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They’re Taking Our Tires!

In the early 1980s, Aedes albopictus, a mosquito species native to Southeast Asia that spreads dengue fever and yellow fever, turned up deep in the American South. Though there were no reported disease outbreaks, epidemiologists were still worried, especially when huge swarms arrived in Houston. The so-called Asian tiger mosquito had clearly gained a foothold in the U.S., but no one knew how it had gotten there. So medical entomologist Paul Reiter headed to the city, situated near the Gulf of Mexico, to search for larvae (and answers) in containers of standing water — especially inside discarded, used tires. There, a chance encounter along a road on the outskirts of town put Reiter on the trail to solving the mystery.

In His Own Words …

I found myself in Houston, accompanied by a colleague, kicking tires and gathering information on the character and location of infested sites – the sort of things that medical entomologists like to do. We concentrated our efforts on a profusion of discarded tires on a lonely acre of wasteland not far from the city’s port. Nearly all contained water and were infested with tiny larvae. They were obviously thriving, but the puzzle remained: How had they gotten there?

On the second day of my visit, toward sundown, we were packing to leave when a pickup truck drove by and stopped some 150 yards away. Two men got out and started sifting through tires. They would occasionally chuck one into their vehicle.

Our tires! We had marked them for study!

I summoned up courage and approached them. “Good evening, gentlemen. May I ask why you are collecting these tires?”

“Our company ships them to Mexico and Guatemala,” they said. “They also ship them in from India.”

A moment of bewilderment, then: Eureka! The men looked puzzled that I was so excited.

A. albopictus was an Asian mosquito. And they’d said these tires were coming from India.

The next morning, I raced to the importing company. The boss was unsmiling and suspicious. Yes, his company imported used tires, he said, but from Japan, not India. Nineteen containers a month. Yes, he did export to Mexico and to several countries in Central America. Lots of people did, and they imported them from many other countries.

I was at the local Department of Commerce by the afternoon, leafing through annual volumes of monthly trade data, import and export. Sure enough, for every month of every year, there were entries under a series of categories: automobile tires, used; truck tires, used; tractor tires, used; airplane tires, used; and so on. Thus it was that I became the world’s foremost used-tire epidemiologist!

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Health

People Were Definitely High For the 2017 Solar Eclipse, Study Finds

(Credit: Thanakrit/Santikunaporn)Shutterstock)

Day turning to dusk in the span of minutes, sunsets all around, a jewel-bright ring in the sky where the sun once stood — an eclipse is an otherworldly experience. But, if there’s one thing we like to do with amazing experiences, it’s try to make them better. Though you may have already guessed, a new study provides the confirmation: Lots of people got high for the 2017 solar eclipse.

The new data comes courtesy of a study from a group of researchers from Murray State University in Kentucky looking at how celebratory events affect drug use. They compared two towns in Kentucky on a normal week and the Fourth of July, and looked at the solar eclipse in one town and the first week of a college semester in the other.

In the Water

Drug use being the kind of thing people don’t necessarily like to make public, the researchers turned to a clever, and increasingly common, method of assessing what and how much people were putting into their bodies: They simply analyzed the sewage water. What goes into our bodies must come back out, and most drugs show up in our urine wholesale or betray their presence through signature metabolites our bodies break them down into. It’s a much more accurate and timely method of measuring drug use than relying on self-reported surveys or estimates based on drug busts, and it’s been used all over the world, though not often in the U.S.

“We can utilize this technique to determine the level of drugs people are consuming yesterday, today,” says Bikram Subedi, an assistant professor at Murray State University and a co-author of the study. “Within 24 hours we can get all the results.”

The researchers took samples from wastewater treatment plants before, during and after big events and sampled them in the lab for the markers of drug use. Big celebrations, unsurprisingly, have a noticeable effect on drug use, they found, in research presented today at the 256th National Meeting & Exposition of the American Chemical Society. Both the Fourth of July and the solar eclipse produced significant spikes in levels of a range of drugs, from weed to cocaine to MDMA, when compared to a baseline reading.

Black Hole Sun

Compared to a more prosaic celebration like the Fourth of July, though, the eclipse seems to have encouraged a somewhat different kind of drug use. Marijuana, MDMA and amphetamine (a broad class of stimulants that includes drugs like Adderall and Vyvanse) use were all significantly higher during the eclipse than during the Fourth. More worryingly, though, drugs like morphine, cocaine and methamphetamine all spiked during the eclipse, though not as much as during the Fourth. The researchers didn’t look at other psychedelic drugs like LSD, psilocybin or DMT.

