Pregnant women who are exposed to tetrachloroethylene (PCE) in drinking water may have a higher risk of stillbirth and placental abruption.
A new study compared 1,091 PCE-exposed pregnancies and 1,019 unexposed pregnancies among 1,766 women living in Cape Cod, Massachusetts, where water was contaminated in the late 1960s to the early 1980s by the installation of vinyl-lined asbestos cement pipes.Related Articles On Futurity
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Exposure was estimated using water-distribution system modeling software. Data on pregnancy complications were self-reported by mothers.
Of the more than 2,000 pregnancies, 9 percent were complicated by pregnancy disorders associated with placental dysfunction. Pregnancies among women with high PCE exposure had 2.38 times the risk of stillbirth and 1.35 times the risk of placental abruption, compared to unexposed pregnancies.
The study also found an elevated risk of vaginal bleeding in pregnancies where women had PCE exposure greater than or equal to the sample median.
The study findings support a small body of prior research indicating that PCE exposure may impact placental function and fetal growth, says lead researcher Ann Aschengrau, professor of epidemiology at Boston University School of Public Health. However, further investigation of related disorders is needed.
“We need to have a better understanding of the impact of this common drinking water contaminant on all aspects of pregnancy.”Common contaminant
For the study, published in the journal Environmental Health, researchers used data from the Cape Cod Family Health Study, a population-based retrospective study designed to examine the influence of prenatal exposure to PCE-contaminated drinking water on multiple outcomes during pregnancy and childhood.
Women were considered eligible for the parent cohort if they gave birth to at least one child between 1969 and 1983 and were living in one of eight Cape Cod towns with some contaminated pipes at the time of the child’s birth.
The study found no link between PCE exposure and preeclampsia or delivery of small-for-gestational-age (SGA) infants.
“Our results suggest that prenatal PCE exposure is not associated with all obstetric complications, but may increase the risk of certain ones, including stillbirth and placental abruption,” the study says.
The study was conducted as part of BU’s Superfund Research Program.
Source: Boston University
“We need to have a better understanding of the impact of this common drinking water contaminant on all aspects of pregnancy,” says Ann Aschengrau. (Credit:
The family of viruses to which Ebola and its lethal relative Marburg belong likely existed in the Miocene Epoch at least 16 to 23 million years ago.
At that time, the evolutionary lines leading to Ebola and Marburg had already diverged, according to research that adds to scientists’ developing knowledge about known filoviruses.Related Articles On Futurity
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Experts once believed filoviruses came into being some 10,000 years ago, coinciding with the rise of agriculture. The new study pushes back the family’s age to the time when great apes arose.
“Filoviruses are far more ancient than previously thought,” says lead researcher Derek Taylor, professor of biological sciences at University at Buffalo. “These things have been interacting with mammals for a long time, several million years.”
Knowing more about Ebola and Marburg’s comparative evolution could “affect design of vaccines and programs that identify emerging pathogens,” researchers write in the journal PeerJ.
The research does not address the age of the modern-day Ebola virus. Instead, it shows that Ebola and Marburg are each members of ancient evolutionary lines, and that these two viruses last shared a common ancestor sometime prior to 16 to 23 million years ago.‘Fossil gene’ clues
Taylor and coauthor Jeremy Bruenn, professor of biological sciences, research viral “fossil genes”—chunks of genetic material that animals and other organisms acquire from viruses during infection.
In the new study, the authors report finding remnants of filovirus-like genes in various rodents. One fossil gene, called VP35, appeared in the same spot in the genomes of four different rodent species: two hamsters and two voles. This means the material was likely acquired in or before the Miocene Epoch, prior to when these rodents evolved into distinct species some 16-23 million years ago.
In other words, it appears the known filovirus family is at least as old as the common ancestor of hamsters and voles.
“These rodents have billions of base pairs in their genomes, so the odds of a viral gene inserting itself at the same position in different species at different times are very small,” Taylor says. “It’s likely that the insertion was present in the common ancestor of these rodents.”
The genetic material in the VP35 fossil was more closely related to Ebola than to Marburg, indicating that the lines leading to these viruses had already begun diverging from each other in the Miocene.
The new study builds on Taylor’s previous work, which used viral fossil genes to estimate that the entire family of filoviruses was more than 10 million years old. However, those studies used fossil genes only distantly related to Ebola and Marburg, which prevented the researchers from drawing conclusions about the age of these two viral lines.
The new findings fill this viral “fossil gap,” to allow scientists to explore Ebola’s historical relationship with Marburg.First Ebola outbreak
The first Ebola outbreak in humans occurred in 1976, and scientists still know little about the virus’ history. The same dearth of information applies to Marburg, which was recognized in humans in 1967 and implicated in the death of a Ugandan health worker this month.
Understanding the virus’ ancient past could aid in disease prevention, Taylor says. If a researcher were trying to create a single vaccine effective against both Ebola and Marburg, it could be helpful to know that their evolutionary lineages diverged so long ago.
Knowing more about filoviruses in general could provide insight into which host species might serve as “reservoirs” that harbor undiscovered pathogens related to Ebola and Marburg, Taylor says.
