October 7, 2013
For years, doctors have observed a strange effect of alcohol abuse: People who drink heavily are more likely break their bones, and the risk can’t be fully explained by more frequent careless falls and alcohol-induced car accidents.
“As an orthopedic surgery resident, time after time, I see people come in with broken limbs while under the influence of alcohol,” says Roman Natoli, a doctor at Loyola University in Chicago.
Statistics suggest that their risk of a bone fracture is equal to that of a non-drinker a decade or two older than them, and they also tend to go through a slower healing process, filled with more frequent complications.
The reasons for this haven’t been entirely clear. Evidence suggested it had something to do with the way alcohol interfered with the activity of osteoblasts (the cells that synthesize new bone growth), while osteoclasts (the cells that remove old, damaged bone tissue) continued work as usual, leaving small cavities where new tissue was supposed to form. Data also indicated that the problem was dose-dependent—the more alcohol people drank, the greater the problem.
To find out the exact nature of the issue, Natoli and a group of medical researchers from Loyola did the logical thing: They got some mice rather intoxicated.
Specifically, the doctors, who presented their findings yesterday at the American Society for Bone and Mineral Research’s annual meeting, sought to simulate the effects of a single intense bout of binge drinking on mice who’d suffered a bone fracture.
To do so, they gave mice levels of alcohol that were roughly equivalent to a human with .20 blood alcohol content, several times the legal limit for driving. For an average person, reaching this level would require drinking about 6-9 drinks in an hour, and would likely lead to confusion, disorientation, dizziness, exaggerated emotions and severe risk of injury.
We have no idea if the mice experienced mood swings, but the doctors did look closely at the way their tibias healed after an induced fracture, as compared to induced fractures in a control group of mice that hadn’t had any alcohol. They found that, in the mice who’d gone through the alcohol binge, the callus—the mass of temporary bone tissue formed by osteoblasts in the gap between the two broken bone ends—was less dense and softer.
They also uncovered a few underlying reasons why this might be the case. For one, the body generates new bone tissue by recruiting immature stem cells to the site of the break, where they develop into osteoblasts and mature bone cells. The researchers found, however, that one of the main two proteins that the body uses to bring these stem cells to the fracture site—a protein called osteopontin, or OPN—was present in much lower levels in the mice who’d had so much alcohol.
Additionally, the alcohol-exposed mice seemed to suffer from a general problem that affects a range of cellular functions: oxidative stress. In essence, this type of stress results for an overabundance of oxidizing molecules—such as peroxides and free radicals—that can damage a variety of cell components, including proteins and DNA. It’s been implicated in a huge range of disorders in humans (including cancer, heart failure and Alzheimer’s).
The mice who’d been drinking had much higher levels of a molecule that scientists use as a proxy marker for oxidative stress (malondialdehyde), which jibes with previous studies that show alcohol can lead to higher production of oxidizing molecules and interfere with the body’s ability to break them down, especially in the liver. These higher stress levels, the researchers say, could inhibit bone growth and healing for reasons we still don’t fully understand.
If these findings apply to effects of drinking on the bone-healing process in humans, they could suggest some intriguing novel therapies for speeding bone growth in people who suffer from alcoholism, and perhaps even in non-drinkers. “The basic goal is to get these fractures to heal normally,” Natoli says.
One possibility that his team plans to test in future studies is injecting mice with extra stem cells, so that even with diminished quantities of the stem cell-recruiting protein OPN, they’d be able to get sufficient levels to the healing site. Another option could be giving mice an antioxidant called NAc, which combats oxidative stress throughout the body, perhaps speeding bone healing as well.
Of course, potential remedies notwithstanding, the findings should serve as a warning: if you’re a heavy drinker, your bones are likely weaker and have more difficulty healing. The silver lining, though, comes from other research, which has indicated that the problem is reversible—simply abstain from alcohol, and your bones will eventually regain most of their density and be able to heal normally again.
