and avoid peers, and that the risk associated with withdrawal depends on the underlying reason or motivation.

Different reasons

Some people withdraw out of fear or anxiety. This type of social withdrawal is associated with shyness. Others appear to withdraw because they dislike social interaction. They are considered socially avoidant.

But some people withdraw due to non-fearful preferences for solitude. These individuals enjoy spending time alone, reading, or working on their computers. They are unsociable. Unlike shyness and avoidance, research consistently shows that unsociability is unrelated to negative outcomes. But, Bowker’s study is the first to link it to a positive outcome, creativity.

Why a little loneliness can be a powerful thing

“Although unsociable youth spend more time alone than with others, we know that they spend some time with peers. They are not antisocial. They don’t initiate interaction, but also don’t appear to turn down social invitations from peers. Therefore, they may get just enough peer interaction so that when they are alone, they are able to enjoy that solitude. They’re able to think creatively and develop new ideas—like an artist in a studio or the academic in his or her office,” says Bowker.

In the study, shyness and avoidance were related negatively to creativity. Bowker thinks that, “shy and avoidant individuals may be unable to use their solitude time happily and productively, maybe because they are distracted by their negative cognitions and fears.”

For the study, 295 participants reported on their different motivations for social withdrawal. Other self-report measures assessed creativity, anxiety sensitivity, depressive symptoms, aggression, the behavioral approach system (BAS)—which regulates approach behaviors and desires, and the behavioral inhibition system (BIS)—which regulates avoidant behaviors and desires.

Bowker says there is some overlap in the types of social withdrawal. Someone might be high in shyness, but also have some tendency toward unsociability. But, the results from her study show that when the research controls for all the subtypes, the three types of social withdrawal are related differently to outcomes.

Not only was unsociability related positively to creativity, but the study findings also showed other unique associations, such as a positive link between shyness and anxiety sensitivity.

Oxytocin amps up good and bad social experience

“Over the years, unsociability has been characterized as a relatively benign form of social withdrawal. But, with the new findings linking it to creativity, we think unsociability may be better characterized as a potentially beneficial form of social withdrawal,” Bowker says.

The researchers report their findings in the journal Personality and Individual Differences.

Source: University at Buffalo

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Ancient bacteria shed light on turning water to energy

Mon, 2017-11-20 18:06

Researchers have traced the paths of three water channels in an ancient photosynthetic organism—a strain of cyanobacteria—to provide the first comprehensive, experimental study of how that organism uses and regulates water to create energy.

The finding advances photosynthesis research but also presents an advance in green fuels research.

Photosynthesis is the chemical conversion of sunlight into chemical energy via an electron transport chain essential to nearly all life on our planet. All plants operate by photosynthesis, as do algae and certain varieties of bacteria.

‘Damage trails’

To convert sunlight into a usable form of energy, photosynthetic organisms require water at the “active site” of the Photosystem II protein complex. But the channels through which water arrives at the active site are difficult to measure experimentally. Reactive oxygen species are produced at the active site and travel away from it, in the opposite direction as water, leaving a “damage trail” in their wake.

“We know for sure that nature devised this machine only once, then transferred it from cyanobacteria to algae and to plants.”

“We identified the damaged sites in Photosystem II using high-resolution mass spectrometry and found that they reveal several pathways centered on the active site and leading away from it all the way to the surface of the complex,” says lead study author Daniel A. Weisz, a postdoctoral researcher in biology at Washington University in St. Louis.

“We propose that these pathways represent channels within the complex that could be used to deliver water to the active site,” he explains.

“Photosystem II has a very complex mechanism, and it’s really important to understand its processes and evolution,” says Himadri B. Pakrasi, a professor and director of the International Center for Energy, Environment, and Sustainability who has researched cyanobacteria extensively for more than 25 years.

“There is a growing interest in green energy, and our knowledge of this enzyme’s behavior could someday be put to use to create an artificial system that mimics the real enzyme to produce an abundant amount of sustainable energy.”

The active site of Photosystem II is a cluster of manganese, calcium, and oxygen ions buried deep within the complex, far away from the watery medium of the cell. Researchers have long speculated that the active site, or manganese cluster, must have a channel system, and theoretical, supercomputer-generated models tenuously have predicted their existence. But water motion is hard to characterize experimentally.

Mapping the path

The researchers took a roundabout path to delineate the channels. The “damage trail” comprises 36 amino acid residues from essentially three proteins found near the manganese cluster by a highly sophisticated mass spectrometer.

The instrument is part of the Mass Spectrometry Research Resource, which study coauthor Michael L. Gross, professor of chemistry, of immunology and pathology, and of medicine in the School of Medicine at Washington University in St. Louis, directs.

The “damage trail” is similar to that caused in a protein footprinting approach Gross developed, where researchers purposefully modify proteins with free radicals to map out solvent exposure. In this study, the modifications take place naturally where the protein is exposed to water solvent.

Amoeba stole genes to get photosynthesis

These damaging reactive oxygen species, also known as radicals, emanate and disperse from the cluster outward toward the cell’s watery medium. The radicals pass through Photosystem II like a tornado, attacking and damaging the nearest amino acid components of Photosystem II that they encounter along their path.

Because the radicals and water have similar properties, such as size and hydrophilicity, the researchers propose that the damage trail pathways going out from the cluster are very similar to the paths that water takes inward toward the active site.

Leaving bread crumbs

“We’re directly observing the paths that the radicals take, not those of water,” Weisz says. “But given the radicals’ similar properties to water as well as previous computer modeling results, we believe that those pathways are the same ones that water takes inward.”

Such an approach to discovering the water channels is considered a proxy because it’s based on the movement of the highly reactive radicals and not of the water itself.

The proxy, Weisz says, “is like leaving a trail of bread crumbs along a path in the forest. If someone is able to find the bread crumbs, they can retrace the path taken out of the forest.”

The researchers identified the many damaged residues because of the incredible accuracy, speed, and sensitivity of Gross’ mass spectrometry instrument.

“With earlier instruments that were slower and less sensitive, it was harder to confidently identify large numbers of damaged sites,” Weisz says. “The powerful capabilities of this instrument enabled us to obtain these results.”

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“Cyanobacteria are the progenitors of chloroplasts in plants,” Pakrasi says. “Photosystem II is conserved across all oxygenic photosynthetic organisms. We know for sure that nature devised this machine only once, then transferred it from cyanobacteria to algae and to plants.”

The researchers report their findings in the journal Science Advances.

The Chemical Sciences, Geosciences, and Biosciences Division, Office of Basic Energy Sciences in the Office of Science of the US Department of Energy (DOE); the Photosynthetic Antenna Research Center, an Energy Frontier Research Center funded by the US DOE, Office of Basic Energy Sciences; and the National Institutes of Health funded the work.

Source: Washington University in St. Louis

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Colliding and fusing nanoparticles caught on tape

Mon, 2017-11-20 11:49

Researchers have captured organic nanoparticles colliding and fusing on video for the first time.

This unprecedented view of “chemistry in motion” will aid nanoscientists developing new drug delivery methods, as well as demonstrate how an emerging imaging technique opens a new window on a very tiny world.

“I had an image in my mind, but the first time I saw these fusing nanoparticles in black and white was amazing…”

This is a rare example of particles in motion. The dynamics are reminiscent of two bubbles coming together and merging into one: first they join and have a membrane between them, but then they fuse and become one larger bubble.

