A new device could one day give real-time measurements of the head impacts sustained by football players.
The research could also help characterize the forces sustained in more common head traumas, such as car accidents and falls.
The debilitating effects of repeated concussions on NFL players have been well documented. What scientists still don’t clearly know is whether those injuries are the result of thousands of tiny impacts, or singular, crushing blows to the brain.
For the past few years, David Camarillo, an assistant professor of bioengineering at Stanford University, and his colleagues have been supplying Stanford football players with special mouthguards equipped with accelerometers that measure the impacts players sustain during a practice or game.
Previous studies have suggested a correlation between the severity of brain injuries and the biomechanics associated with skull movement from an impact.
Camarillo’s group uses a sensor-laden mouthguard because it can directly measure skull accelerations—by attaching to the top row of teeth—which is difficult to achieve with sensors attached to the skin or other tissues.
So far, the researchers have recorded thousands of these impacts, and have found that players’ heads frequently sustain accelerations of 10 g forces, and, in rarer instances, as much as 100 g forces. By comparison, space shuttle astronauts experience a maximum of 3 g forces on launch and reentry.Building a better mouthguard
Although these mouthguards have provided a wealth of data, they were not very discerning: A player tossing his mouthguard to the ground can register the same force as if he had been run over by a linebacker.Related Articles On Futurity
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This has required Camarillo’s team to spend hours going through videos of games and practices to determine whether each player’s time-stamped data matches a true impact or a spurious event, says Lyndia Wu, a bioengineering doctoral student in Camarillo’s lab and the lead author of a new paper in IEEE Transactions on Biomedical Engineering.
To overcome this dilemma, the researchers incorporated infrared proximity sensors into the mouthpiece, so that it can detect when the device is firmly seated against the player’s teeth. (Teeth have a special property whereby they absorb and scatter infrared light, allowing the sensor to be triggered when in direct contact with the teeth.)
Furthermore, machine-learning algorithms sift out additional “noisy” signals to only focus on real impacts.
Wu says that both of these improvements make it faster to collect data, which will become critical for expanding research to other subject populations and collecting a larger data set to ultimately prove what specific aspects of head acceleration cause concussions.
“We do know that sustaining a second injury right after the first injury will exacerbate the trauma, so detecting that injury is critical,” Wu says. “However, diagnosis often relies on players to self-report injuries, which doesn’t work often for a variety of reasons.
“A player typically shakes it off, thinking he will be fine, without telling the coaches or trainers. Eventually, we hope to have a device that is able to screen for injury in real time.”Off the field
The newly developed technology has been tested on an impact dummy in the lab, and shows 99 percent accuracy in detecting head impacts. The next step involves refining the algorithms using field data.
A common issue with some of the commercially available systems is that they can provide too many warning alerts. Camarillo says it will be critical to make sure that the mouthguard can separate true impacts from other events, such as chewing, and to also conduct further studies to understand the true physiological significance of impacts.
Camarillo’s lab is also interested in developing new helmets or other protective headgear; with the instrumented mouthguard, they can collect head biomechanics data to gain insight into injury mechanisms, which will in turn guide preventative technology design.
The work also has important implications off the football field. Although football players are at heightened risk, Camarillo says, the number one cause of traumatic brain injuries is falling, which is most common among children and the elderly.
“Our football team has been extremely cooperative and interested in helping solve this problem,” Camarillo says. “Football players willingly put themselves at risk at a well-defined point and time in space for us to carry out our research in this ‘lab.’ What we are learning from them will help lead to technologies that will one day make bike-riding and driving in your car safer, too.”
Source: Stanford University
New research finds that personality can determine a spider’s specialization—caregiver or hunter-warrior.
While most spiders are soloists, a few species, such as the Anelosimus studiosus (found in Tennessee, among other places) live in groups. And unlike ants, for example, their specialization isn’t a matter of size or physical structure.
PhD student Colin Wright and his mentor Jonathan Pruitt, assistant professor of behavioral ecology at the University of Pittsburgh, separated the docile spiders from the aggressive by observing how much space they demanded from fellow colony members. Aggressive females demand more space than docile ones.Related Articles On Futurity
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The team ran the spiders through a series of tests, examining their performance in colony defense, prey capture, parenting skills, and web repair.
The aggressive cohort was great at defending the web, capturing prey, and repairing their web. But they were awful parents.
“We didn’t know what the docile spiders did,” Wright says. “Were they just freeloaders?” No, it turns out, they were the ones who were capable of rearing large numbers of offspring.
In a separate study, Pruitt also created all docile, all aggressive, and mixed colonies of spiders.
The docile colonies died out first. No one was there to protect them from “parasite” spiders that picked off their young and stole their prey. The all-aggressor group died off second, as they became cannibalistic toward their young.
The mixed group thrived.
The findings appear in the Proceedings of the National Academy of Sciences.
Source: University of Pittsburgh
A new study links prolonged episodes of sepsis—a life-threatening infection and leading cause of death in hospitals—to the reactivation of dormant viruses in ill patients.
In healthy people, latent viruses are kept in check by the immune system. But new research provides strong evidence that when sepsis lingers for more than a few days, which is common, viruses re-emerge and enter the bloodstream, signaling that the immune system has become suppressed.
This state of immune suppression may leave patients unable to fight off secondary infections, such as pneumonia.
A research team at Washington University School of Medicine in St. Louis published their findings in PLOS ONE. Their work suggests that drugs that “rev up” the immune system could be incorporated into the treatment of prolonged sepsis.Therapy shift
“A controversy has existed over whether patients with sepsis progress to a state of immune suppression,” says co-senior author Gregory Storch, a virologist and chief of the Division of Pediatric Infectious Diseases. “The finding that critically ill patients with sepsis have a number of different viruses circulating in the bloodstream is compelling evidence they are immune-suppressed and dramatically could alter therapy for sepsis.”
Surprisingly, the researchers detected levels of viruses in sepsis patients that were on par with those seen in patients who have had organ transplants and are taking immune-suppression drugs to prevent rejection.
“This is an indicator of the degree of immune suppression in septic patients, and it tells us they are highly immune-suppressed,” explains senior author Richard S. Hotchkiss, professor of anesthesiology.Sepsis infections
More than 200,000 patients in the United States die annually of sepsis. The condition develops when the body mounts a massive immune response to infection, triggering excessive inflammation that can lead quickly to organ failure. While some patients die soon after the condition develops, most sepsis deaths occur four or more days after onset.Related Articles On Futurity
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“We’ve gotten much better at getting sepsis patients through the initial phase,” says Hotchkiss, who also is a professor of medicine and of surgery. “But too many patients die several weeks or months after sepsis sets in, primarily of secondary infections.”
Earlier research has hinted that lingering sepsis may be linked to immune suppression. But a lack of compelling evidence has kept the debate going.
For the current study, first authors Andrew Walton and Jared Muenzer used polymerase chain reaction (PCR) testing to detect a range of viruses in blood and urine samples from 560 critically ill patients with sepsis, who were treated in the surgical and medical intensive care units at Barnes-Jewish Hospital.
As a comparison, they performed the same test on 161 critically ill patients in the hospital who did not have sepsis and 164 healthy patients who were having outpatient surgery.Latent viruses
“We were looking for viruses that people are commonly exposed to early in life and that persist in the body in a latent form that doesn’t cause sickness,” says Storch, the professor of Pediatrics. “No one had really looked at this in a comprehensive fashion before. These viruses have the potential to reactivate if the immune system is suppressed.”
Patients with lingering sepsis had markedly higher levels of viruses detectable in the blood, compared with the healthy controls and critically ill patients without sepsis. Among the sepsis patients, for example, the researchers found that 53 percent had Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had herpes-simplex virus, and 10 percent had human herpes simplex virus-7.