October 3, 2013
The importance of bees in our food system often goes unappreciated. Just by going about their daily business, these insects are responsible for pollinating three-quarters of the 100 crop species that provide roughly 90 percent of the global food supply. The most recent estimate for the economic value of this bee activity is that it’s worth over $200 billion.
But in recent years, an alarming number of bee colonies across North America and Europe have begun to collapse. As part of the phenomenon, formally known as Colony Collapse Disorder, worker bees fail to return to the hive after their pollen-collecting trips nearby. We still don’t fully understand what’s driving this trend, but the list of culprits likely includes pesticides, viral infections, intensive agriculture and perhaps even the practice of feeding bees high fructose corn syrup in place of the honey we take from them.
New research, though, suggests there may be an overlooked problem: the exhaust fumes produced by diesel-powered engines. As described in a study published today in Scientific Reports, a group of researchers from the UK’s University of Southampton found that the pollution produced by diesel combustion reduces bees’ ability to recognize the scent of various flowers—a key sense they use in navigating and finding food sources.
“Honeybees have a sensitive sense of smell and an exceptional ability to learn and memorize new odors,” Tracey Newman, a neuroscientist who worked on the study, said in a press statement. “Our results suggest that that diesel exhaust pollution alters the components of a synthetic floral odor blend, which affects the honeybee’s recognition of the odor. This could have serious detrimental effects on the number of honeybee colonies and pollination activity.”
To come to the finding, the group used extract from rapeseed flowers to create a scent that mimics the natural smell of several different flowers that the bees normally pollinate. In a sealed glass vessel, they mixed the scented air with diesel exhaust at a variety of concentrations, ranging from those that meet the EPA’s standards for ambient air quality to worst-case scenarios—concentrations of diesel pollutants (specifically the highly reactive NOx gases, nitric oxide and nitrogen dioxide) that greatly exceed these standards but are commonly detected in urban areas.
At all concentrations, just one minute after they added the pollutants, gas chromatography testing revealed that two of the main flower-scented chemicals in the original blend were rendered undetectable, degraded by the nitrogen dioxide. Previously, they’d trained 30 honeybees to remember the flowers’ scent—by rewarding them with a sip of sucrose when they extended their proboscis in response to smelling it—but when the scent had been altered by the exposure to diesel fumes, just 30 percent of the bees were still able to recognize it and extend their proboscis. They confirmed that the NOx gases in particular were to blame by repeating the experiments with isolated versions of them, instead of the whole range of diesel pollutants, and arriving at the same results.
It’s a small study on one bee population using one flowers’ scent, but it’s a concern. That’s because, although the study specifically looked at NOx gases that resulted from the burning of diesel, the gases are also produced by your car’s gasoline-burning engine. When NOx measurements are averaged out, few areas exceed the EPA’s standards, but in many urban locales during periods of high traffic, NOx levels can be much higher—high enough, this testing suggests, to disrupt bees’ ability to smell flowers.
It follows that diesel fumes could play a role in Colony Collapse Disorder: If bees are less effective at navigating and finding nectar, they might be more likely to get lost in large numbers. Colony collapse is typically characterized by the continual disappearance of worker bees during their travels—so it’s possible that the effects of engine exhaust plays a role.
“Diesel exhaust is not the root of the problem,” said Newman said in a press briefing. “But if you think of a situation where a bee is dealing with viral infections, mites, all the other stresses it has to deal with—another thing that makes it harder for the bee to work in its environment is likely to have detrimental consequences.”
October 2, 2013
Editor’s Note, Oct. 9: Based on several comments that mentioned that the Josephine Brine Treatment Facility stopped treating fracking wastewater in 2011, we did a bit of digging and found that the treated water downstream from the plant still showed signatures that fresh fracking water had run through it, according to the study’s authors. The post has been revised with this information, along with the fact that treatment does remove a good bit of contamination.
In the state of Pennsylvania, home to the lucrative Marcellus Shale formation, 74 facilities treat wastewater from the process of hydraulic fracturing (a.k.a. “fracking”) for natural gas and release it into streams. There’s no national set of standards that guides this treatment process—the EPA notes that the Clean Water Act’s guidelines were developed before fracking even existed, and that many of the processing plants “are not properly equipped to treat this type of wastewater”—and scientists have conducted relatively little assessment of the wastewater to ensure it’s safe after being treated.