“I had an image in my mind, but the first time I saw these fusing nanoparticles in black and white was amazing,” says study leader Nathan C. Gianneschi, professor in the chemistry department in the Weinberg College of Arts and Sciences and in the materials science and engineering departments in the McCormick School of Engineering at Northwestern University.

“To me, it’s literally a window opening up to this world you have always known was there, but now you’ve finally got an image of it. I liken it to the first time I saw Jupiter’s moons through a telescope. Nothing compares to actually seeing,” he says.

The research team used liquid-cell transmission electron microscopy to directly image how polymer-based nanoparticles, or micelles, that Gianneschi’s lab is developing for treating cancer and heart attacks change over time. The powerful new technique enabled the scientists to directly observe the particles’ transformation and characterize their dynamics.

“We can see on the molecular level how the polymeric matter rearranges when the particles fuse into one object,” says Lucas R. Parent, first author of the paper and a postdoctoral fellow in Gianneschi’s research group.

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“This is the first study of many to come in which researchers will use this method to look at all kinds of dynamic phenomena in organic materials systems on the nanoscale,” Parent says.

In the study, organic particles in water bounced off each other, and some collided and merged, undergoing a physical transformation. The researchers captured the action by shining an electron beam through the sample. The tiny particles—the largest are only approximately 200 nanometers in diameter—cast shadows that a camera below captures directly.

“We’ve observed classical fusion behavior on the nanoscale,” says Gianneschi. “Capturing the fundamental growth and evolution processes of these particles in motion will help us immensely in our work with synthetic materials and their interactions with biological systems.”

Nanoparticles improve fight against breast cancer in bone

The researchers report their findings in the Journal of the American Chemical Society.

The National Institutes of Health, the National Science Foundation, the Air Force Office of Scientific Research, and the Army Research Office supported the research.

Source: Northwestern University

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How do brains drain? Not how textbooks say

Mon, 2017-11-20 11:08

Scientists have disproved a decades-old orthodoxy: Cerebrospinal fluid does not leave the cranial cavity via blood vessels, but instead through the lymphatic system.

This finding has far-reaching implications in new treatments for dementia.

The brain sits fully immersed in an aqueous liquid called cerebrospinal fluid. Every day, the human body produces about half a liter of new cerebrospinal fluid in the cerebral ventricles; this liquid originates from the blood. This same quantity then has to exit the cranial cavity again every day.

Researchers in the group led by Michael Detmar, professor of pharmacogenomics at ETH Zurich, have now published a study showing that in mice, the cerebrospinal fluid exits the cranial cavity through the lymph vessels.

The work, published in Nature Communications, identifies another central role of the lymphatic system.

Two paths

Past research has inadequately explained how cerebrospinal fluid exits the cranial cavity. Scientists knew that two paths were available—blood vessels (veins) and lymphatic vessels—but for a long time, and due to insufficient research tools, they had assumed that drainage through the veins was by far the predominant pathway.

The researchers, led by Steven Proulx, senior scientist in Detmar’s group, have now been able to refute this assumption. They injected tiny fluorescent dye molecules into the ventricles (cavities) of the brain in mice and observed how these molecules exited the cranial cavity.

They used a sensitive non-invasive imaging technique to examine the blood vessels in the periphery of the animals’ bodies, as well as the lymphatic and blood vessels directly draining the skull.

It turned out that the dye molecules appeared after just a few minutes in the lymphatic vessels and lymph nodes outside the brain. The researchers were unable to find any molecules in blood vessels so quickly after the injection.

They were also able to determine the exact path of the dye molecules and thus the cerebrospinal fluid: It leaves the skull along cranial nerve sheaths—in particular around the olfactory and optic nerves. “Once in tissue outside the brain, it is removed by the lymphatic vessels,” explains Qiaoli Ma, a doctoral student in Detmar’s group and lead author of the study.

The scientists are not entirely able to rule out whether a small portion of the cerebrospinal fluid also leaves the brain through the veins. However, based on their research findings, they are convinced that the lion’s share travels through the lymphatic system, and that the anatomy textbooks will require editing.

Flushing the brain

Scientists assume that the circulation of cerebrospinal fluid has a purifying function. “The immune system eliminates toxins elsewhere in the body, but the brain is considered to be largely disconnected from this system. Only a few immune cells have access under normal conditions,” explains Proulx.

“The cerebrospinal fluid steps into the breach here. By constantly circulating, it flushes the brain and removes unwanted substances.”

This pathway may cause synapse loss in brain diseases

This flushing function could offer a starting point for treatment of neurodegenerative diseases such as Alzheimer’s. Misfolded proteins that accumulate in the brain cause Alzheimer’s. Proulx and his colleagues speculate that these misfolded proteins could be eliminated by, for example, drugs that induce lymphatic flow.

Similarly, studies could take place to examine whether it is possible to manage inflammatory diseases of the central nervous system, such as multiple sclerosis, through influence of the lymphatic flow.

Slower flow in old age

The scientists also showed that much less cerebrospinal fluid flows out of the brain in older mice than in younger ones, presumably because less fluid is produced in old age. Since Alzheimer’s and other forms of dementia occur in old age, the researchers think it will be interesting to examine whether stimulation of the flow of cerebrospinal fluid could slow down the progression of dementia. This is the question the scientists would like to explore next in a mouse model.

Humans brains aren’t ‘hungrier’ than other animals’

Detmar’s group has already shown that other diseases outside the brain can be treated by stimulation of the lymphatic flow. In the case of rheumatoid arthritis and psoriasis, the researchers succeeded in relieving symptoms through stimulation of the lymphatic flow.

The researchers say that studies on cerebrospinal outflow in humans may be conceivable in the future. The fluorescent marker molecule does not trigger an immune reaction and is efficiently eliminated by the body. Before the molecule can be used in humans, the scientists must first apply for the necessary approval.

“Research on the lymphatic system did not receive the attention it deserved until recently. Some in the scientific world have even ignored the lymphatic system altogether,” says Proulx.

Source: ETH Zurich

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To predict population booms, borrow from economics

Mon, 2017-11-20 10:46

A new “landscape portfolio” theory uses insights from economics to predict animal population growth and the spread of disease.

The work melds Harry Markowitz’s “portfolio theory” in economics with ecological landscape theory to predict population growth of living things.

Population demography of plants, animals, and microbes that cause diseases is central to understanding many problems in ecology, evolution, and conservation biology.

Scientists have had limited information on collections of living populations to understand and predict what happens when you have many populations spread across vast geographic areas. Most research has focused only on local populations at small scales.

Coauthor Jessica Gurevitch, professor in the department of ecology and evolution at Stony Brook University, and colleagues discovered by using this landscape portfolio theory—verified with data on gypsy moth populations—something surprising occurs: When groups of populations are assessed over a large area, the total numbers of all of them together can grow even when none of the individual populations is growing. This is called “growth inflation”—a concept similar to diversified financial investing and total investment growth.

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When growth inflation happens with living populations, the risk of population volatility or plummeting population numbers becomes very small. Synchronicity among the populations was key to their discovery.

“This theory incorporates new developments based on the relationships among populations, which can potentially help scientists better predict geographically widespread growth of populations,” says Gurevitch. “The theory can also offer new insights to growth in fields as diverse as medicine and economics.”

The findings appear in PNAS. Coauthors of the paper are from Stellenbosch University in South Africa and the University of South Florida.

Source: Stony Brook University

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These Black Friday deals can trick you into spending more

Mon, 2017-11-20 09:50

Promotions that involve spending a certain amount at a store to get a gift card may make you spend more than you normally, report researchers.