These viruses generally don’t lead to significant illness in people who are healthy but can cause problems in patients who are immune-suppressed.
The researchers noted that 43 percent of patients with sepsis had two or more viruses detected in their blood or urine during their hospital stays. However, this finding may underestimate the frequency of viral infections because some of these patients were not tested for all viruses. In a subgroup of 209 sepsis patients tested for all viruses, 54 percent were positive for two or more.Trigger for additional infections
Additionally, the researchers found that septic patients with higher levels of viruses detected in their blood were more likely than critically ill patients without sepsis to have more severe illnesses, secondary fungal, and bacterial infections, and longer stays in the intensive care unit.
Also, septic patients with evidence of cytomegalovirus in plasma, a component of blood, had significantly higher 90-day death rates than septic patients who tested negative for the virus, although it is not clear whether the cytomegalovirus contributed to the additional deaths.Viral testing
“We stumbled onto more viruses than we expected, and we don’t know yet whether some of these viruses are causing problems in their own right,” Storch says. “We think this paper will stimulate others to carry out further investigations of the role of latent viruses in sepsis.”
A further direction for researchers is to determine whether PCR testing for a panel of latent viruses could be used as a read out of the state of a person’s immunity. If this is the case, doctors could perform PCR testing in patients with cancer, autoimmune diseases and infections and use results to guide treatments.
The findings also open the door to new ways of treating sepsis. Over the years, a number of treatments have been evaluated to treat sepsis, but none has worked well. The new research indicates that, in addition to using powerful antibiotics to fight off infections in patients with sepsis, immunotherapy drugs that boost the immune system may be an effective therapy.
The team is planning several clinical trials of such drugs in sepsis patients in the near future.
Thee National Institutes of Health funded the research.
Wild African elephants might offer ranchers their best chance to eradicate the “Sodom apple”—a toxic invasive plant that has overrun vast swaths of East African savanna and pastureland.
Should the reference to the smitten biblical city be unclear, the Sodom apple, or Solanum campylacanthum, is a wicked plant.
Not a true apple, the relative of the eggplant smothers native grasses with its thorny stalks, while its striking yellow fruit provides a deadly temptation to sheep and cattle.
A five-year study shows that elephants and impalas, among other wild animals, can not only safely gorge themselves on the plant, but can efficiently regulate its otherwise explosive growth. Without elephants ripping the plant from the ground, or impalas devouring dozens of its fruits at a time, the shrub easily conquers the landscape.
Just as the governments of nations such as Kenya prepare to pour millions into eradicating the plant, the findings, published in Proceedings of the Royal Society B, present a method for controlling the Sodom apple that is cost-effective for humans and beneficial for the survival of African elephants, says first author Robert Pringle, assistant professor of ecology and evolutionary biology at Princeton University.Win-win for elephants, ranchers
“The Holy Grail in ecology is these win-win situations where we can preserve wildlife in a way that is beneficial to human livelihoods,” Pringle says. Similarly, two earlier studies showed that allowing livestock to graze with wild animals such as zebras greatly improved the quality of the domesticated animals’ diet.Related Articles On Futurity
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“It’s a nice example of how conservation needn’t be about sacrifice. It often is—let’s be honest. But there are situations where you can get a win-win,” he says. “This opens the door for people whose main interest is cattle to say, ‘Maybe I do want elephants on my land.’ Elephants have a reputation as destructive, but they may be playing a role in keeping pastures grassy.”
Elephants and impalas can withstand the poison of S. campylacanthum because they belong to a class of herbivores known as “browsers” that subsist on woody plants and shrubs, many species of which pack a toxic punch. On the other hand, “grazers” such as cows, sheep, and zebras primarily eat grass, which is rarely poisonous.
Grazers easily succumb to to the Sodom apple, that causes emphysema, pneumonia, bleeding ulcers, brain swelling, and death.Ecological mayhem
As more African savanna is converted into pasture, the proliferation of the Sodom apple may only get worse, Pringle says, which means that the presence of elephants to eat it may become more vital to the ecosystem and livestock.
The Sodom apple thrives on ecological mayhem, such as the stress of overgrazing put on the land, Pringle says. “Typically, people will overload the land with more cattle than it can support. Then they remove the animals that eat the plant.”
The researchers present enough data to potentially determine the amount of pastureland that wild Sodom-apple eaters would be able to keep free of the noxious plant, says Ricardo Holdo, a savanna ecologist and assistant professor of biological sciences at the University of Missouri.
Holdo, who is familiar with the research but had no role in it, says that beyond removing the Sodom apple, animals such as elephants and impalas could potentially increase the food available to cattle. This is a departure from the conventional view in Africa that livestock and wild animals compete for the same scarce resources.
“There is enough quantitative information in this paper that they can probably model this effect in a meaningful way,” Holdo says. “When you add the wild (herbivores), they have a negative effect on the Solanum, so they’re actually promoting a higher biomass of high-quality habitat for livestock. So, it’s a win-win in the sense that you’re creating a situation in which you can both have livestock and wild animals, and probably actually increase your yield for livestock.”Functional redundancy
Researchers say this is one of the first studies to examine “functional redundancy” in land animals. Functional redundancy refers to the situation in which one species declines or goes extinct and another species steps in to fulfill the same ecological role. This consideration helps ecologists predict the overall effect of extinction on an entire ecosystem.
In this case, the effect of large mammals such as elephants and impalas on the Sodom apple population—and perhaps the populations of other plants—is unlikely to be duplicated by another animal species.
“That’s an important question because some species are quite vulnerable to extinction and others aren’t,” Pringle says. “The ones that go first tend to be the biggest, or the tastiest, or the ones with ivory tusks. We’re trying to gauge how the world is changing, and we need to understand to what extent these threatened animals have unique ecological functions.”
The majority of studies on functional redundancy have been conducted in aquatic systems because large land animals can be hard to control in an experiment. The new study is also unusually long by ecology standards, Pringle says—the researchers observed similar patterns year after year.Keeping elephants out
“A big part of the reason we don’t understand functional redundancy very well in terrestrial ecosystems is because it’s difficult to manipulate land species,” he says. “Doing these experiments in the kind of environment like you have in Kenya is really challenging—keeping elephants out of anything is really a huge challenge.”
Pringle was roughly three years into a study about the effects of elephants on plant diversity when he noticed that the Sodom apple was conspicuously absent from some experiment sites. He and other researchers had set up 36 exclosures—designed to keep animals out rather than in—totaling nearly 89 acres (36 hectares) at the Mpala Research Centre in Kenya, a multi-institutional research preserve with which Princeton has been long involved.
There were four types of exclosure: one type open to all animals; another where only elephants were excluded; one in which elephants and impalas were excluded; and another off limits to all animals.
It was in the sites that excluded elephants and impala that the Sodom apple particularly flourished, which defied everything he knew about the plant.Who’s eating the apple?
“This study was really fortuitous. I had always thought that these fruits were horrible and toxic, but when I saw them in the experiment, I knew some animal was otherwise eating them. I just didn’t know which one,” Pringle says. “The question became, ‘Who’s eating the apple?’ It’s a very interesting and simple question, but once you get the answer it raises a lot of other questions.”
Using the exclosures established for the original experiment, Pringle and his co-authors used cameras to document the zest with which wild African browsers will eat S. campylacanthum.