Recently, a group of Duke University scientists decided to do some testing. They contacted the owners of one treatment plant, the Josephine Brine Treatment Facility on Blacklick Creek in Indiana County, Pennsylvania, but, “when we tried to work with them, it was very difficult getting ahold of the right person,” says Avner Vengosh, an Earth scientist from Duke. “Eventually, we just went and tested water right from a public area downstream.”
Their analyses, made on water and sediment samples collected repeatedly over the course of two years, were even more concerning than we’d feared. As published today in the journal Environmental Science and Technology, they found elevated concentrations of the element radium, a highly radioactive substance. The concentrations within sediments in particular were roughly 200 times higher than background levels. In addition, amounts of chloride and bromide in the water were two to ten times greater than normal.
This is despite the fact that treatment actually removes most of the contaminants from the wastewater–including 90 percent of the radium. “Even if, today, you completely stopped disposal of the wastewater,” Vengosh says, there’s enough contamination built up in sediments that “you’d still end up with a place that the U.S. would consider a radioactive waste site.”
In recent years, the use of fracking to extract natural gas from shale formations has boomed in several areas, most notably Pennsylvania’s Marcellus Shale, which has been called “the Saudi Arabia of natural gas.” The process involves injecting mix of water, sand and proprietary chemicals deep into rock at high pressure, causing the rock to fracture and allowing methane gas to seep upward for extraction.
Much of the concern over fracking has related to the seepage of these chemicals or methane from drilling wells into groundwater or the fact that high-pressure injection can trigger earthquakes, but the wastewater recently tested presents a separate, largely overlooked problem.
Between 10 and 40 percent of fluid sent down during fracking resurfaces, carrying contaminants with it. Some of these contaminants may be present in the fracking water to begin with. But others are leached into the fracking water from groundwater trapped in the rock it fractures.
Radium, naturally present in the shales that house natural gas, falls into the latter category—as the shale is shattered to extract the gas, groundwater trapped within the shale, rich in concentrations of the radioactive element, is freed and infiltrates the fracking wastewater.
Other states require this wastewater to be pumped back down into underground deposit wells sandwiched between impermeable layers of rock, but because Pennsylvania has few of these cavities, it allows fracking wastewater to be processed by normal wastewater treatment plants and released into rivers.
In 2011, Pennsylvania Department of Environmental Protection (PADEP) issued a recommendation that plants, including Josephine, voluntarily stop treating fracking wastewater. But Jim Efstathiou Jr. at Bloomberg News reports that, even though spokespeople at PADEP and Josephine say that the plant has stopped treating fracking wastewater, those claims are “contradicted by today’s study, which shows that the Josephine plant continued to treat Marcellus Shale wastewater through the beginning of this year,” according to Vengosh.
“Based on the isotopes that we measured we can see that the effluent that’s coming from Josephine in the last three years, including two months ago, still has the fingerprint of the Marcellus,” Vengosh told Efsathiou.
The treatment plants, many scientists note, are not designed to handle the radioactive elements present in the wastewater. Neither are they required to test their effluent for radioactive elements. As a result, many researchers have suspected that the barely-studied water they release into local streams retains significant levels of radioactivity.
This new work confirms that suspicion for at least one plant—which as about an hour east of Pittsburgh, and releases effluent into the watershed that supplies the city’s drinking water—and Vengosh believes that the findings would likely be similar for many of the other facilities in Pennsylvania. Especially concerning is the fact that, apart from in the water, the team found high levels of radioactivity accumulating on the sediments at the bottom of the stream over time. Radium has a half-life of 1600 years, so unless these sediments are removed, they’ll keep releasing radiation into the water for an extremely long period.
In addition, the high levels of bromide found in the wastewater is a concern, because even in slight quantities, the compound can trigger the formation of a toxic class of chemicals called halomethanes when it’s combined with chlorine. This is a problem because in rural areas, many residents treat well water by chlorinating it.