This is thanks to a phenomenon called “mental discounting.”

“…consumers should carefully consider these offers before taking advantage of them…”

“Price promotions that feel too good to be true are always an opportunity for consumers to take an extra moment for reflection,” says Cynthia Cryder, associate professor of marketing at Washington University in St. Louis’ Olin Business School, author of a new paper that will appear in the Journal of Marketing Research.

“Instead of thinking about how much money they are ‘saving,’ consumers might want to stop to ask themselves: How much am I actually paying for this product, and am I willing to pay that much?”

With certain price promotions, such as a receiving a gift card to spend in the future, consumers mentally deduct the gift card’s value from the initial purchase as well as from the second purchase when they use the gift card. Multiple mental deductions based on a single price promotion result in consumers’ perceptions that their costs feel lower than they actually are, and can increase spending, Cryder says.

“Consider a situation in which a college student purchases a $900 Macbook and receives a $100 gift card to spend in an Apple store in the future,” Cryder and coauthor Andong Cheng of the University of Delaware write in the paper.

“Feeling confident that she will use the gift card, the student may mentally reduce the laptop cost and think: ‘I am spending only $800 (instead of $900) on this laptop because I am receiving $100 worth of credit back in my pocket.’

“Now imagine that later, the student is back in the store purchasing a $300 iPad. At this point, she applies the $100 gift card, resulting in a final $200 charge for the iPad,” they write.

This mistake makes us buy junky stuff online

“She may think: ‘I am spending only $200 (instead of $300) for this tablet, because my gift card covers some of the cost.’ In total, this consumer has paid $1100 for the laptop and tablet, yet, because she mentally applied the price promotion to both purchases, she may feel as if she paid substantially less.”

According to industry research, Cryder says, businesses will load $14.5 billion onto promotional credit offers in 2017, triple the amount from 10 years ago.

“These promotions create opportunities for retailers, and consumers should carefully consider these offers before taking advantage of them,” Cryder says. “Although consumers might feel like they are spending less, these offers can sometimes encourage them to spend more.”

Source: Washington University in St. Louis

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How boosting cognition could prevent anxiety

Mon, 2017-11-20 09:16

People at-risk for anxiety are less likely to develop the disorder if they have higher activity in a region of the brain responsible for complex mental operations, according to a new study.

“We are looking for variables that actually confer resiliency and protect individuals from developing problems.”

The findings may be a step toward tailoring psychological therapies to the specific brain functioning of individual patients.

“These findings help reinforce a strategy whereby individuals may be able to improve their emotional functioning—their mood, their anxiety, their experience of depression—not only by directly addressing those phenomena, but also by indirectly improving their general cognitive functioning,” says Ahmad Hariri, a professor of psychology and neuroscience at Duke University.

Previous findings from Hariri’s group show that people whose brains exhibit a high response to threat and a low response to reward are more at risk of developing symptoms of anxiety and depression over time.

Individuals whose brains exhibit a high response to threat in the amygdala (left) and a low response to reward in the ventral striatum (middle) are more at risk of developing symptoms of anxiety and depression over time. The new study shows that these at-risk individuals were less likely to develop anxiety if they also had high activity in the dorsolateral prefrontal cortex (right). (Credit: Matthew Scult/Duke) ‘Flip side of risk’

In the current work, which appears in Cerebral Cortex, Hariri and Matthew Scult, a clinical psychology graduate student in the psychology and neuroscience department, wanted to investigate whether higher activity in a region of the brain called the dorsolateral prefrontal cortex could help shield these at-risk individuals from future mental illness.

The dorsolateral prefrontal cortex is our brain’s “executive control” center.

“We wanted to address an area of understanding mental illness that has been neglected, and that is the flip side of risk,” Hariri says. “We are looking for variables that actually confer resiliency and protect individuals from developing problems.”

The dorsolateral prefrontal cortex is our brain’s “executive control” center, helping us focus our attention and plan complex actions. It also plays a role in emotion regulation.

Well-established types of psychotherapy, including cognitive behavioral therapy, engage this region of the brain by offering patients strategies to reframe or re-evaluate their emotions.

The team drew on data from 120 undergraduate students who participated in the Duke Neurogenetics Study. Each participant completed a series of mental health questionnaires and underwent functional Magnetic Resonance Imaging (fMRI), a type of non-invasive brain scan while engaged in tasks meant to activate specific regions of the brain.

The researchers asked each participant to answer simple memory-based math problems to stimulate the dorsolateral prefrontal cortex. Participants also viewed angry or scared faces to activate a region of the brain called the amygdala, and played a reward-based guessing game to stimulate activity in the brain’s ventral striatum.

Scult was particularly interested in “at-risk” individuals with the combination of high threat-related activity in the amygdala and low reward-related activity in the ventral striatum.

Depression and anxiety can cost you retirement savings

By comparing participants’ mental health assessments at the time of the brain scans, and in a follow-up occurring on average seven months later, he found they were less likely to develop anxiety if they also had high activity in the dorsolateral prefrontal cortex.

“We found that if you have a higher functioning dorsolateral prefrontal cortex, the imbalance in these deeper brain structures is not expressed as changes in mood or anxiety,” Hariri says.


The dorsolateral prefrontal cortex is especially skilled at adapting to new situations, researchers say. Individuals whose brains exhibit the at-risk signatures may be more likely to benefit from strategies that boost the brain’s dorsolateral prefrontal activity, including cognitive behavioral therapy, working memory training, or transcranial magnetic stimulation (TMS).

But, the jury is still out on whether many brain-training exercises improve the overall functioning of the dorsolateral prefrontal cortex, or only hone its ability to complete the specific task being trained, researchers warn. Additional studies on more diverse populations are also needed to confirm their findings.

Ads about ‘home’ can capitalize on anxiety

“We are hoping to help improve current mental health treatments by first predicting who is most at-risk so that we can intervene earlier, and second, by using these types of approaches to determine who might benefit from a given therapy,” Scult says.

The National Institutes of Health, Duke University, and a National Science Foundation Graduate Research Fellowship supported the work.

Source: Duke University

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Smaller, quieter wind turbines could boost public support

Mon, 2017-11-20 08:34

Vertical axis wind turbines, which may have fewer effects on birds and nearby people, could increase public support for new wind energy installations, new research suggests.

With global carbon emissions on the rise, wind power continues to be an attractive option for states and countries looking to limit fossil fuel use and increase renewable energy. Wind already accounts for over 5 percent of electricity generation in the United States.

A number of issues plague the low-carbon energy source, however, such as complaints from nearby residents about noise and the killing of hundreds of thousands of birds and bats each year that collide with turbine blades.

Last week, in a setback to wind energy proponents, the Vermont Public Utility Commission adopted new regulations that limited the amount of sound new wind projects are allowed to produce. And in counties across California, similar restrictions have been passed limiting wind energy expansion. While some states are growing their wind power sectors, California has seen a plateau in growth over the last four years.

Researchers surveyed Californians on how they felt about traditional versus vertical axis wind turbines in a rural setting. (Credit: Iris Hui/Stanford)

To better understand these concerns over wind energy, researchers conducted a poll examining how receptive people in California are to vertical axis wind turbines in various settings.

“For California, even with the state’s support for climate action and reducing emissions, wind farms can be a tough sell for residents,” says Iris Hui, a coauthor of the paper and senior researcher with the Bill Lane Center for the American West at Stanford University.