Pringle worked with Corina Tarnita, a mathematical biologist and assistant professor of ecology and evolutionary biology. They specifically observed the foraging activity of elephants, impalas, small-dog-sized antelopes known as dik-diks, and rodents. They captured about 30,000 hours of foraging using cameras they had focused on particular plants. The researchers also marked several hundred Sodom-apple fruit to track how many were eaten, and measured the average height, mortality and reproducibility of Sodom-apple plants in all the exclosures.In one end, out the other
The Sodom apple proliferated with each group of animal that was excluded. At one point, the plant’s density was three-times greater in areas restricted to all animals than those that permitted all of them.
In February 2011, the researchers counted an average of less than one fruit per plant in the exclosure open to all animals, meaning that nearly every fruit produced by the plants was being consumed. In the plots closed to elephants, that average increased to three fruits per plant. When both impala and elephants were kept away, the average jumped to around 50 fruits per plant, and fruits were more likely to be eaten by insects rather than dik-diks or rodents.
There is a catch to the elephants’ and impalas’ appetite for the Sodom apple: When fruit goes in one end, seeds come out the other. Though some seeds are destroyed during digestion, most reemerge and are potentially able to germinate.
The researchers developed a mathematical model to conduct a sort of cost-benefit analysis of how the Sodom apple’s ability to proliferate is affected by being eaten. The model weighed the “cost” to the plant of being partially consumed against the potential benefit of having healthy seeds scattered across the countryside in an animal’s droppings. They then used the model to determine whether different animal species had an overall positive or negative influence on the population of Sodom-apple plants.The whole plant
While elephants ate an enormous amount of Solanum seeds, they also often destroyed the entire plant, ripping it out of the ground and stuffing the whole bush into their mouths. The model showed that to offset the damage an elephant wreaks on a plant, 80 percent of the seeds the animal eats would have to emerge from it unscathed. On top of that, each seed would have to be 10-times more likely to take root than one that simply fell to the ground from its parent.
Impalas, on the other hand, can have a positive overall effect on the plants. Impalas ate the majority of the fruit consumed—one impala ate 18 fruit in just a few minutes. But they don’t severely damage the parent plant while feeding and also spread a lot of seeds in their dung. Of the seeds eaten by an impala, only 60 percent would need to survive, and those seeds would have to be a mere three-times more likely to sprout than a seed that simply fell from its parent.
“A model allows you to explore a space you’re not fully able to reach experimentally,” says Tarnita. “Once you’ve explored it, however, the conclusions and predictions need to be confronted with reality. This model helped us conclude that although it is theoretically possible for elephants to benefit the plant, that outcome is extremely unlikely.”
Researchers from University of Wyoming, University of Florida, University of California, Davis, the Mpala Center, and University of British Columbia are coauthors of the study. The National Science Foundation, the National Sciences and Engineering Research Council of Canada, the Sherwood Family Foundation, the National Geographic Committee for Research and Exploration, and the Princeton Environmental Institute’s Grand Challenges Program supported the work.
Source: Princeton University
The post Why African ranchers should let elephants gorge on poison apples appeared first on Futurity.
Researchers have found a new drug target to treat Alzheimer’s—one that also has the potential to serve as a diagnostic tool for the disease.
The recent failure in clinical trials of once-promising Alzheimer’s drugs under development by large pharmaceutical companies prompted the new study.
“Billions of dollars were invested in years of research leading up to the clinical trials of those Alzheimer’s drugs, but they failed the test after they unexpectedly worsened the patients’ symptoms,” says Gong Chen, a professor of biology at Penn State.Related Articles On Futurity
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The research behind those drugs had targeted the long-recognized feature of Alzheimer’s brains: the sticky buildup of the amyloid protein known as plaques, which can cause neurons in the brain to die.
“The research of our lab and others now has focused on finding new drug targets and on developing new approaches for diagnosing and treating Alzheimer’s disease,” Chen explains.
“We recently discovered an abnormally high concentration of one inhibitory neurotransmitter in the brains of deceased Alzheimer’s patients,” Chen says.GABA gateway
The neurotransmitter, called GABA (gamma-aminobutyric acid), showed up in deformed cells called “reactive astrocytes” in a brain structure called the dentate gyrus. This structure is the gateway to hippocampus, an area of the brain that is critical for learning and memory.
The GABA neurotransmitter was drastically increased in the deformed versions of the normally large, star-shaped “astrocyte” cells which, in a healthy individual, surround and support individual neurons in the brain.
“Our research shows that the excessively high concentration of the GABA neurotransmitter in these reactive astrocytes is a novel biomarker that we hope can be targeted in further research as a tool for the diagnosis and treatment of Alzheimer’s disease,” Chen says.
His lab also found that the high concentration of the GABA neurotransmitter in the reactive astrocytes is released through an astrocyte-specific GABA transporter, a novel drug target found in this study, to enhance GABA inhibition in the dentate gyrus.
With too much inhibitory GABA neurotransmitter, the neurons in the dentate gyrus are not fired up like they normally would be when a healthy person is learning something new or remembering something already learned.Improved memory
Importantly, Chen says, “After we inhibited the astrocytic GABA transporter to reduce GABA inhibition in the brains of the AD mice, we found that they showed better memory capability than the control AD mice.
“We are very excited and encouraged by this result because it might explain why previous clinical trials failed by targeting amyloid plaques alone. One possible explanation is that while amyloid plaques may be reduced by targeting amyloid proteins, the other downstream alterations triggered by amyloid deposits, such as the excessive GABA inhibition discovered in our study, cannot be corrected by targeting amyloid proteins alone,” Chen says.
“Our studies suggest that reducing the excessive GABA inhibition to the neurons in the brain’s dentate gyrus may lead to a novel therapy for Alzheimer’s disease. An ultimate successful therapy may be a cocktail of compounds acting on several drug targets simultaneously.”
In addition to Chen, other members of the research team include Zheng Wu and Ziyuan Guo at Penn State and Marla Gearing at Emory University.
The National Institutes of Health and Penn State University’s Eberly College of Science Stem Cell Fund supported the study, which appears in Nature Communications.
Source: Penn State
Scientists are using X-rays to take a closer look at the detailed structure of milk and how its fats interact with our digestive system. What they’re learning could provide a blueprint to create new milk products, including formula for premature babies.
“By unlocking the detailed structure of milk we have the potential to create milk loaded with fat-soluble vitamins and brain-building molecules for premature babies, or a drink that slows digestion so people feel fuller for longer,” says Stefan Salentinig of Monash University Institute of Pharmaceutical Sciences.
“We could even harness milk’s ability as a ‘carrier’ to develop new forms of drug delivery.”Milk’s unique structure
By chemically recreating the digestive system in a glass beaker and adding cows’ milk, the team found that milk has a unique structure—an emulsion of fats, nutrients, and water forms a structure that enhances digestion.Related Articles On Futurity
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The researchers used specialized instruments at the Australian Synchrotron to simulate digestion. Enzymes and water were added to milk fat to break it down, and the synchrotron’s small angle X-ray scattering beam showed that when digested, the by-products of milk become highly organized.
The structure is similar to a sponge, Salentinig says.
“We knew about the building blocks of milk and that milk fat has significant influence on the flavor, texture, and nutritional value of all dairy food. But what we didn’t know was the structural arrangement of this fat during digestion.
“We found that when the body starts the digestion process, an enzyme called lipase breaks down the fat molecules to form a highly geometrically ordered structure. These small and highly organized components enable fats, vitamins, and lipid-soluble drugs to cross cell membranes and get into the circulatory system Salentinig says.
The next phase of the research will see the team work with nutritionists to better make the link between these new findings and dietary outcomes, and utilize these findings to design and test improved medicines.
The Australian Research Council funded the research, which appears in the journal ACS Nano.