The study—which is part of a larger Duke project studying the effect of fracking on water—doesn’t show that fracking is inherently unsafe, but does show that without proper controls, the wastewater being dumped into the environment daily represents a very real danger for local residents.
Vengosh notes that there are better methods of treating fracking wastewater (he points to the plants operated by Eureka Resources as a model for adequately removing radioactivity), but these are more expensive to operate. But currently, without the push of federal regulations, companies looking to dispose of wastewater have no incentive to pay for this type of solution.
October 1, 2013
Last Tuesday, a 7.7-magnitude earthquake hit Pakistan, causing widespread destruction, the creation of a new island off the country’s coastline and at least 515 deaths.
Of course, there’s nothing we can do to prevent such disasters—earthquakes result from the shifting and collision of enormous, continent-scale tectonic plates over which we have no control. If we know a massive quake is about to strike, though, there may be measures we can take to better protect ourselves.
But how could we possibly know when a quake is about to hit? Seismologists are extremely good at characterizing the overall hazards that those living in fault zones face, but they’re far away from being able (and may never have the ability) to predict exactly when an earthquake will strike.
Undeterred, several different teams of scientists are hatching plans for a new kind of solution. And the key to their success may may be the smartphone in your pocket.
Their idea takes advantage of the fact that most new smartphones include a tiny chip called an accelerometer. These chips measure the movement of the phone in three directions (up-down, left-right, and backward-forward) to customize your experience as you use the phone—for example, rotating the display if you turn the device.
As it happens, seismometers (the large, expensive instruments used by geologists to detect and measure earthquakes) do essentially the same thing, albeit with much more accuracy. Still, the tiny accelerometers we already carry around with us all the time could allow scientists to gather much more real-time data than is currently available—there are countless times more smartphones than seismometers, they’re much cheaper and they’re already deployed in a wide range of locations—if they can actually measure earthquake movement with sufficient precision.
Recently, Antonino D’Alessandro and Giuseppe D’Anna, a pair of seismologists at Italy’s Istituto Nazionale di Geofisica e Vulcanologia, set out to resolve this question. To assess the accelerometers—specifically, the LIS331DLH MEMS accelerometer used in iPhones—the duo placed five iPhones on a vibrating table in a variety of positions (flat, angled on top of a wedge-shaped piece, and vertical) and compared the data they recorded with a professional-quality earthquake sensor for reference.
Their results, published Sunday in the Bulletin of the Seismological Society of America, showed that the iPhone accelerometers performed even better than they expected. “When we compared the signals, we pleasantly surprised by the result—the recordings were virtually identical,” D’Alessandro says. “An accelerometer that costs a few dollars was able to record acceleration with high fidelity, very similar to a professional accelerometer that costs a few thousand.”
There are some limitations: the iPhone accelerometers aren’t as sensitive to weak vibrations, so during the tests, they were only able to record movements that correspond to earthquakes that would register as magnitude 5 or higher. But ”these limits will be overcome in the near future,” says D’Alessandro. “Because these chips are widely used in laptops, games controllers and mobile phones, research into improving them is going on around the world.”
The next step would be developing software to allow normal users to harness these accelerometers’ capabilities, turning their smartphones into mobile earthquake sensing systems. Last December, Berkeley researchers announced plans to develop an app that would allow users to donate their accelerometer data to earthquake research. Stanford’s Quake-Catcher Network and Caltech’s Community Seismic Network—both of which use small purpose-built seismometers that are distributed to volunteers and plugged into their computers—could serve as a model for this sort of network.
Once in place, the network would be able to gather a huge amount of data from thousands of geographically-dispersed users, allowing researchers to see how quakes move with finer resolution. If enough phones are on this network, emergency workers may be able to quickly gauge where they could most efficiently devote their time after a quake hits.
But how do you go from documenting earthquakes to warning people about when dangerous shaking will occur? As The Atlantic points out, the key is that earthquakes are actually comprised of two types of waves that ripple through the earth: P-waves, which arrive first and are difficult for humans to sense, and S-waves, which typically come a few seconds later and cause the majority of the physical damage.