“We wanted to see if the potential for lower impacts from vertical axis turbines might persuade Californians to be more receptive to large-scale wind projects,” Hui says.

‘Opinion matters’

Vertical axis turbines have been around for decades but have been less popular options for large wind farms because of concerns that current models are less reliable and produce less energy per unit. But the tide could turn with public concern over the effects that wind energy has on people as well as birds and other wildlife.

“Because vertical axis turbines operate at lower speeds, lower height, and have a different visual signature than conventional wind turbines, we anticipated that they would have less impact on birds and wildlife,” says coauthor John Dabiri, professor of civil and environmental engineering and of mechanical engineering at Stanford University.


The researchers also asked how Californians felt about traditional versus vertical axis wind turbines in an open space setting. (Credit: Iris Hui/Stanford)

“Our field testing over the past eight years has shown this to be anecdotally true. We also expected the fact they they’re less noisy and harder to see from a distance would make them more attractive for communities. But it was important to test these assumptions in practice.”

This results of the poll could help California and other states make better use of abundant wind energy, says coauthor and political science professor Bruce Cain.

“The issue is both a technical engineering problem and a political science problem because opinion matters so much to which technologies get adopted and implemented. That’s why we brought people from both disciplines together on this,” says Cain.

Better for bats and birds

The team devised an online opt-in survey that asked respondents about their feelings on the different turbine technologies. The most desirable feature for vertical axis turbines was the idea that they may kill fewer birds and bats.

Cost remained a big concern, however, as did where to put the turbines. While support for installation was 75 percent for turbines that would be 50 miles from their home, support plummeted significantly as the distance from the turbine installation to the respondent’s home got smaller.

Wind turbines change visitors to tortoise burrows

Dabiri’s lab is working on ways to develop vertical axis turbines that can reach parity on energy output with horizontal axis turbines and has research showing the potential of deploying smaller vertical axis turbines (about 30 feet high compared to the iconic white horizontal axis turbines stretching over 300 feet tall) in clusters to further perpetuate wind.

Due to their smaller stature, there is also more potential to deploy these turbines in a more urban setting than is possible with larger horizontal axis turbines. However, neither of these ideas gave vertical axis wind turbines a significant advantage over conventional wind turbines with the respondents.

Respondents with higher educational levels who value action on climate change were more likely to support integrating vertical axis turbines into an urban setting.

The researchers stress these findings indicate that, rather than being competing technologies, vertical and horizontal wind turbines can be complementary.

“Vertical axis turbines could be favored in areas of significance to wildlife or in certain urban settings where larger turbines are not viable,” says Hui.

In addition to this study, Dabiri’s lab has funding through the Stanford Woods Institute for the Environment’s Realizing Environmental Innovation Program to study how to lower the impacts of wind energy expansion on birds and ecosystems.

“The real challenge that remains is to do more rigorous testing on how vertical axis turbines impact birds,” says Dabiri. “If our anecdotal evidence of lower avian impacts can be supported by formal biological studies, it could make a real difference in public acceptance.”

To cut power use, put a price tag on carbon

The researchers report their findings in the journal Energy Policy. The Bill Lane Center for the American West funded the work.

Source: Stanford University

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These ER tests don’t actually spot heart attacks

Mon, 2017-11-20 08:21

People who go to the ER with chest pain often receive unnecessary tests to evaluate whether they are having a heart attack, a practice that provides no clinical benefit and adds to health-care costs, according to a new study.

Specifically, computed tomography (CT) scans and cardiac stress tests are overused in the ER for patients with chest pain and provide no information to determine whether a patient is in the midst of a heart attack, the researchers report.

A typical clinical evaluation includes a medical history, physical exam, electrocardiogram, and blood test for a protein that becomes elevated after the heart is damaged. In addition, hospitals give many patients a CT scan of the arteries that deliver blood to the heart or a cardiac stress test. A stress test measures heart function during exercise.

“Our study suggests that in the emergency room, stress testing and CT scans are unnecessary for evaluating chest pain in possible heart attack patients,” says cardiologist and senior author David L. Brown, a professor of medicine at Washington University in St. Louis.

“Patients don’t do any better when given these additional tests. Our study is not a definitive randomized clinical trial, but it does suggest that we are over-testing and over-treating these patients.”

Looking for the wrong thing

In recent years, Brown says doctors can more accurately diagnose heart attacks largely because of advances in the blood test that measures levels of a protein called troponin. High troponin levels signal injury to the heart.

“This troponin test is super-sensitive,” Brown says. “But earlier blood tests were much less accurate. A patient could be having a heart attack and these older tests often would come back normal. Doctors didn’t trust the tests, so they looked for other ways to evaluate the patient. CT scans and stress tests were among the methods used. But now that the blood testing method is so much better, there is less reason to continue doing these screening tests in the emergency room.”

The investigators evaluated data from 1,000 patients who visited nine medical centers across the country that were a part of the Rule Out Myocardial Ischemia/Infarction by Computer Assisted Tomography (ROMICAT-II) clinical trial. The current study revisited data from that trial, looking for any differences in outcomes for patients who received a clinical evaluation alone (118 patients) compared with those who received a clinical evaluation plus either a CT scan or a stress test (882 patients).

In the study, 88 percent of patients received the extra testing. Nationwide, the overwhelming majority of patients evaluated for chest pain in the ER get such extra tests, Brown says.

Why hospital doctors should cut back on blood tests

During the nearly month-long follow-up period, there were no differences between the two groups in the percentages of patients who had a stent placed to open an artery, underwent coronary artery bypass surgery, returned to the emergency room, or experienced a major cardiac event, such as heart attack.

Other drawbacks

While providing no clear health benefit to emergency room patients, the extra tests also led patients to stay in the hospital longer than may have been necessary and exposed them to radiation from testing that was not required to diagnose a heart attack. Length-of-stay for patients who received less testing was, on average, 20 hours compared with 28 hours for those who did receive either of the two additional tests.

The analysis also showed that, on average, a patient receiving more testing accrued $500 more in health-care costs during the ER visit. Patients who received more testing during the initial ER visit also received more follow-up tests, leading to $300 more in health-care costs for this group during the 28-day follow-up period. With 10 million patients coming to the ER for chest pain each year in the United States, these extra costs add up, according to the investigators.

“It’s important to keep in mind that CT scans and stress tests are used to diagnose coronary disease—whether someone has plaque in the arteries,” Brown says. “Many people have coronary plaque but are not having a heart attack.

“The goal of evaluating patients with chest pain in the ER is not to screen for coronary artery disease,” he says. “Anyone who goes to the ER for chest pain and gets sent home should make an appointment to see their primary care doctor to talk about their recent hospital visit. It’s important to follow up to see if additional testing is warranted because screening tests are not appropriate in this specific emergency situation.”

Doctors blame extra treatment on fear of lawsuits

The researchers report their findings in JAMA Internal Medicine. They will also present of the study at the American Heart Association’s Scientific Sessions in Anaheim, California. The investigators report no external funding.

Source: Washington University in St. Louis

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NIH funding cuts could paralyze drug development

Sun, 2017-11-19 19:12

More than 90 percent of new drugs received funding from the National Institutes of Health. Now, US President Donald Trump’s proposed budget calls for cutting the NIH budget by 21 percent, or about $7.2 billion.

“Cutting the NIH budget could dismantle our ability to address real problems,” says Michael S. Kinch, a professor of biochemistry and molecular biophysics at Washington University in St. Louis.