Source: Monash University
Pregnant women living in close proximity to chemical pesticide application had a two-thirds higher risk of having a child with autism spectrum disorder or other developmental delay, according to a new study.
The associations were stronger when the exposures occurred during the second and third trimesters of the women’s pregnancies.
The large, multisite California-based study examined associations between specific classes of pesticides, including organophosphates, pyrethroids, and carbamates, applied during the study participants’ pregnancies and later diagnoses of autism and developmental delay in their offspring. It appears online in Environmental Health Perspectives.
“This study validates the results of earlier research that has reported associations between having a child with autism and prenatal exposure to agricultural chemicals in California,” says lead study author Janie F. Shelton, a University of California, Davis, graduate student who now consults with the United Nations.Related Articles On Futurity
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“While we still must investigate whether certain sub-groups are more vulnerable to exposures to these compounds than others, the message is very clear: women who are pregnant should take special care to avoid contact with agricultural chemicals whenever possible.”
California is the top agricultural producing state in the nation, grossing $38 billion in revenue from farm crops in 2010. Statewide, approximately 200 million pounds of active pesticides are applied each year, most of it in the Central Valley, north to the Sacramento Valley and south to the Imperial Valley on the California-Mexico border.
While pesticides are critical for the modern agriculture industry, certain commonly used pesticides are neurotoxic and may pose threats to brain development during gestation, potentially resulting in developmental delay or autism.
The study was conducted by examining commercial pesticide application using the California Pesticide Use Report and linking the data to the residential addresses of approximately 1,000 participants in the Northern California-based Childhood Risk of Autism from Genetics and the Environment (CHARGE) Study.
The study includes families with children between two and five diagnosed with autism or developmental delay or with typical development. The majority of study participants live in the Sacramento Valley, Central Valley, and the greater San Francisco Bay Area.
Twenty-one chemical compounds were identified in the organophosphate class, including chlorpyrifos, acephate, and diazinon. The second most commonly applied class of pesticides was pyrethroids, one quarter of which was esfenvalerate, followed by lambda-cyhalothrin permethrin, cypermethrin, and tau-fluvalinate. Eighty percent of the carbamates were methomyl and carbaryl.What the maps show
For the study, researchers used questionnaires to obtain study participants’ residential addresses during the pre-conception and pregnancy periods. The addresses then were overlaid on maps with the locations of agricultural chemical application sites based on the pesticide-use reports to determine residential proximity. The study also examined which participants were exposed to which agricultural chemicals.
“We mapped where our study participants’ lived during pregnancy and around the time of birth. In California, pesticide applicators must report what they’re applying, where they’re applying it, dates when the applications were made, and how much was applied,” says principal investigator Irva Hertz-Picciotto, a MIND Institute researcher and professor and vice chair of the department of public health sciences at UC Davis.
“What we saw were several classes of pesticides more commonly applied near residences of mothers whose children developed autism or had delayed cognitive or other skills.”
The researchers found that during the study period approximately one-third of CHARGE Study participants lived in close proximity—within 1.25 to 1.75 kilometers—of commercial pesticide application sites.
Some associations were greater among mothers living closer to application sites and lower as residential proximity to the application sites decreased, the researchers found.
Organophosphates applied over the course of pregnancy were associated with an elevated risk of autism spectrum disorder, particularly for chlorpyrifos applications in the second trimester.
Pyrethroids were moderately associated with autism spectrum disorder immediately prior to conception and in the third trimester. Carbamates applied during pregnancy were associated with developmental delay.Pesticides and the fetal brain
Exposures to insecticides for those living near agricultural areas may be problematic, especially during gestation, because the developing fetal brain may be more vulnerable than it is in adults.
Because these pesticides are neurotoxic, in utero exposures during early development may distort the complex processes of structural development and neuronal signaling, producing alterations to the excitation and inhibition mechanisms that govern mood, learning, social interactions, and behavior.
“In that early developmental gestational period, the brain is developing synapses, the spaces between neurons, where electrical impulses are turned into neurotransmitting chemicals that leap from one neuron to another to pass messages along,” Hertz-Picciotto says.
“The formation of these junctions is really important and may well be where these pesticides are operating and affecting neurotransmission.”Reducing exposure
Research from the CHARGE Study has emphasized the importance of maternal nutrition during pregnancy, particularly the use of prenatal vitamins to reduce the risk of having a child with autism.
While it’s impossible to entirely eliminate risks due to environmental exposures, Hertz-Picciotto says that finding ways to reduce exposures to chemical pesticides, particularly for the very young, is important.
“We need to open up a dialogue about how this can be done, at both a societal and individual level,” she says. “If it were my family, I wouldn’t want to live close to where heavy pesticides are being applied.”
The National Institute of Environmental Health Sciences and the US Environmental Protection Agency supported the work.
Source: UC Davis
The post Living near pesticides in pregnancy ups autism risk appeared first on Futurity.
People are natural accomplices who like to conspire together to enjoy a small indulgence, but also to resist temptation together when it matters most.
Researchers staged a series of experiments that paired consumers against different temptations and gauged how closely their reactions mirrored each other and how they felt about each other afterward.
“We like moral support when the stakes are high, but we enjoy having a ‘partner in crime’ when the stakes are lower,” says Kelly L. Haws, an associate professor at Vanderbilt Owen Graduate School of Management.Ties that bind
When researchers tracked how many pieces of candy test subjects consumed during a short film, they found that most duos ate about the same amount.Related Articles On Futurity
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“We find evidence of a general tendency for peers to ultimately match behaviors when facing a mutual temptation,” write Haws and Michael L. Lowe of Texas A&M in the study published in the Journal of Consumer Research.
Further, test subjects who ate a small amount of candy each later reported liking their partner more than when the study began. But participants who say they ate large amounts of candy reported liking their partner less than when the study began.
“We feel a greater sense of affiliation with a person when we eat or buy something considered bad, but not terrible, with a friend,” Haws says. “Likewise, we feel a stronger affiliation when a friend reaffirms a decision not to overindulge.”Indulgences
Haws says this research is applicable to diverse self-control decisions from eating to spending money.
“The basic finding holds that if we’re with a friend and there’s a large amount of money at stake, it helps us feel better about the relationship if together we decline to waste a large amount of money,” Haws says.
The findings have relevance for marketers, policymakers, and consumers, the researchers say.
“Marketers can apply these findings to inform a number of important decisions related to promoting goods perceived as indulgences,” Haws says.
“Knowing that consumers prefer partners in crime when indulging on a small scale can inform decisions regarding communication strategies and messages, as well as promotional offers, perhaps by using a friends-and-family type of approach.”
On the other hand, knowing that mutually abstaining is also rewarding can help policy makers wishing to combat behaviors such as overspending, drug use, and overeating, the researchers say.
“You see this idea manifested in programs such as Weight Watchers, which builds around the idea of accountability and moral support for abstention,” Haws says.
Finally, consumers can use the knowledge to their advantage as they seek to control their decisions in social settings.
Source: Vanderbilt University
The post ‘Partners in crime’ let us indulge and keep us in check appeared first on Futurity.
Women who are 55 and younger are twice as likely to suffer a heart attack, require artery-opening procedures, or die from heart disease if they are moderately or severely depressed.Related Articles On Futurity
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“Women in this age group are also more likely to have depression, so this may be one of the ‘hidden’ risk factors that can help explain why women die at a disproportionately higher rate than men after a heart attack,” says study author Amit Shah, assistant professor of epidemiology and assistant professor of medicine (cardiology) at Emory University.