If we had software installed on our phones that automatically detected strong P-waves and sounded an alarm, we might have a few scant seconds to take cover before the S-waves hit (officials recommend dropping to the ground, huddling under a stable table or desk and getting away from windows and doors). It’s not much, but in some cases, a just a few crucial seconds of warning could make all the difference.
September 30, 2013
That hairless, wrinkly, fanged rodent in the photo above? It’s a naked mole rat, and deep inside its cells, its molecular machinery might hold the secret to living a very, very long time.
“They are an incredibly striking example of longevity and resistance to cancer,” says Vera Gorbunova, a biologist at the University of Rochester who studies the long-lived rodents, which have been shown to survive for up to 28 years—a lifespan eight times that of similarly-sized mice—and have never once been observed to develop cancer, even in the presence of carcinogens.
In recent years, Gorbunova and her husband Andrei Seluanov have looked closely at the species, which lives in underground colonies in East Africa, hoping to figure out how exactly it manages to survive so long. As revealed in new research her team published today in Proceedings of the National Academy of Sciences, their team thinks they’ve found at least part of the answer: naked mole rats have strange ribosomes.
Every one of our cells (and, for that matter, every living organism’s cells) converts the genetic instructions present in our DNA into proteins—which control a cell’s overall operation—through a process called translation. Tiny microscopic structures called ribosomes handle this translation, reading genetic instructions that specify a particular recipe and churning out the protein accordingly.
The ribosomes in almost every multicellular organism on the planet is made up of two large pieces of RNA, a genetic substance similar to DNA. But last year, one of the Rochester lab’s students was isolating RNA from cells taken from the naked mole rats when he noticed something unusual. When he separated the RNA pieces, instead of seeing two distinct pieces of ribosomal RNA, he saw three.
“At first, we thought we were doing something wrong and it’d gotten damaged,” Gorbunova says. “Because for all mammals, you’d see two, but we kept seeing three.”
After a variety of testing confirmed that it wasn’t an experimental error, they decided to look more closely at the potential effects of this unusual structure. Other research had suggested that artificially interrupting the translation process to make ribosomes less accurate could produce poorly-built proteins that accumulate and lead to cell death, which raised the possibility that the mole rats’ unusual ribosomes did the opposite—producing fewer transcription errors and extending lifespan. To test the idea, Gorbunova developed a means of seeing just how accurate the mole rats’ ribosomes were at converting genetic instructions into proteins.
It turned out that, compared to mouse ribosomes, these three-part structures made between four and forty times fewer errors during the translation process. At this point, it’s unclear how exactly that might lead to longer lifespans, but the researchers believe it plays a key role.
Even so, the rodents appear to benefit from other, unrelated mechanisms that allow them to live uncommonly long lives. In June, Gorbunova and Seluanov announced the discovery that the rodents also produce a novel cellular compound that appears to prevent them from getting cancer.
Both of these mechanisms prompt an obvious question: Why are naked mole rats blessed with these anomalous, life-extending characteristics? “It’s not random,” Gorbunova says. “It has to do with the ecology of the species.”
Because the rodents live underground, in ultra-social colonies, she explains, they’re much less prone to random deaths caused by accidents or predation. The fact that the risk of dying randomly is so much lower means that, from an evolutionary standpoint, it makes more sense to invest in cellular mechanisms that might allow the creatures to live longer. Even if a mouse had three-part ultra-accurate ribosomes and cancer-fighting substances, in other words, it’d probably be eaten within a year by a predator anyway, so it never had the chance to evolve mechanisms that would allow it to live to 28.
But the naked mole rats did. Gorbunova and Seluanov want to proceed by seeing whether either of their special mechanisms—longevity or cancer resistance—could be introduced into mouse cells, and whether they might lead to corresponding extensions in lifespan. If they’re successful, they hope that, someday, we might even be able to extend our own lifespans by copying the naked mole rats’ success.