Hear Kinch explain the research: https://www.futurity.org/wp/wp-content/uploads/2017/11/NIH-cuts-.mp3

“Take antibiotics, for example. We’ve grown accustomed to being able to treat infections, but now bacteria are becoming resistant to existing drugs. If funding cuts slow the development of new infection-fighting medicines, then in future years, many people may die from infections that once were treatable.”

Researchers analyzed budget data from the NIH and the Food and Drug Administration (FDA) to learn how much NIH support contributed to the early development of commonly prescribed drugs. They also zeroed in on newer drugs that were approved by the FDA in the past decade.

An analysis of the 100 most commonly prescribed drugs in the US—such as Synthroid, which replaces the hormone normally secreted by the thyroid gland; Crestor, a statin used to lower cholesterol; and albuterol, an inhaled treatment for people with lung diseases such as asthma—show that 93 percent had received NIH funding. For drugs approved by the FDA from 2010 to 2016, the percentage that relied on NIH support was even higher: 97 percent.

The findings appear as a letter in Cell Chemical Biology.

“NIH funding is instrumental in the early research needed to develop FDA-approved medicines,” says Kinch, director of the Center for Research Innovation in Biotechnology and Center for Drug Discovery. “Our data suggest that the development of newer drugs is becoming even more dependent on NIH funding.”

Further, because it can take 10 years or more for a drug to move through the pipeline and receive FDA approval, cuts in NIH funding now could continue to impair the development of new and better drugs for decades.

US is #1 in biomed research, but this country is catching up

“The average cost of developing a new medicine is $1 billion to $3 billion,” Kinch says. “And at the earliest stages of research, there is more uncertainty and the risks are bigger, so pharmaceutical companies have focused their efforts on spending during later stages of development, as drugs move through clinical trials.”

For decades, pharmaceutical companies have been moving further away from the earliest stages of research. That withdrawal of private-sector funding was less noticeable because new biotech companies were appearing on the scene, and those firms helped pay for the early research that pharma companies no longer funded. But in recent years, many biotech firms have disappeared, and the creation of new biotech companies has fallen by about 50 percent.

That leaves the NIH as the primary funder of early-stage research and development now and, presumably, in the future, so further NIH budget cuts could slow drug development and leave the public without access to new therapies for years to come.

Source: Washington University in St. Louis

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How social justice and the environment connect

Sun, 2017-11-19 18:38

In his new book, author David Pellow argues that environmental issues and social justice are connected.

In What is Critical Environmental Justice? (Polity Press, 2017), Pellow, a chair in environmental studies at the University of California, Santa Barbara, examines the complicated connections between humans and ecosystems. He provides a framework for making environmental justice more inclusive and discusses how that concept applies to areas not usually associated with the field: the Black Lives Matter movement, the US prison industrial complex, and the Israel-Palestine conflict.

“Every one of us is an indispensable member of our community and is needed for moving us toward ecological sustainability and social justice, which I see as symbiotic issues,” says Pellow, who also directs the University of California, Santa Barbara’s Global Environmental Justice Project.

“But we need to expand our theories and practices of environmental justice beyond just human beings,” he says.

Changing ideas of justice

Is it possible to reframe the way people think about environmental issues and solutions? Pellow addresses the question in his book. As he sees it, he says, the scholarly debate about whether exposure to environmental pollution is primarily a function of economics or of racial inequalities is limited because both are almost always in evidence.

“We also need to think of climate change and environmental health issues as examples of violence,” Pellow remarks. “In fact, our bodies themselves can be viewed as sites of struggle for environmental justice.”

While the Black Lives Matter movement protests the violence and systemic racism toward black people by police and vigilantes, Pellow is troubled by the rhetoric people use on both sides of the issue.

For example, there is a common refrain that police are shooting black people “like dogs.” That rhetoric, he notes, rightly points to the longstanding problem of state-sanctioned racist violence, but it also implies that it’s OK to go out and indiscriminately slaughter nonhumans. He calls it the “social discourse of animality,” a term meant to capture the language people use to describe human behavior via nonhuman references and analogies.

According to Pellow, this signals a set of assumptions surrounding what is viewed as acceptable behavior and how different bodies are valued.

“The language we use sometimes masks and other times makes visible the fact that many people think it’s perfectly fine to have open season on certain beings but not on others,” he adds.

“If we had a broader vision of environmental justice, we could simultaneously acknowledge the unique ways in which African Americans have a troubling relationship with law enforcement and, at the same time, be more inclusive and pay attention to how violence often spills over the species boundary.”

Why so little grassroots action against climate change?

Another key point in Pellow’s book: Relying on governments to solve environmental justice problems may not always be the best option. After all, he says, governments are in some ways the primary engines of climate change and certain environmental harms.

“It’s fairly illogical to expect the perpetrators of the problem to be the ones to solve it,” he adds. “It is far more empowering and democratizing when communities take direct action to improve their lot.”

People power

To that end, Pellow also underscores the power of ordinary people to secure meaningful victories for environmental justice.

Bryant Arroyo is a case in point. During the time he served at Pennsylvania’s State Correctional Institution at Mahanoy, the township was considering a proposal for a coal gasification plant right next to the prison, which would have led to a public health threat from increased air pollution.

Despite restrictions on inmates’ activities, Arroyo organized 900 of his fellow prisoners to sign letters of protest and made sure they reached the township supervisors. They agreed with the arguments put forth by the inmates and halted the project, earning Arroyo the informal title of “jailhouse environmentalist.”

Maps track spread of U.S. social movements

Pellow says, “If Bryant Arroyo could shut down a coal gasification plant from within a prison, then surely everyone else in the ‘free world’ has far greater power and potential than we ever imagined—and that is really inspiring.”

He makes a similar case for the conflict between Israel and Palestine. Pellow sees the struggle over unequal access to the same land as an environmental justice issue—one that would benefit from thinking about and acting on environmental issues on many levels: local, national, and global.

“While I am not an expert on this conflict, I see no reason why we can’t pursue justice for people on all sides in ways that are respectful and that recognize the historic, ongoing human rights struggles for all faiths and origins,” Pellow says. “However, I do think that there has been a troubling unwillingness on both sides to really see the humanity of the other.

“In this, as in all critical environmental justice issues,” he continues, “we’ve got to find a way to see all of us—both humans and nonhumans—as having shared fates.”

Source: Nicoletta Lanese for UC Santa Barbara

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Swabbing dolphin mouths reveals bacterial ‘dark matter’

Fri, 2017-11-17 10:47

Researchers have found two previously unknown phyla of bacteria inside the mouths of dolphins.

A phylum is a broad taxonomic rank that groups together organisms that share a set of common characteristics due to common ancestry.

The discovery of two bacterial phyla, as well as additional novel genes and predicted products, provides new insights into bacterial diversity, dolphin health, and the unique nature of marine mammals in general, says David Relman, professor of medicine and of microbiology and immunology at the Stanford University School of Medicine and senior author of a new paper describing the findings.

(Credit: National Marine Mammal Foundation via Stanford) Bacterial ‘gold’

The US Navy’s Marine Mammal Program reached out to Relman more than 10 years ago for help in keeping its dolphins healthy. The animals are highly trained and perform missions at sea.

“We knew there was gold in those dolphin mouths, and we decided it was time to go after it…”

Previous research by Relman’s group, in collaboration with the Marine Mammal Center, revealed a surprising number of never-before-seen bacteria in dolphin and other marine mammal samples, particularly those swabbed from the dolphins’ mouths, says Relman. Some of the bacteria found in the current study are affiliated with poorly understood branches of the bacterial tree.