For the study, published in the Journal of the American Heart Association, investigators assessed symptoms of depression in 3,237 people with known or suspected heart disease (34 percent women, average age 62.5 years) scheduled for coronary angiography, an X-ray that diagnoses disease in the arteries that supply blood to the heart.After nearly three years of follow-up, they found:
- In women 55 and younger, after adjusting for other heart disease risk factors, each 1-point increase in symptoms of depression was associated with a 7 percent increase in the presence of heart disease.
- In men and older women, symptoms of depression didn’t predict the presence of heart disease.
- Women 55 and younger were 2.2 times as likely to suffer a heart attack, die of heart disease, or require an artery-opening procedure during the follow-up period if they had moderate or severe depression.
- Women 55 and younger were 2.5 times as likely to die from any cause during the follow-up period if they had moderate or severe depression.
“All people, and especially younger women, need to take depression very seriously,” Shah says. Depression itself is a reason to take action, but knowing that it is associated with an increased risk of heart disease and death should motivate people to seek help.”
Providers should ask more questions and be aware that young women are especially vulnerable to depression, and that it may increase the risk to their heart, Shah says.
“Although the risks and benefits of routine screening for depression are still unclear, our study suggests that young women may benefit from special consideration,” says senior study author Viola Vaccarino, professor of medicine. “Unfortunately, this group has largely been understudied before.”
Source: Emory University
The post Depressed young women more likely to die from heart disease appeared first on Futurity.
Some cells don’t recycle their own worn-out parts. Instead, they let their neighbors handle waste disposal.
Those are the findings of a new study that challenges the belief that healthy cells are universally responsible for cleaning up after themselves.
Scientists found that nerves in the eyes of mice pass off old, damaged energy-producing mitochondria to nearby support cells. The results could offer clues to the origins of glaucoma, researchers say. The findings may also offer insights into Parkinson’s and Alzheimer’s diseases, amyotrophic lateral sclerosis, and other illnesses that involve a buildup of “garbage” in brain cells.
“This was a very surprising study for us, because the findings go against the common understanding that each cell takes care of its own trash,” says Nicholas Marsh-Armstrong, research scientist at the Kennedy Krieger Institute and associate professor of neuroscience at Johns Hopkins University School of Medicine.Cell powerhouses
Marsh-Armstrong and Mark H. Ellisman, a neuroscientist at the University of California, San Diego, had previously discovered that retinal ganglion cells, which transmit visual information from the eye to the brain, might be handing off bits of themselves to astrocytes, cells that surround and support the signal-transmitting neurons.Related Articles On Futurity
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The retinal ganglion cells appeared in that earlier research to make the transfer to astrocytes at the optic nerve head, the beginning of the long tendril that connects the eye and the brain. The two researchers suspected that the neuronal bits being passed on to astrocytes were mitochondria, which are known as the powerhouses of the cell.
To find out if this was the case, researchers genetically modified mice so that they produced indicators that glowed in the presence of chewed-up mitochondria. They then used cutting-edge electron microscopy to reconstruct 3D images of what happened at the optic nerve head.
As reported in the June 17 online early edition of the Proceedings of the National Academy of Sciences, the astrocytes were, indeed, breaking down large numbers of mitochondria from neighboring retinal ganglion cells.A leading cause of blindness
The location of the process at the optic nerve head is particularly interesting, Marsh-Armstrong notes. That is the site thought to be at fault in glaucoma, a condition that damages the optic nerve, resulting in vision loss.
He plans to investigate whether the mitochondria disposal process is relevant to this disease, the second leading cause of blindness worldwide.
But the implications of the results go beyond the optic nerve head, since a buildup of “garbage” inside cells causes neurodegenerative diseases such as Parkinson’s, Alzheirmer’s, and ALS.
“By showing that this type of alternative disposal happens, we’ve opened up the door for others to investigate whether similar processes might be happening with other cell types and cellular parts other than mitochondria,” he says.
The National Eye Institute, the Glaucoma Research Foundation, the Melza M. and Frank Theodore Barr Foundation, the National Center for Research Resources, the National Institute on Drug Abuse’s Human Brain Project, the National Institute of General Medical Sciences, and the National Science Foundation funded the study.
Source: Johns Hopkins University
Radar images of Ligeia Mare, the second-largest sea on Saturn’s moon Titan, taken by NASA’s Cassini spacecraft reveal a bright, mysterious geologic object where one never existed before.
Scientifically speaking, this spot is considered a “transient feature,” but the astronomers also call it “Magic Island.”
Reporting in Nature Geoscience, the scientists say this may be the first observation of dynamic, geological processes in Titan’s northern hemisphere.
“This discovery tells us that the liquids in Titan’s northern hemisphere are not simply stagnant and unchanging, but rather that changes do occur,” says Jason Hofgartner, a Cornell University graduate student in the field of planetary sciences and the paper’s lead author.
“We don’t know precisely what caused this ‘magic island’ to appear, but we’d like to study it further.”
Titan, the largest of Saturn’s 62 known moons, is a world of lakes and seas. The moon—smaller than our own planet—bears close resemblance to watery Earth, with wind and rain driving the creation of strikingly familiar landscapes.Related Articles On Futurity
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Under its thick, hazy nitrogen-methane atmosphere, astronomers have found mountains, dunes, and lakes. But in lieu of water, liquid methane and ethane flow through river-like channels into seas the size of Earth’s Great Lakes.
To discover this geologic feature, the astronomers relied on an old technique—flipping. The Cassini spacecraft sent data on July 10, 2013, to the Jet Propulsion Laboratory at the California Institute of Technology for image processing.
Within a few days, Hofgartner and his colleagues flipped between older Titan images and the newly processed pictures for any hint of change. This is a long-standing method used to discover asteroids, comets, and other worlds. “With flipping, the human eye is pretty good at detecting change,” says Hofgartner.
Prior to the July 2013 observation, that region of Ligeia Mare had been completely devoid of features, including waves.
Titan’s seasons change on a longer time scale than Earth’s. The moon’s northern hemisphere is transitioning from spring to summer. The astronomers think the strange feature may result from changing seasons.
In light of the changes, Hofgartner and the other authors speculate on four reasons for this phenomenon:
- Northern hemisphere winds may be kicking up and forming waves on Ligeia Mare. The radar imaging system might see the waves as a kind of “ghost” island.
- Gases may push out from the sea floor of Ligeia Mare, rising to the surface as bubbles.
- Sunken solids formed by a wintry freeze could become buoyant with the onset of warmer temperatures during the late Titan spring.
- Ligeia Mare has suspended solids, which are neither sunken nor floating, but act like silt in a terrestrial delta.
“Likely, several different processes—such as wind, rain, and tides—might affect the methane and ethane lakes on Titan. We want to see the similarities and differences from geological processes that occur here on Earth,” Hofgartner says. “Ultimately, it will help us to understand better our own liquid environments here on the Earth.”
In addition to Hofgartner, Cornell authors include: Alex Hayes, assistant professor of planetary sciences; Jonathan Lunine, professor of physical sciences; and Phil Nicholson, professor of astronomy. A portion of the research took place at the Jet Propulsion Laboratory, under a contract with NASA.
Source: Cornell University
Combining two different medications could help patients with Type 1 diabetes at least partially regain the ability to produce their own insulin.
For a new study, Michael Haller, an endocrinologist at University of Florida, looked for problematic cells of the immune system that could be behind a patient’s inability to produce insulin and wiped them out with a medication called Thymoglobulin, a drug initially developed for use in organ transplantation.Related Articles On Futurity
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Then he used a medication called Neulasta, a drug designed to improve the lives of people with certain forms of cancer, to stimulate the production of new and potentially beneficial immune cells.