The one drawback to the work, however, is that they weren’t able to control for the massive influx of people the eclipse, and to a lesser extent events like the Fourth, brought. Some towns in the path of totality saw more than 10,000 people flood in for the event, so it’s impossible to say whether people did more drugs during the eclipse, or if there were simply more people around to do them.

The takeaway here is two-fold. One, we can prove that, yes, people did get high during the eclipse, using the stunning celestial alignment as a opportunity to try and expand their minds further under the influence of psychoactive substances. (No one seems to have gone blind while tripping on LSD , though, as one bit of 1960s anti-drug propaganda had it.)

On another level, however, it reveals that celebrations present an even greater danger for people addicted to already harmful drugs like meth and opioids. What’s more, that correlation holds whether it’s an established holiday like the Fourth of July or a more uncommon event like the eclipse. As the opioid crisis continues, the information could be helpful for everyone from police officers to hospital administrators who must deal with the the effects of addiction and overdose.

Their work, and similar analyses worldwide, are indicating that we may have underestimated howe many drugs are actually being consumed, something that has real implications for public health agencies. In the future, Subedi hopes that such wastewater monitoring can be carried out in larger cities and over extended periods of time. Such a project would track the ebb and flow of drug use to better inform the ways that we as a society deal with illicit substances.

And, with another eclipse set to blaze a path across the U.S. in 2024, the study offers a preview of what we might expect in terms of some people’s viewing plans.

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Health

Uncertain Hope Blooms for Tasmanian Devils

Using remote camera traps, photographer Heath Holden captured rare images like this one of wild Tasmanian devils (Sarcophilus harrisii) in their natural habitat. The animals’ bright red ears and eerie, raucous scuffles earned the scrappy marsupials their haunting common name. (Credit: Heath Holden)

On a misty summer morning in 2015, Manuel Ruiz ditched his pickup truck along a dusty two-track road in northwest Tasmania and trod into a grove of eucalyptus. He was searching for a devil. “If I were a devil, this would be a nice place to spend the night,” thought Ruiz, a wildlife veterinarian and doctoral candidate at the University of Tasmania.

The Tasmanian devil (Sarcophilus harrisii) is the world’s largest carnivorous marsupial. Despite that distinction, the animal is only about the size of a raccoon. But what the species lacks in heft, it makes up for with tenacity. At night, devils hunt and scavenge wallabies, possums, and other small mammals under the cover of their black fur. During the day, they retreat to underground dens and sleep off the rigors of their nighttime exploits.

As picturesque and wild as northwest Tasmania’s landscape may be, it is also a battleground for disease, and in 2015, Ruiz was patrolling the epidemic front lines. It didn’t take him long to find evidence of the fight. A few dozen paces into the undergrowth, he knelt to inspect a white cylindrical trap nestled amidst a lush cluster of ferns. Inside, a female devil peered down her pointed, whiskered snout at Ruiz. He had seen this individual, nicknamed Leesa, once before. A raw, oozing tumor as large as a ping-pong ball gaped behind the right corner of her mouth—the mark of a debilitating cancer.

Leesa and thousands of other devils suffer from what’s known as devil facial tumor disease. The cancer was first detected in 1996 in eastern Tasmania. Since then, it has spread rapidly across the island state, causing an overall species decline of 80 percent, with localized declines of more than 90 percent. A decade ago, scientists predicted imminent extinction for the critically endangered species.

Since then, some wild devils have begun to show signs of resistance, offering new hope for the species’ survival. And while the quickly spreading cancer has wrought great devastation, it has also offered scientists a rare window into the progression of cancer at large. Researchers are monitoring the disease as it runs its course, searching for clues that will help them derail it. They’re hopeful that their findings might soon be applied to combatting cancers in other species—maybe even in humans someday.

A Tasmanian devil with two large facial tumors walks along a fire trail at night. These tumors, caused by a form of cancer, can grow so large that they ultimately prevent the animal from feeding.

A Tasmanian devil with two large facial tumors walks along a fire trail at night. These tumors, caused by a form of cancer, can grow so large that they ultimately prevent the animal from feeding. (Credit: Heath Holden)

no matter what species it’s in,” says Greg Woods, an immunologist who recently retired from the Menzies Institute for Medical Research at the University of Tasmania after two decades studying the devils. Genetic mutations trigger runaway tissue growth, which leads to detectable tumors in most forms of cancer. “It’s the same mechanism,” says Woods, “just in the devils’ case it’s transmissible.”