“These organisms, about which we have known just a tiny bit, are basically the dark matter of the biological world,” he says. “We knew there was gold in those dolphin mouths, and we decided it was time to go after it with more comprehensive methods.”

In the new study, the researchers identified bacterial lineages by reconstructing their genomes from short bits of DNA. The genome of a given cell serves as its blueprint and contains all its operating instructions, encoded in DNA.

The researchers named one of the newly identified lineages Delphibacteria in honor of the dolphins (Delphinidae is the Latin name for oceanic dolphins).

Earth may be home to 1 trillion species of microbes

By looking at the genes encoded in the genomes of Delphibacteria representatives, the researchers gained insight into the bacteria’s lifestyle.

Researchers predict the bacteria express a property called denitrification that may affect dolphins’ oral health: The chemical process can cause inflammation and could be connected to gum disease. Denitrification also occurs in plaque on human teeth, suggesting that something about mammalian mouths selects for this process.

Putting the puzzle together

The researchers differentiated between bacteria and predicted their behavior by looking broadly at their genomes.

“What we do first is shear the DNA into a bunch of little bits and pieces, the mix of DNA is sequenced, and we then try to figure out how the genomes were originally assembled,” says lead author Natasha Dudek, a graduate student at the University of California, Santa Cruz.

If a gene is one piece of a puzzle, the researchers put together the whole puzzle.

“Typically, people are interested in small Cas9 proteins that might be easy to manipulate and deliver into cells,” says Relman. “These are the opposite—they’re enormously big.”

Different structures in the genes that encode these proteins account for the size difference, and the researchers suggest these large Cas9 proteins have different properties from those known before. Dudek plans to pursue this line of research further.

‘Competing’ ocean bacteria may collaborate instead

The study also feeds nicely into ongoing work in Relman’s lab. A large, comparative study is underway to investigate how adaptation to life in the sea might affect marine mammal microbiomes. Beyond discovering and characterizing novel bacteria, Relman wants to apply his research to conservation.

“Marine mammals are becoming increasingly endangered,” he says. “They are sentinel species for the health of the sea, and the more we can understand their biology, the better we can anticipate changes in the health of their environment.”

The researchers report their findings in Current Biology.

Additional researchers from the UC Berkeley, UC Santa Cruz, and Stanford also contributed to the study. The Office of Naval Research supported the study, as did Stanford’s medicine and microbiology and immunology departments.

Source: Nicoletta Lanese for Stanford University

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Here’s when to buy LED light bulbs

Fri, 2017-11-17 10:46

A new study recommends replacing all incandescent and halogen light bulbs in your home now with compact fluorescent lamps (CFLs) or LEDs.

But immediate replacement is not advised for existing CFLs and LEDs, unless your main concern is helping to reduce power-plant emissions, according to the study in Environmental Research Letters.

“Estimating the right time to switch over to LEDs is not a straightforward problem. If your goal is to help reduce carbon dioxide emissions, then maybe you should switch to LEDs now,” says Lixi Liu, first author of the study and a doctoral student at the University of Michigan School for Environment and Sustainability and in the department of mechanical engineering.

“But if your main concern is lowering costs and home energy use, then holding on to existing CFLs and LEDs, and waiting until LEDs use even less energy and are even lower in cost, may be desirable.”

For a CFL that’s used an average of three hours per day, it may be best—both economically and energetically—to delay the adoption of LEDs until 2020, she says.

Lighting accounted for 10 percent of US residential energy use in 2016. Home lighting upgrades are an easy way to lower your utility bill, reduce energy use, and help cut greenhouse gas emissions.

LEDs are long-lasting light bulbs that use less energy than incandescent, halogen, or fluorescent bulbs to provide the same light output. But the initial purchase price for LEDs is higher than other types of bulbs, so many consumers haven’t made the switch.

Previous studies have noted that LEDs reduce spending on energy over time and are a cost-effective alternative to other light bulbs. But those studies did not look at the best time to replace an existing bulb.

In their newly published study, the researchers examined cost, energy use, and greenhouse gas emissions for different types of 60-watt-equivalent bulbs and created a computer model to generate multiple replacement scenarios, which they then analyzed.

Specifically, they used a method called life cycle optimization to construct a lighting replacement optimization model. Researchers at the university’s Center for Sustainable Systems have previously used the model to study replacement of automobiles, refrigerators, washing machines, and air conditioners.

How LED light bulbs could fight disease

In the lighting study, the researchers considered factors such as how often the current bulb is used and its condition. And they looked at trajectories for lighting technology and energy generation: light bulb technologies are improving, costs continue to drop, and electricity generation in this country is becoming cleaner.

By 2040, the share of US electricity from natural gas is expected to increase by 6 percent, and the share from renewables is expected to increase 13 percent. By 2040, the share of US electricity from nuclear power is expected to decrease by 4 percent, and the share from coal is expected to decrease 15 percent.

The new lighting study provides specific replacement strategies for maximizing the cost, energy, and emissions savings from home lighting.

The study also finds that:

  • In general, bulbs that are used more often should be replaced first to maximize energy savings.
  • Replacing a bulb before it burns out may seem wasteful, but consumers can cut energy use by doing so.
  • Strategies for replacing light bulbs vary from place to place, depending on regional energy costs and the power-generation mix (i.e., coal, natural gas, nuclear, and renewables).
  • In general, LED upgrades should be made earlier and more frequently in places—such as California, Washington, DC, and Hawaii—where electricity costs are high.

The National Science Foundation’s Graduate Research Fellowship Program supported the work.

Source: University of Michigan

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Ancient North Americans played high-stakes games

Fri, 2017-11-17 10:39

From games of chance to tests of physical skill, ancient North America Indians took their sport and recreation seriously, research shows.

“Games are ubiquitous. Every society seems to have them,” says Barbara Voorhies, a research professor of anthropology at the University of California, Santa Barbara. Gambling was especially prevalent—because with nothing at stake the games would simply be incredibly boring.

“Based on the ethnographic record, gambling must be very deep-seated in human prehistory because it shows up everywhere, from the arctic to the tropical lowlands, and in hunter-gatherer to more complex societies,” says Voorhies, a specialist in archaeology, human ecology, and Mesoamerica. “It’s everywhere.”

Voorhies is editor of a new book, Prehistoric Games of North American Indians: Subarctic to Mesoamerica (University of Utah Press, 2017), that examines the role of games among ancient indigenous people throughout North America.

For the book, 20 archaeologists looked at how games fit into the social logic of ancient societies; how games influence economies, religion, politics, and health care; and how they promote cooperation or competition among participants.

Some of the findings derive from diaries of Spaniards who arrived in Central Mexico. They described a dice game the Aztecs played, and it seems the ancient Maya enjoyed similar games.

“Dice games are pretty widespread across the continent,” says Voorhies, who is also a contributor to the book. “By and large they are women’s games,” though not in these two societies. There were also several types of ball games played across Mesoamerica, some played with rubber balls.

“One generalization we can make about North American games is that women play against women and men play against men,” Voorhies says. “Gambling might be between the players, but also among onlookers.”

Sisters might have played a dice game and bet on who would cook dinner or get firewood. Sometimes, people would gamble on a game with the loser becoming the winner’s slave for a time.

Voorhies’ interest in ancient games began in 1988 when she was excavating a shell mound in southern Mexico. On a floor-like surface, she found a puzzling semicircular pattern of 24 holes, with a rock imprint in its center.