“The treatment is almost like trying to hit the reset button on the immune system,” Haller says. “We’re trying to wipe out the bad cells and stimulate the good cells at the same time.”
Haller treated 17 adult Type 1 diabetes patients for two weeks with the cocktail therapy and then followed them for a year. Another eight patients were given a placebo.
By the end of the year, the patients treated with the cocktail had increased their ability to produce insulin, which indicates that the Thymoglobulin was successful in killing the bad immune system cells, and the Neulasta was successful in stimulating new, healthy immune cells.
The patients’ ability to produce insulin also indicates they had an increase in beta cells—the cells responsible for producing insulin in the pancreas.
Haller presented his findings this month at the annual meeting of the American Diabetes Association in San Francisco.Profound results
Conventional diabetes wisdom says that within just a few months of the onset of Type 1 diabetes, there are very few of the insulin-producing beta cells left in the pancreas, says Mark Atkinson, a co-investigator of the study and member of the department of pathology, immunology, and laboratory medicine.
That the treatment seemed to stimulate insulin production in people with established Type 1 diabetes made the researchers “cautiously optimistic,” Atkinson says. “The results that Dr. Haller saw in his first study are profound.”
Another new aspect of the study is that it worked with patients who had been long diagnosed with the disease. Typically, studies examine patients who are newly diagnosed and still have a reasonable number of beta cells producing insulin. The patients in Haller’s study had been living with Type 1 diabetes between four months and two years.
“The model has mostly been to test therapies aimed at beta cell preservation in people who have just been diagnosed,” Haller says. “But obviously, the majority of patients living with the disease have been living with the disease for a long time, so people become disenfranchised from the research process. We’re interested in making life better for these patients.”Combination therapies
Atkinson began considering Thymoglobulin as a treatment for diabetes nearly a decade ago. He and fellow co-investigator Desmond Schatz, associate chairman of the department of pediatrics, authored a paper advocating a combination approach to treating Type 1 diabetes.
Based on Schatz’s belief in combination therapies, the group began shepherding a cocktail of Thymoglobulin and Neulasta through early studies done with mouse models.
“Despite tremendous strides in our understanding of the natural history of Type 1 diabetes, we are as yet unable to cure and prevent the disease,” Schatz says. “This study is a step in that direction, toward a biological cure.”
The patients in Haller’s study will be followed for three to five years to see if their bodies will preserve the insulin-producing beta cells. The researchers’ next step will be to recruit patients who have been newly diagnosed with the disease to conduct a larger trial.
Haller says he hopes the approach will help patients manage their disease more easily.
“If we can confirm the results in a larger effort, the study could potentially be paradigm-shifting for our field in that it documents we should really be looking at combination therapies in treating Type 1 diabetes,” Haller says.
“Our ultimate goal is to prevent and cure this disease, but we have to crawl before we walk, and walk before we run. This study is an important step forward in our efforts to make life easier for patients with Type 1 diabetes.”
Source: University of Florida
A new study shows that a potassium ion channel called hERG in the uterus is responsible for difficult labor among overweight pregnant women.
Acting as a powerful electrical brake, hERG works during pregnancy to suppress contractions and prevent premature labor. However, at the onset of labor a protein acts as a switch to turn hERG off, removing the brake and ensuring that labor can take place.Related Articles On Futurity
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Specifically, testing the electrical signals in small amounts of uterine tissue taken from women who had an elective caesarean before labor started and women who needed an emergency caesarean during their labor, proved that hERG was dysregulated in overweight women.
Pregnant women who are overweight often continue pregnant past their due date or progress slowly when labor begins.
Overweight women have higher rates of medical interventions around labor and birth, including higher rates of induction for prolonged pregnancy, and higher rates of Caesarean section as a result of failure to progress in labor.
Lead researcher Professor Helena Parkington of Monash University says this “switch” needs to be turned off to allow labor contractions to occur, but remains turned on in overweight women.
“The reason it stays on is that the ‘molecular hand’ that should turn the switch off fails to appear in sufficient quantities in the uterine muscle of overweight women when labor should be occurring. These women also respond poorly to our current methods of induction,” says Parkington.
Professor Shaun Brennecke of the University of Melbourne and Royal Women’s Hospital says the finding significantly advances understanding of how labor progresses, with implications for all women who have complicated labors.
“The clinical significance of this discovery is that, having identified the problem responsible for dysfunctional labor in overweight women, we are now able to look at developing a safe, effective, and specific treatment to correct the problem.”
“For example, a drug to turn off the switch to allow normal labor to start and progress,” he says.
The study appears in Nature Communications.
Cities in the US north and northeast tend to be destination cities for cocaine trafficking, while cities in the south and along the west coast are source cities, according to a new tracking system.
Cities in other regions, like Chicago and Atlanta, are major hubs.
Researchers say law enforcement authorities need to get a better handle on cocaine trafficking patterns if they are to take control of one of the world’s largest illegal drug markets.
Siddharth Chandra, an economist at Michigan State University, studied wholesale powdered cocaine prices in 112 cities to identify city-to-city links for the transit of the drug, using data published by the National Drug Intelligence Center of the US Department of Justice from 2002 to 2011.
Field intelligence officers and local, regional and federal law enforcement sources collected the data during drug arrests and investigations.
“These data enable us to identify suspected links between cities that may have escaped the attention of drug enforcement authorities,” says Chandra, director of the Asian Studies Center.
“By identifying patterns and locations, drug policy and enforcement agencies could provide valuable assistance to federal, state and local governments in their decisions on where and how to allocate limited law enforcement resources to mitigate the cocaine problem.”Spikes in cocaine prices
Chandra analyzed prices for 6,126 pairs of cities for possible links. If two cities are connected, prices will move in lockstep. So if there’s a spike in cocaine prices in the city of origin—or a source city, where the drug originates—that spike will be transmitted to all cities dependent upon that source.Related Articles On Futurity
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Cocaine will flow from the city with the lower price to the city with the higher price. It takes a number of transactions for cocaine to reach its end price, and prices tend to go up as drugs move from one city to another, he says.
While cities in the north and northeast are destination cities for cocaine, Chandra found cities in the southern US and along the west coast are source cities. In addition, cities in other regions, like Chicago and Atlanta, are major hubs for cocaine.
Chandra also created a map of possible drug routes, which he compared with a map produced by the National Drug Intelligence Center, and found that a number of his routes hadn’t been identified.Drug trafficking puzzle
Chandra cautions his methodology shouldn’t be used in isolation. Instead, it is one piece of the larger drug trafficking puzzle. Individual bits of the publicly available NDIC data may or may not be accurate based on whether drug smugglers tell the truth. However, the combined data could lead to better drug enforcement.
The NDIC was closed in 2012 and Chandra isn’t sure if another agency is continuing to collect data. But his research shows the importance of doing so.
“As an economist, the big takeaway is that prices carry some valuable information about trafficking in illegal goods,” Chandra says.
The study is published in the Journal of Drug Issues.
Source: Michigan State University
Researchers have created a simple and scalable method of making strong, stretchable graphene oxide fibers that are easily scrolled into yarns and have strengths approaching that of Kevlar.
This method opens up multiple possibilities for useful products. For instance, removing oxygen from the graphene oxide fiber results in a fiber with high electrical conductivity.
Adding silver nanorods to the graphene film would increase the conductivity to the same as copper, which could make it a much lighter weight replacement for copper transmission lines.
In addition, the researchers believe that the material lends itself to many kinds of highly sensitive sensors.