“When they first started looking for reservoirs for Ebola, they were crashing through the rainforest, looking at everything—mammals, insects, other organisms. The more we know about the evolution of filovirus-host interactions, the more we can learn about who the players might be in the system.”
Source: University at Buffalo
Startups that work with a few carefully chosen larger companies will get the most benefit, according to new research.
Forthcoming in Organization Science, the study finds that by aligning with established companies, a young firm gains valuable access to additional resources and markets. However, as a startup adds more outside partners, eventually the firm’s internal capability will weaken and the cost of maintaining its alliances will exceed any remaining benefits.
“Partnerships offer many mutual benefits; established companies can tap into a startup’s cutting-edge technologies and innovative potential, while young firms acquire knowledge and status from experienced partners,” says study coauthor Ramin Vandaie, assistant professor of operations management and strategy in the University at Buffalo School of Management.Related Articles On Futurity
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“But more is not necessarily better,” he adds. “We found the benefits of alliances with larger companies do not increase proportionally with the number of partners, but instead start to level off and turn negative as more partnerships are formed.”
The study examined 150 independent film production studios and tracked their partnerships with major studios and performance from 1990 to 2010. Vandaie says the data can be applied to many industries, particularly creative fields like publishing or advertising, as well as professional services like accounting or law firms.
In addition, the research revealed that highly specialized firms experience greater benefits from inter-firm alliances than more generalist competitors.
For example, in its early years, the Weinstein Co. focused on a limited number of genres that were distributed through deals with major studios. With that strategy, the company found and sustained critical and commercial success and has since grown into a “mini-major” that produces and distributes a wide range of films.
“Small, specialized firms that have the opportunity to align with larger firms should put their expansion plans on hold to gain the full benefits of those partnerships,” Vandaie recommends. “Later, they can use their newly developed capabilities as a basis for growth and a more reliable path to expansion.”
Vandaie collaborated on the project with Akbar Zaheer the of University of Minnesota Carlson School of Management.
Source: University at Buffalo
In a new study, researchers show that neurons controlling hunger and appetite in the brain also control the “browning” of white fat.
That discovery suggests that modulating this connection may be a new way to fight obesity.
Previous research showed that energy-storing white fat has the capacity to transform into energy-burning “brown-like” fat.
This process impacts how much energy we burn and how much weight we can lose.
Excess fatty tissue is a major risk factor for type 2 diabetes, cardiovascular disease, hypertension, neurological disorders, and cancer. People become overweight and obese when energy intake exceeds energy expenditure, and excess calories are stored in the adipose tissues.Related Articles On Futurity
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The adipose organ is made up of both white and brown fat. While white fat primarily stores energy as triglycerides, brown fat dissipates chemical energy as heat.
The more brown fat you have, the more weight you can lose.
The team stimulated this browning process from the brain in mice and found that it protected the animals from becoming obese on a high-fat diet. The team then studied the molecular changes in hunger-promoting neurons in the hypothalamus and found that the attachment of a unique sugar called “O-GlcNAc” to potassium ion channels acts as a switch to control brain activity to burn fat.
“Our studies reveal white fat ‘browning’ as a highly dynamic physiological process that the brain controls,” says lead author Xiaoyong Yang, associate professor of comparative medicine and physiology at Yale School of Medicine.
“This work indicates that behavioral modifications promoted by the brain could influence how the amount of food we eat and store in fat is burned.”
Yang says hunger and cold exposure are two life-history variables during the development and evolution of mammals.
“We observed that food deprivation dominates over cold exposure in neural control of white fat browning. This regulatory system may be evolutionarily important as it can reduce heat production to maintain energy balance when we are hungry.
“Modulating this brain-to-fat connection represents a potential novel strategy to combat obesity and associated illnesses.”
The National Institutes of Health, American Diabetes Association, Ellison Medical Foundation, American Heart Association, and CNPq/Brazil funded the work, which appears in Cell.
Researchers have teased apart the separate biological responses of the human eye to blue light, revealing an unexpected contest for control.
Their work addresses the properties of melanopsin, a light-sensitive protein in the eye that establishes the rhythm of our day-night cycle and the familiar constriction of the pupil to bright light.Related Articles On Futurity
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They measured the pupil response to stimulation of melanopsin and of short-wave-sensitive (S) cones, the other blue light-sensing cells that operate in daylight. Surprisingly, they found that melanopsin and S-cones have opposite effects and compete for control of the pupil in blue light.
“The challenge of studying melanopsin is that it is very sensitive to blue light, a short-wave light emitted by digital devices including smartphones, tablets, and computers, as are S-cones,” says lead author, Manuel Spitschan, a graduate student in psychology at the University of Pennsylvania.
“Previous studies in the human eye have not separately studied the S-cones and melanopsin because flashing a blue light stimulates both of these cells, so we didn’t know if what a person saw or the response of the pupil was from one or both.”