Most cancers arise within their hosts and die along with them. But some are infectious, shuttled by agents like viruses (as in California sea lions), bacteria, or other microscopic vehicles. In devil facial tumor disease, the cancer cells themselves are the infectious agents—making the tumors transmissible from one individual to another. Transmissible cancers are not well understood, partly because they only recently landed on researchers’ radar screens. Of the eight known transmissible cancers identified so far in devils, dogs, and marine invertebrates, seven were detected within the past three decades.

A devil is captured with a visible DFTD (Devil Facial Tumour Disease) near the upper canine and is checked out and a biopsy is taken for further study.

A devil is captured with a visible DFTD (Devil Facial Tumour Disease) near the upper canine and is checked out and a biopsy is taken for further study. (Credit: Heath Holden)

Devil facial tumor disease is passed from devil to devil through physical contact. Individuals brawl, bite, and scratch one another in competition for food and throughout the breeding season. (Early European settlers likened the haunting hisses and growls of their scuffles to the sounds of the Devil, and the name stuck.) During these clashes, an infected individual can transfer live tumor cells from its open wounds to a healthy devil’s face. The cells then grow into disfiguring, puffy blights that bloom in and around the animal’s mouth, face, and neck. Once contracted, the cancer is almost always the kiss of death.

Tumors may take down their host in a number of ways: by acquiring deadly bacterial infections; by growing so large they physically prevent the devil from feeding; or by metastasizing to other systems in the body and eventually causing organ failure. Once facial tumors appear, the cancer typically kills its host within six months to a year.

Scientists from government agencies and research institutions across Tasmania are tracking how devil populations fare in the wake of the cancer’s swift spread. Monitoring teams routinely visit sites across the island, staggering their data collection geographically to complement one another. Ruiz, who is a member of the University of Tasmania team, tracks the devil’s physiological response at several sites stricken by cancer in the northwest region. Out in the field, he and his colleagues snap mugshots of all individual devils they capture, which, when viewed as a collection, are reminiscent of a Most Wanted poster. Along with tissue samples, these photos allow the team to assess tumor growth over time.

Visitors observea captiveTasmanian devilat Trowunna Wildlife Sanctuary, one of the first facilities to successfully breed devils in captivity and now a recognized authority on devil husbandry.

Visitors observea captiveTasmanian devilat Trowunna Wildlife Sanctuary, one of the first facilities to successfully breed devils in captivity and now a recognized authority on devil husbandry. (Credit: Heath Holden)

The scientists also analyze blood samples to chart the devils’ immune response as the cancer progresses. “We can be collecting blood samples, and the devils are just snoring away without a care in the world,” says Ruiz, who has trapped, micro-chipped, and tracked more than 400 devils. “They seem like a little teddy bear when they’re asleep—but with big jaws that can chop your finger off at any time.”

Even perfectly healthy devils are short-lived: Most individuals live just six years. Since the cancer’s outbreak two decades ago, several generations of devils have come and gone, and that short generation time may confer a selective advantage. People often think of evolution as happening over thousands or millions of years, but, according to Ruiz, it’s happening right now in Tasmanian devils and their cancer. “This is one of the most interesting systems in the world for understanding the evolution of pathogens and their hosts,” Ruiz says.

Once it emerged, devil facial tumor disease moved swiftly. Its progression through Tasmania was so alarming that the government launched the multi-stakeholder Save the Tasmanian Devil Program a mere seven years later. As an insurance measure, the program established a disease-free population of devils on an island off the Tasmanian coast. Nearly two-dozen zoos and wildlife parks across mainland Australia and Tasmania also pitched in to help maintain genetic diversity in captive populations. By 2013, the program had raised more than 500 captive, healthy devils. But officials were reluctant to re-introduce these individuals into the wild; odds were too high that the animals would contract the cancer and die.

An expectant mother will lay down a trail of saliva for newborn pups to follow as they wriggle from the birth canal to her pouch. There they find warmth, protection, and nourishment.