“We found this graphene oxide fiber was very strong, much better than other carbon fibers,” says Mauricio Terrones, professor of physics, chemistry and materials science and engineering, Penn State. “We believe that pockets of air inside the fiber keep it from being brittle.”Graphene slurry film
The researchers made a thin film of graphene oxide by chemically exfoliating graphite into graphene flakes, which were then mixed with water and concentrated by centrifugation into a thick slurry.Related Articles On Futurity
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The slurry was then spread by bar coating—something like a squeegee—across a large plate. When the slurry dries, it becomes a transparent film that can be carefully lifted off without tearing.
The film is then cut into narrow strips and wound on itself with an automatic fiber scroller, resulting in a fiber that can be knotted and stretched without fracturing. The researchers reported their results in a recent issue of ACSNano.
“The importance is that we can do almost any material, and that could open up many avenues—it’s a lightweight material with multifunctional properties,” says Terrones. And the main ingredient, graphite, is mined and sold by the ton.”
Penn State and Shinshu University in Japan have applied for a joint patent on the process.
The Research Center for Exotic Nanocarbons in Japan and the Center for Nanoscale Science at Penn State supported the research.
Source: Penn State
The post Stretchy, bendy, stronger-than-ever graphene fiber appeared first on Futurity.
The centuries-long search for the fountain of youth has yielded only a few promising leads, one of which entails an extreme, emaciating diet. A new study of the tiny nematode worm C. elegans begins to explain this marvel of calorie restriction and hints at an easier way to achieve longevity.
Researchers have found that taking food away from C. elegans triggers a state of arrested development: while the organism continues to wriggle around foraging for food, its cells and organs are suspended in an ageless, quiescent state.
When food becomes plentiful again, the worm develops as planned, but can live twice as long as normal.
The results appear in PLOS Genetics.
“It is possible that low-nutrient diets set off the same pathways in us to put our cells in a quiescent state,” says David R. Sherwood, an associate professor of biology at Duke University.Related Articles On Futurity
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“The trick is to find a way to pharmacologically manipulate this process so that we can get the anti-aging benefits without the pain of diet restriction.”
Over the last 80 years, researchers have put a menagerie of model organisms on a diet, and they’ve seen that nutrient deprivation can extend the lifespan of rats, mice, yeast, flies, spiders, fish, monkeys, and worms anywhere from 30 percent to 200 percent longer than their free-fed counterparts.
Outside the laboratory and in the real world, organisms like C. elegans can experience bouts of feast or famine that no doubt affect their development and longevity.
Sherwood’s colleague Ryan Baugh, an assistant professor of medicine, showed that hatching C. elegans eggs in a nutrient-free environment shut down their development completely. He asked Sherwood to investigate whether restricting diet to the point of starvation later in life would have the same effect.Arrested development
Sherwood and his postdoctoral fellow Adam Schindler decided to focus on the last two stages of C. elegans larval development—known as L3 and L4—when critical tissues and organs like the vulva are still developing.
During these stages, the worm vulva develops from a speck of three cells to a slightly larger ball of 22 cells. The researchers found that when they took away food at various times throughout L3 and L4, development paused when the vulva was either at the three-cell stage or the 22-cell stage, but not in between.
When they investigated further, the researchers found that not just the vulva, but all the tissues and cells in the organism seemed to get stuck at two main checkpoints. These checkpoints are like toll booths along the developmental interstate.
If the organism has enough nutrients, its development can pass through to the next toll booth. If it doesn’t have enough, it stays at the toll booth until it has built up the nutrients necessary to get it the rest of the way.
“Development isn’t a continuous nonstop process,” says Schindler, who is lead author of the study. “Organisms have to monitor their environment and decide whether or not it is amenable to their development. If it isn’t, they stop, if it is, they go.
“Those checkpoints seem to exist to allow the animal to make that decision. And the decision has implications, because the resources either go to development or to survival.”‘The meter isn’t running’
The study found that C. elegans could be starved for at least two weeks and still develop normally once feeding resumed. Because the meter isn’t running while the worm is in its arrested state, this starvation essentially doubles the two-week lifespan of the worm.
“This study has implications not only for aging, but also for cancer,” says Sherwood. “One of the biggest mysteries in cancer is how cancer cells metastasize early and then lie dormant for years before reawakening. My guess is that the pathways in worms that are arresting these cells and waking them up again are going to be the same pathways that are in human cancer metastases.”
The researchers are now performing a number of genetic studies to see if they can find another way to force C. elegans into these development holding patterns.
The American Cancer Society Postdoctoral Fellowship Award and the National Institutes of Health supported the research.
Source: Duke University
Water on the moon could be embedded in rocks or, if cold enough, “stuck” on the rocks’ surfaces, but chances of finding water on the moon’s sunlit side are pretty slim, new research suggests.
Ultraviolet photons emitted by the sun likely cause H2O molecules, which are predominately found at the poles, to either quickly desorb or break apart. The fragments of water may remain on the lunar surface, but the presence of useful amounts of water on the sunward side is not likely.Related Articles On Futurity
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“Overall, the moon will lose water efficiently when the solar photons are hitting it,” says Thomas Orlando, professor in the School of Chemistry and Biochemistry at Georgia Tech.
“The water also desorbs thermally. When they photodesorb or thermally desorb, the velocities are too low for the water to escape so it will bounce around until it gets trapped in the permanently shadowed regions at the poles or break apart in transit.”
Researchers built an ultra-high vacuum system that simulates conditions in space, then performed the first-ever reported measurement of the water photodesorption cross section from an actual lunar sample. The machine zapped a small piece of the moon with ultraviolet (157 nm) photons to create excited states and watched what happened to the water molecules. They either came off with a cross section of ~ 6 x 10−19 cm2 or broke apart with a cross section of ~ 5 x 10−19 cm2.
According to the team’s measurements, approximately one in every 1,000 molecules leave the lunar surface simply due to absorption of UV light.
The cross section values can now be used by scientists attempting to find water throughout the solar system and beyond.
“The cross section is an important number planetary scientists, astrochemists, and the astrophysics community need for models regarding the fate of water on comets, moons, asteroids, other airless bodies, and interstellar grains,” Orlando says.Fixed solar flux
The number is relatively large, which establishes that solar UV photons are likely removing water from the moon’s surface. This research, which was carried out primarily by former Georgia Tech PhD student Alice DeSimone, indicates the cross sections increase even more with decreasing water coverage. That’s why it’s not likely that water remains intact as H2O on the sunny side of the moon. Orlando compares it to sitting outside on a summer day.
“If a lot of sunlight is hitting me, the probability of me getting sunburned is pretty high,” he says. “It’s similar on the moon. There’s a fixed solar flux of energetic photons that hit the sunlit surface, and there’s a pretty good probability they remove water or damage the molecules.”
The result is the release of molecules such as H2O, H2, and OH as well as the atomic fragments H and O.
The research is published in two companion articles in the Journal of Geophysical Research: Planets. The first discusses the water photodesorption. The second paper details the photodissociation of water and the O(3PJ) formation on a lunar impact melt breccia.
NASA supported the work.
Source: Georgia Tech
Chance events may profoundly shape history. We can speculate about alternative possibilities, but a team of evolutionary biologists studying ancient proteins has turned speculation into experiment.
They resurrected an ancient ancestor of an important human protein as it existed hundreds of millions of years ago and then used biochemical methods to generate and characterize a huge number of alternative histories that could have ensued from that ancient starting point.
Tracing these alternative evolutionary paths, the researchers discovered that the protein—the cellular receptor for the stress hormone cortisol—could not have evolved its modern-day function unless two extremely unlikely mutations happened to evolve first.
These “permissive” mutations had no effect on the protein’s function, but without them the protein could not tolerate the later mutations that caused it to evolve its sensitivity to cortisol.