“It looked like somebody was playing marbles,” she says. “That was the first thing that occurred to me. At the time I didn’t think anybody in Mesoamerica played marbles so I discounted that and was perplexed about this whole thing.”

Bones hint at lives of Maya middle class

Then in 2009, she returned to the site, expanded the excavation to expose more of the floor, and found several more of the same features. “Whatever it was, people were doing it a lot. So I renewed my efforts to figure out what it was.”

A colleague referred her to American ethnographer Stewart Culin’s 1907 book titled Games of the North American Indians, considered to be the most complete work ever prepared on the games of North American Indians living during Culin’s lifetime.

She then realized her discovery in Mexico was most likely a game board, since it closely resembled dice game scoreboards from several groups in the American southwest and northwest Mexico that Culin describes in his book.

Source: UC Santa Barbara

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To prevent eczema, promote breastfeeding?

Fri, 2017-11-17 10:17

Babies whose mothers had received support to breastfeed exclusively for a sustained period from birth have a 54 percent lower risk of eczema at the age of 16, a new study shows.

Eczema causes the skin to become itchy, dry, cracked, sore, and red. It affects around 1 in 5 children and 1 in 10 adults in the developed world.

Eczema affects around 1 in 5 children and 1 in 10 adults in the developed world.

The study examined more than 13,000 Belarussian teenagers enrolled in the PROmotion of Breastfeeding Intervention Trial (PROBIT).

“The WHO recommends between four and six months of exclusive breastfeeding to aid prevention of allergy and associated illnesses. Our findings add further weight to the importance of campaigns like the Baby-Friendly Hospital Initiative (BFHI), which is tackling low rates of breastfeeding globally,” says lead author Carsten Flohr of King’s College London.

The PROBIT study recruited a total of 17,046 mothers and their newborn babies between June 1996 and December 1997. Half of the maternity hospitals and pediatric clinics involved in the study provided additional support based on the recommendations of the WHO and United Nations Children’s Fund’s BFHI, while the other half continued their usual practices.

While the study found that the breastfeeding promotion intervention provided protection against eczema, there was no reduction in risk of asthma with 1.5 percent of the intervention group (108/7,064) reporting asthma symptoms compared with 1.7 percent (110/6,493) in the control group.

PROBIT is “the largest randomized trial ever carried out in the area of human lactation,” says principal investigator of PROBIT Michael Kramer, senior scientist from the Child Health and Human Development Program at the Research Institute of the McGill University Health Centre and a professor in pediatrics at McGill University.

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The researchers report their findings in JAMA Pediatrics.

Additional researchers contributed to the work from King’s College London, Harvard University, the University of Bristol, McGill University, and the Research Institute of the McGill University Health Centre (R-MUHC).

The National Institute for Health Research Biomedical Research Centre at Guy’s and St Thomas’ and King’s College London supported Flohr’s work.

Source: McGill University

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3D-printed ‘schwarzites’ could build all kinds of stuff

Fri, 2017-11-17 08:54

Engineers are using 3D printers to turn largely theoretical structures into strong, light and durable materials with complex, repeating patterns.

The porous structures called schwarzites are designed with computer algorithms, but Rice University researchers found they could send data from the programs to printers and make macroscale, polymer models for testing. Their samples strive to use as little material as possible and still provide strength and compressibility.

The results, reported in Advanced Materials, are works of art that may someday lead to nanoscale electronic devices, catalysts, molecular sieves, and battery components, and on the macroscale could become high-load-bearing, impact-resistant components for buildings, cars, and aircraft.

It may even be possible to one day print an entire building as one schwarzite “brick.”

‘Everything is curved’

Schwarzites, named after German scientist Hermann Schwarz, who hypothesized the structures in the 1880s, are mathematical marvels that have inspired a large number of organic and inorganic constructs and materials. The discovery at Rice of the Nobel Prize-winning buckminsterfullerene (or buckyball) provided further inspiration for scientists to explore the design of 3D forms from 2D surfaces.

“You don’t want things to break catastrophically; you want them to break slowly.”

The structures remained theoretical until 3D printers provided the first practical way to make them. The Rice lab of materials scientist Pulickel Ajayan, in collaboration with researchers at the University of Campinas, São Paulo, investigated the bottom-up construction of schwarzites through molecular dynamics simulations and then printed those simulations in the shapes of polymer cubes.

“The geometries of these are really complex; everything is curved, the internal surfaces have negative curvature, and the morphologies are very interesting,” says Rice postdoctoral researcher Chandra Sekhar Tiwary.

“Schwarzite structures are very much the same. The theory shows that at the atomic scale, these materials can be very strong. It turns out that making the geometry bigger with polymer gives us a material with a high load-bearing capacity.”

The structures also have excellent deformation characteristics. “The way a material breaks is important,” Tiwary says. “You don’t want things to break catastrophically; you want them to break slowly. These structures are beautiful because if you apply force to one side, they deform slowly, layer by layer.

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“You can make a whole building out of this material, and if something falls on it, it’s going to collapse slowly, so what’s inside will be protected.”

Beyond blocks

Because they can take a variety of forms, researchers limited their investigation to primitive and gyroid structures, which have periodic minimal surfaces as originally conceived by Schwarz.

In tests, both transferred loads across the entire geometry of the structures no matter which side was compressed. That held true in the atom-level simulations and for the printed models.

That was unexpected, says Douglas Galvão, a professor at the University of Campinas who studies nanostructures through molecular dynamics simulations.

“It is a little surprising that some atomic-scale features are preserved in the printed structures. We discussed that it would be nice if we could translate schwarzite atomic models into 3D printed structures. After some tentatives, it worked quite well.”

The next step will be to refine the surfaces with higher-resolution printers and further minimize the amount of polymer to make the blocks even lighter. In the far future, they envision printing 3D schwarzites with ceramic and metallic materials on a grander scale.

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“There’s no reason these have to be blocks,” says coauthor and Rice graduate student Peter Owuor. “We’re basically making perfect crystals that start with a single cell that we can replicate in all directions.”

The Air Force Office of Scientific Research and its Multidisciplinary University Research Initiative, the São Paulo Research Foundation, and the Center for Computational Engineering and Sciences at the State University of Campinas supported the work.

Source: Rice University

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Gene mutation extends life and health of some Amish

Thu, 2017-11-16 19:30

Scientists have discovered the first genetic mutation that appears to protect against multiple aspects of biological aging in humans in an extended family of Old Order Amish living in the vicinity of Berne, Indiana.

An experimental “longevity” drug that recreates the effect of the mutation is now being tested in human trials to see if it provides protection against some aging-related illnesses.

“Not only do they live longer, they live healthier.”

Indiana Amish kindred (immediate family and relatives) with the mutation live more than 10 percent longer and have 10 percent longer telomeres (a protective cap at the end of our chromosomes that is a biological marker of aging) compared to Amish kindred members who don’t have the mutation, reports the study.

Amish with this mutation also have significantly less diabetes and lower fasting insulin levels. A composite measure that reflects vascular age also is lower—indicative of retained flexibility in blood vessels in the carriers of the mutation—than those who don’t have the mutation, the research also found.

The paper appears in the journal Science Advances.

These Amish individuals have very low levels of PAI-1 (plasminogen activator inhibitor,) a protein that comprises part of a “molecular fingerprint” related to aging or senescence of cells. It was previously known that PAI-1 was related to aging in animals but unclear how it affected aging in humans.