An expectant mother will lay down a trail of saliva for newborn pups to follow as they wriggle from the birth canal to her pouch. There they find warmth, protection, and nourishment. (Credit: Heath Holden)

That same year, scientists discovered that devil facial tumor disease had the capacity to hide markers on its cell surfaces. These molecules are what typically signal to the immune system that an intruder is present. With this discovery in mind, a team led by Woods at the Menzies Institute set out to develop a vaccine that could direct the devil’s immune system to recognize and target the cancer cells despite the inherent absence of more obvious signals. They first treated dead cancer cells with cytokines, special molecules that force the disease cells to express their surface markers. This makes the cancer recognizable to the body’s immune defenses. The team then injected these modified cancer cells into healthy devils. By delivering two types of immune-activating molecules known as antigens and adjuvants at the same time, the devils’ immune systems sprang into action—flagging the injected cells and producing antibodies to fight back. “We’re fighting cancer with cancer,” says Woods.

The scientific community was buoyed by the promise of this finding. But the trials had their limitations. Sample sizes were small, and vaccinated individuals released into the wild were sometimes difficult to catch again, making it a challenge to measure the vaccine’s effectiveness. Additionally, most of the animals that were eventually recaptured came back with malignant growths, indicating that while the vaccine could stimulate the immune system to produce tumor-fighting antibodies, it wasn’t protecting the devils from contracting cancer in the wild.
A year later, just as vaccine research was gaining momentum, researchers detected a new transmissible facial cancer in devils—a genetically distinct cell line that also causes tumorous boils across the face. So far, scientists have diagnosed only about a dozen devils with the new cancer. But they already know that it’s possible for an individual to contract both types simultaneously.

“There’s something that might make devils more susceptible to disease,” says Rodrigo Hamede, a research fellow at the University of Tasmania, and one of Ruiz’s advisors, who studies the ecology of transmissible cancer. According to Hamede, the emergence of a second transmissible cancer in the same species is rare and raises many questions about the perfect storm of factors that has targeted devils twice in just 20 years. He hopes to identify what makes devils susceptible; his findings may shed light on whether we could see a transmissible cancer emerge in humans someday.

A curious Tasmanian devil peeks through a window at Trowunna Wildlife Sanctuary.In the wild, devils roam highly diverse habitats, from sandy beaches to lush rainforests and the high alpine.

A curious Tasmanian devil peeks through a window at Trowunna Wildlife Sanctuary.In the wild, devils roam highly diverse habitats, from sandy beaches to lush rainforests and the high alpine. (Credit: Heath Holden)

When Ruiz first trapped Leesa in the summer of 2015, four of her teats were engorged, a sign that she had nursing pups awaiting her return to the den. Despite the gaping wound on her face, she was docile and calm when he interacted with her, which is typical of wild devils. (Captive devils often show more aggression toward humans.) When Leesa showed up in one of his traps a third time, five months later, Ruiz was happy to see that she had survived the disease long enough to raise and wean her pups. And to his delight, her tumor had taken an unexpected turn.

Once raw and red, the lump on her right cheek now gleamed with healthy tissue. Ruiz thumbed through Leesa’s previous datasheets in excitement to confirm before phoning Hamede from the field: Leesa’s tumor had naturally regressed. Somehow, she had developed antibodies to fight the disease.

Leesa was not the first wild devil to show spontaneous tumor regression. The University of Tasmania team had detected six other individuals with naturally regressing tumors before Leesa’s case was documented. Since then, eight more animals—a total of 15 devils at northwest monitoring sites—have shown signs of regression. And other individuals are simply living longer with their tumors; although transmission rates have remained high in northwest Tasmania, mortality rates and the overall devil population in the region have stabilized.

Adult female devil, Leesa is released from the scientist, Manuel Ruiz's mesh bag after her checkup. Leesa is one of very few devils who has been recored to have tumour regression in the wild.

Adult female devil, Leesa is released from the scientist, Manuel Ruiz’s mesh bag after her checkup. Leesa is one of very few devils who has been recored to have tumour regression in the wild. (Credit: Heath Holden)

Armed with this information, scientists have been working to understand why some individuals are responding differently to the disease. Two years ago, a team that included Hamede looked at whether the species could be evolving natural mechanisms to combat devil facial tumor disease. They compared individuals from three sites across Tasmania, all born four to six generations after the cancer’s outbreak, and detected rapid changes in their genomes; two regions of genetic code in particular looked different. These regions contain genes that are known to influence cancer risk and immune function in humans—suggesting that devils could be evolving resistance. If scientists can firmly establish that certain devils have evolved resistance to the cancer, they may be able to accelerate the recovery of the species by introducing immune individuals into populations that currently lack genes for resistance.