In screening thousands of alternative histories, the researchers found no alternative permissive mutations that could have allowed the protein’s modern-day form to evolve. The researchers describe their findings online in Nature.‘Unlikely chance events’
“This very important protein exists only because of a twist of fate,” says study senior author Joe Thornton, professor of ecology & evolution and human genetics at the University of Chicago.Related Articles On Futurity
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“If our results are general—and we think they probably are—then many of our body’s systems work as they do because of very unlikely chance events that happened in our deep evolutionary past,” he adds.
Thornton specializes in ancestral protein reconstruction, a technique that uses gene sequencing and computational methods to travel backwards through the evolutionary tree and infer the likely sequences of proteins as they existed in the deep past.
Through biochemical methods, these ancient proteins can be synthesized and introduced into living organisms to study their function.
Thornton and others have previously shown that the evolution of modern-day proteins required permissive mutations in the past. But no one had ever investigated whether there were many or few other possible permissive mutations that could have happened, so it remained unknown how unlikely it is that evolution discovered a permissive pathway to the modern function.Going back 450 million years
To answer this question, Thornton and co-author Michael Harms of the University of Oregon focused on the glucocorticoid receptor (GR), a key protein in the endocrine system that regulates development and stress responses in response to the hormone cortisol.
They resurrected the gene for ancestral GR as it existed around 450 million years ago, before it evolved its capacity to specifically recognize cortisol. They included a handful of mutations that occurred slightly later that allowed the protein to evolve its cortisol recognition, but they left out the permissive mutations, rendering the protein nonfunctional.
Thornton and Harms then created millions of copies of this genetic template, using a method that introduced random mutations into every new copy, thus mimicking the variation that evolution could have produced in the protein under alternative scenarios.
To identify permissive mutations in these “might-have-been” pathways, they engineered yeast cells that could grow only if they contained a functional GR and then introduced their “library” of mutated versions of ancestral GR into them. If any of the mutations were permissive, they would restore the GR’s function and allow the yeast to grow when exposed to cortisol.
Thornton and Harms tested many thousands of variants but found none that restored the function of GR other than the historical mutations that occurred in actuality. “Among the huge numbers of alternate possible histories, there were no other permissive mutations that could have opened an evolutionary path to the modern-day GR,” Thornton says.Permissive mutations are rare
By studying the effects of mutations on the ancient protein’s physical architecture, Harms and Thornton also showed why permissive mutations are so rare. To exert a permissive effect, a mutation had to stabilize a specific portion of the protein—the same part destabilized by the function-switching mutations—without stabilizing other regions or otherwise disrupting the structure. Very few mutations, they showed, can satisfy all these narrow constraints.
“These results show that contingency—the influence of chance events on the way evolution unfolds—is built into the atomic structure of molecules,” said Irene Eckstrand of the National Institutes of Health’s National Institute of General Medical Sciences, which provided substantial funding for the research.
“If the results hold true for other systems, this will be a highly significant contribution to our understanding of exactly how proteins can evolve new functions—a process that accounts for the diversity of life and the origins of genetic variation.”‘Radically different biology’
While most prior discussions of historical contingency in evolution have focused on external events such as asteroid impacts, mass extinctions, climate change, Thornton and Harms showed that the intrinsic complexity of proteins as physical objects also makes evolution depend profoundly on low-probability chance events.
“It’s very exciting to have been able to directly study alternative ancient histories,” Thornton says.
“If evolutionary history could be relaunched from ancestral starting points, we would almost certainly end up with a radically different biology from the one we have now. Unpredictable genetic events are constantly opening paths to some evolutionary outcomes and closing the paths to others, all within the biochemical systems of our cells.”
Source: University of Chicago
A drug commonly used for arthritis may be an effective way to reverse alopecia universalis, a condition that results in loss of all body hair.
There is currently no cure or long-term treatment for the condition. A new study, published online June 18 in the Journal of Investigative Dermatology, is the first reported case of successful targeted treatment.Related Articles On Futurity
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A 25-year-old patient had previously been diagnosed with both alopecia universalis and plaque psoriasis, a condition characterized by scaly red areas of skin.The only hair on his body was within the psoriasis plaques on his head.
He was referred to dermatologists at Yale University for treatment of the psoriasis. The alopecia universalis had never been treated.
Doctors believed it might be possible to address both diseases simultaneously using an existing FDA-approved drug for rheumatoid arthritis called tofacitinib citrate.
The drug had been used successfully for treating psoriasis in humans. It had also reversed alopecia areata, a less extreme form of alopecia, in mice.Full head of hair
After two months on tofacitinib at 10 mg daily, the patient’s psoriasis showed some improvement, and the man had grown scalp and facial hair—the first hair he’d grown there in seven years.
After three more months of therapy at 15 mg daily, the patient had completely regrown scalp hair and also had clearly visible eyebrows, eyelashes, and facial hair, as well as armpit and other hair.
“The results are exactly what we hoped for,” says Brett A. King, assistant professor of dermatology and senior author of the paper.
“This is a huge step forward in the treatment of patients with this condition. While it’s one case, we anticipated the successful treatment of this man based on our current understanding of the disease and the drug. We believe the same results will be duplicated in other patients, and we plan to try.”Turns off immune system attack
“There are no good options for long-term treatment of alopecia universalis,” King says. “The best available science suggested this might work, and it has.”
“By eight months there was full regrowth of hair,” says coauthor Brittany G. Craiglow. “The patient has reported feeling no side effects, and we’ve seen no lab test abnormalities, either.”
Tofacitinib appears to spur hair regrowth in a patient with alopecia universalis by turning off the immune system attack on hair follicles that is prompted by the disease. The drug helps in some, but not all, cases of psoriasis, and was mildly effective in this patient’s case.
King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata.
Source: Yale University
The more light absorbed by a solar panel’s active elements, the more power it will produce. But the light has to get there.
A new one-step process to etch nanoscale spikes into silicon lets the maximum amount of sunlight reach a solar cell, unlike current materials that reflect more light.
Various strategies have cut reflectance down to about 6 percent, but the anti-reflection is limited to a specific range of light, incident angle, and wavelength, says Andrew Barron, professor of chemistry and of materials science and nanoengineering at Rice University.Chemical stew
Enter black silicon, so named because it reflects almost no light. Black silicon is simply silicon with a highly textured surface of nanoscale spikes or pores that are smaller than the wavelength of light. The texture allows the efficient collection of light from any angle—from sunrise to sunset.Related Articles On Futurity
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Barron and graduate student Yen-Tien Lu, the study’s lead author, replaced a two-step process that involved metal deposition and electroless chemical etching with a single step that works at room temperature.
The chemical stew that makes it possible is a mix of copper nitrate, phosphorous acid, hydrogen fluoride, and water. When applied to a silicon wafer, the phosphorous acid reduces the copper ions to copper nanoparticles. The nanoparticles attract electrons from the silicon wafer’s surface, oxidizing it and allowing hydrogen fluoride to burn inverted pyramid-shaped nanopores into the silicon.590 nanometer pores
Fine-tuning the process resulted in a black silicon layer with pores as small as 590 nanometers (billionths of a meter) that let through more than 99 percent of light. By comparison, a clean, un-etched silicon wafer reflects nearly 100 percent of light.
The spikes will still require a coating to protect them from the elements, and Barron’s lab is working on ways to shorten the eight-hour process needed to perform the etching in the lab. But the ease of creating black silicon in one step makes it far more practical than previous methods.
Natcore Technology Inc., the Robert A. Welch Foundation, and the Welsh Government Sêr Cymru Program supported the research.
The findings appear in the Journal of Materials Chemistry A.
Source: Rice University