“The findings astonished us because of the consistency of the anti-aging benefits across multiple body systems,” says cardiologist Douglas Vaughan, the lead author of the paper and professor and chairman of medicine at Northwestern University Feinberg School of Medicine and Northwestern Medicine.

“For the first time we are seeing a molecular marker of aging (telomere length), a metabolic marker of aging (fasting insulin levels), and a cardiovascular marker of aging (blood pressure and blood vessel stiffness) all tracking in the same direction in that these individuals were generally protected from age-related changes,” Vaughan says.

“That played out in them having a longer lifespan. Not only do they live longer, they live healthier. It’s a desirable form of longevity. It’s their ‘health span.'”

Northwestern has partnered with Tohoku University in Japan in the development and testing of an oral drug, TM5614, that inhibits the action of PAI-1. The drug has already been tested in a phase 1 trial in Japan and is now in phase 2 trials there. Northwestern will apply for FDA approval to start an early phase trial in the US, possibly to begin within the next six months.

The proposed Northwestern trial will investigate the effects of the new drug on insulin sensitivity on individuals with type 2 diabetes and obesity because of the mutation’s effect on insulin levels in the Amish.

Benefits of the gene mutation

In the new study, Northwestern scientists looked at individuals who had one mutant copy of the gene, rendering their level of PAI-1 about half the level of kindred with two normal copies.

Those carriers of the gene mutation had nearly 30 percent lower fasting insulin levels and were completely protected from diabetes.

“We were definitely surprised,” Vaughan says. “Even when we analyze it factoring for their relatedness, the mutation is still an important predictor of whether they’ll get diabetes.”

“This is the only kindred on the planet that has this mutation.”

He says 7 percent of the kindred with two normal copies of the gene have diabetes, so out of the 177 Amish participants in the study, he would expect three or four of the carriers of the single mutant gene to have the disease as well.

The scientists also saw an improvement in a group of cardiovascular measures—lower blood pressure and more flexible blood vessels—that change with age. The improvement did not reach statistical significance, but the carriers of the mutant gene have a younger appearing cardiovascular system, Vaughan says. In particular, individuals in the oldest third of the group have a reduced pulse pressure, indicative of more flexible arteries.

Cognitive testing will be part of future measurements for the study. Experimental data in mice show lower levels of PAI-1 can protect against Alzheimer’s-like pathology.

“We hope to be able to revisit them regularly and do additional testing to look at the velocity of aging in this kindred and unearth more details about the protective effect of this mutation,” Vaughan says.

A ‘private mutation’

The Amish kindred in Berne, Indiana, have been genetically and culturally isolated and most are at least distantly related. The ancestors of the Indiana Amish emigrated in the middle of the 19th century from Berne, Switzerland. The town recalls the architecture of their original home in Switzerland with its Swiss-style clock tower and architecture.

Farmers from Switzerland who moved into the area introduced the mutation into the Amish kindred. Two of their descendants, who carried the mutation, married into the Amish community. The Amish community outside the Berne area does not carry this mutation.

“This is the only kindred on the planet that has this mutation,” Vaughan says. “It’s a ‘private mutation.'”

People with the mutation live to be 85 on average, significantly longer than their predicted average lifespan of 71 for Amish in general and which hasn’t changed much over the last century.

The age range of Amish in the study was 18 to 85 with the average age of carriers 44 and the unaffected 46 years old.

Intensive testing

On May 5, 2015, a caravan of 40 doctors, nurses, sonographers, and other health care workers drove to Berne before dawn and set up 10 testing stations in a nearby community center. Over the following two days, 177 Amish arrived by horse and buggy for testing, half on each day.

“They are curious about the mutation because they know some of them have a bleeding problem.”

It took an entire day for each person to go through all the testing stations that included: fasting blood samples, echocardiograms, systolic blood pressure testing, pulse wave velocity (a measure of stiffness of their large arteries), pulmonary function tests, and urine samples.

Scientists took fibroblasts (cells) and grew stem cells from those cells in order to investigate the impact of the mutation on cell biology. Scientists can turn those cells into neurons, cardiac cells, or any type of cell and investigate the impact of this genetic alteration on important biology.

Bleeding disorder

Why did so many of the kindred agree to participate in the study? “They are curious about the mutation because they know some of them have a bleeding problem,” Vaughan says.

Individuals affected with the bleeding disorder have two copies of the mutated gene that led to the absence of PAI-1 in the blood and the resulting bleeding. People who carry one copy of the mutated gene did not have a bleeding disorder.

PAI-1 has an important role in the regulation of the part of the human blood clotting system that helps to dissolve clots once formed. When people are missing PAI-1, they have increased breakdown of clots and abnormal bleeding that is associated with heavy menstrual bleeding, bleeding with pregnancy and ovulation, dental work, injury, and trauma.

Scientists found the individuals with two changed PAI-1 genes not only had a bleeding disorder but also had varying degrees of an unusual cardiac disorder that leads to fibrosis (scarring of the heart). One of the affected individuals has died from this complication.

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Shapiro and colleagues at the Indiana Hemophilia & Thrombosis Center treat 11 Amish patients with the double mutation. For bleeding issues, the patients receive a medication that can be taken by either mouth or given intravenously to prevent clots from being dissolved too quickly. There is no treatment for cardiac fibrosis recently identified by the research team.

PAI-1 as drug target

Northwestern is partnering with a Japanese startup company (Renascience) to develop a new class of drugs that specifically target PAI-1. The drugs are the brainchild of Vaughan’s collaborator, Dr. Toshio Miyata, who leads a drug discovery program at Tohoku University in northern Japan.

In the phase 1 Japanese studies, completed this past summer, the drug was given to about 160 healthy individuals to test its safety. After proving to be safe and nontoxic, the drug is now being tested in a phase 2 trial to see if inhibiting PAI-1 affects the migration of stem cells from the bone marrow.

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Scientists want to see if giving the PAI-1 inhibitor drug boosts the number of red and white blood cells and platelets of patients who have undergone chemotherapy, which results in low counts. That could reduce complications, which include infections, bleeding, and anemia. Since PAI-1 controls the mobilization and release of stem cells from the bone marrow, scientists hypothesize that partial inhibition of PAI-1 will accelerate the recovery of normal cell counts in the blood.

Vaughn’s previous research in a 2014 paper published in the Proceedings of the National Academy of Sciences showed the drug prolonged the lifespan in a mouse model of accelerated aging.

In that study, the rapidly aging mice fed the experimental drug lived more than three times longer than a control group, and their lungs and vascular system were protected from aging-like pathology, including emphysema and arteriosclerosis.

When cells or tissue age, they lose the ability to regenerate, and they secrete certain proteins, like a distinctive fingerprint. One of those proteins is PAI-1.

“We made the intellectual leap between a marker of senescence and physiological aging,” Vaughan says. “We asked is this marker for cell aging one of the drivers or mechanisms of rapid physiological aging?”

Vaughan first became interested in PAI-1 because it is the natural inhibitor of the body’s clot dissolving system. It specifically inhibits the clot-dissolving protein called t-PA, which was developed to treat people having heart attacks and strokes.

An earlier formulation of the experimental drug, TM5441, is one of only several chosen each year by the National Institute on Aging to be tested in its Interventions Testing Program, which investigates treatments with the potential to extend lifespan and delay disease in mice.

The National Heart, Lung and Blood Institute of the National Institutes of Health supported the work.

Source: Northwestern University

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