Devils aren’t the only species benefitting from this research. Hamede hopes that what we learn from devils will inform immunotherapy—harnessing the body’s immune system to combat cancer—when treating other cancers, even those in humans. He and his colleagues are investigating differences in immune profiles in wild devils and the role they might have in the animals’ ability to resist tumors. By analyzing facial tumor disease and human cancer side by side, scientists can learn more about the fundamental role the immune system plays in combatting disease. “We have a more holistic view of cancer now that we wouldn’t have had without devils,” says Hamede.

Meanwhile, Woods’s team continues working to develop a vaccine that can prevent devils from contracting facial tumor disease. In the most recent trials, the team vaccinated more than 50 disease-free individuals from insurance populations and released them into the wild. Some animals were fitted with GPS collars to allow for higher recapture success and follow-up immunizations. The study found that 95 percent of vaccinated individuals produced antibodies that combat the disease.

The next step is seeing whether the vaccine can be strengthened in a way that would lead to tumor regression and keep devils from contracting facial tumor disease in the first place. The team remains optimistic that in the not-too-distant future, captive devils destined for the wild might be released with full immunity to the disease. These introductions will bolster wild populations that are still hanging on, despite the dire predictions issued a decade ago.

Ruiz last trapped and released Leesa in August of 2016, when she was an elderly 7 years old. While he assumes she no longer patrols the eucalyptus forests of northwest Tasmania, he feels strongly that Leesa likely died of old age or another natural cause—not from cancer.

[This article originally appeared in bioGraphic.]

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A “Zombie Gene” in Elephants Could Protect Them From Cancer

(Credit: Gregory Zamell/Shutterstock)

Millions of years ago, a gene in mammals became useless. Now scientists have discovered the gene has come back to life in elephants, where it’s exceptionally good at killing damaged cells. The “zombie” gene may explain why the long-lived pachyderms rarely develop cancer and how large animals evolved.

A Cancer Mystery

Elephants are a paradox for scientists. The giants appear largely resistant to cancer, which is odd as their long lifespans and humongous size ought to make them highly susceptible to the disease. The thinking goes that the longer one lives, the more time the body has to pick up cancer-causing mutations. Likewise, big bodies have more cells than small ones. Since all cells are equally vulnerable to damage, more cells mean higher risk for developing the condition. Elephants are guilty on both counts, yet the behemoths get cancer far less than scientists expect.

Vincent Lynch, a geneticist and evolutionary biologist at the University of Chicago in Illinois, wanted to know what gives elephants this cancer immunity. He figured long-lived, sizable animals like elephants must have evolved a way to protect themselves from the disease.

So, he and his team probed the genomes of more than 50 long-living mammals that run the gamut of animal body sizes from bowhead whales to bats, voles and naked mole rats. Their analysis revealed that elephants, as well as manatees and hyraxes, have seven to 11 extra copies of a gene called LIF, whereas every other animal they investigated has only one.

LIF6, the Zombie Gene

In most mammals this single copy of the LIF gene can help prevent cancer development under the right circumstances, so elephants’ numerous duplicates seem like a boon. But it turns out that most of these extra LIF genes don’t do anything anymore.

“We found that elephants and their relatives have many non-functioning copies of the LIF gene,” Lynch said in a statement. But “elephants themselves evolved a way to turn one of these copies, LIF6, back on.”

The researchers had shown in previous work that elephant’s cells are highly sensitive to DNA damage. So, to figure out if LIF6 might play a role, the team stressed the cells with carcinogens. Although LIF6 is normally turned on at very low levels, when DNA damage occurs, it gets expressed at much higher rates. That activates a series of reactions that lead to cellular suicide in the potentially cancerous cells, the team reported August 14 in the journal Cell Reports.

“The elephant cells just died; they were entirely intolerant of DNA damage in a way their relatives’ cells were not,” Lynch said. “Because the elephant cells died as soon as their DNA was damaged, there was no risk of them ever becoming cancerous.”

When the team put the gene into other animals’ cells growing in petri dishes, those cells also died. That makes LIF6, the zombie gene that came back from the dead to kill weak cells, a potential cancer-fighter in other species besides elephants as well.

The work also begins to solve the mystery of elephant’s large size and long lifespan. An evolutionary comparison of LIF6 in elephants, mammoths and mastodons revealed LIF6 came back to life in elephant ancestors around the same time the animals became giants, meaning the gene may have played a role in allowing animals to evolve large bodies.

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