To overcome this problem, the team developed a special class of visual stimuli: they produced flickering light that stimulates melanopsin but is invisible to S-cones, and a second flickering light that stimulates S-cones but is invisible to melanopsin. The lights were created using a machine that can sculpt and switch between computer-designed rainbows of light.Pupils enlarge
The researchers had 16 people watch this flickering light while recording the response of their pupil. The light that stimulates melanopsin made the pupil slowly contract. To their surprise, they also discovered that stimulation of S-cones made the pupil get larger. That is, when the S-cones of the eye captured more light, the pupil enlarged, the opposite of what is generally thought of as the natural pupil response.
This means that blue light sets off a tug-of-war between melanopsin and S-cones to make your pupil smaller or bigger. The melanopsin effect is stronger, resulting in the familiar shrinking of the pupil to bright light of any color.
“For the first time in people we are able to probe the relationship between melanopsin signals and the cones and how they work together or in opposition,” says David Brainard, professor of psychology, and director of the Vision Research Center and director of the Institute for Research in Cognitive Science.
And what do these special flickering lights look like? “The flicker that stimulates S-cones looks like it is switching between a bluish and yellowish color. The flicker that stimulates melanopsin, however, is hard to see, and looks like a soft glow that rises and falls in brightness.”Melanopsin and clinical conditions
Light enters the human eye and is imaged on the retina. It has long been know that the retinal image is sensed by neurons known as the rods and cones. The rods operate in dim light levels and allow us to see at night. It is the signals from rods and cones that the brain converts into the images we see.
Recently, though, another class of retinal cells has been identified that also senses light. These cells are known as intrinsically photosensitive ganglion cells, and they contain the protein melanopsin.
Melanopsin is sensitive to light at wavelengths intermediate to those sensed by the S and M cones. It appears that it primarily mediates light-driven functions other than conscious vision, such as setting our circadian clock and contributing to control of the pupil.
This new work makes it possible to isolate and study the properties of melanopsin in people, separate from the cone cells. We can now ask what we “see” with melanopsin.
“This is important because we think melanopsin could be involved in clinical conditions,” says Geoffrey K. Aguirre, a behavioral neurologist and associate professor in the department of neurology.
“For example, it seems that too much stimulation of melanopsin produces the feeling of pain from light that is too bright, and not having enough melanopsin stimulation may be part of seasonal affective disorder, in which people become depressed when they don’t have enough light exposure.
“Having now teased apart the melanopsin and cone responses to blue light, we can study how the eye is involved in these disorders.”
A patent on this alternative photoreceptor isolation method and its applications has been filed by the University of Pennsylvania with Spitschan, Aguirre, and Brainard as inventors. In addition, they have founded a company with the Penn UpStart incubator with the goal to commercialize a device based upon these techniques.
The NIH supported the work, which appears in the Proceedings of the National Academy of Sciences.
Source: University of Pennsylvania
A cellular probe that combines a tarantula toxin with a fluorescent compound can help scientists observe electrical activity in neurons and other cells.
The probe binds to a voltage-activated potassium ion channel subtype, lighting up when the channel is turned off and dimming when it is activated.
This is the first time researchers have been able to visually observe these electrical signaling proteins turn on without genetic modification. These visualization tools are prototypes of probes that could some day help researchers better understand the ion channel dysfunctions that lead to epilepsy, cardiac arrhythmias, and other conditions.
“Ion channels have been called life’s transistors because they act like switches, generating electrical feedback,” says senior author Jon Sack, assistant professor of physiology and membrane biology at University of California, Davis. “To understand how neural systems or the heart works, we need to know which switches are activated. These probes tell us when certain switches turn on.”
Voltage-gated channels are proteins that allow specific ions, such as potassium or calcium, to flow in and out of cells. They perform a critical function, generating an electrical current in neurons, muscles, and other cells. There are many different types, including more than 40 potassium channels. Though other methods can very precisely measure electrical activity in a cell, it has been difficult to differentiate which specific channels are turning on.
“There are about 40 voltage-gated potassium channel genes that are basically doing the same thing, and it’s been shockingly hard to figure out which ones are doing something that’s physiologically relevant,” Sack says.Why the tarantula?
The tarantula toxin, guangxitoxin-1E, was an ideal choice because it naturally binds to the Kv2 channels. These channels are expressed in most, if not all, neurons, yet their regulation and activity are complex and actively debated. Sack and his laboratory worked closely with Bruce Cohen, a scientist in the Lawrence Berkeley Lab’s Molecular Foundry, who has been studying how fluorescent molecules and nanoparticles can be used to image live cells.Related Articles On Futurity
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To study the channels, the team engineered variants of tarantula toxin that could be fluorescently labeled and retain function. These probes were designed to bind to the potassium channels when they were at rest and let go when they became active. The researchers then tested them on living cells. To their surprise, the probes worked right away.
“A lot of times you see ambiguous results, but when we added the probes to living cells there was a very clear signal,” Sack says. “When we added potassium to stimulate the cells, the probes fell right off.”
While this is just a first step towards imaging the activity of potassium and possibly other ion channels, this approach holds vast potential to help scientists understand the underlying mechanisms behind cardiac arrhythmias, muscle defects, and other channelopathies.
“There are dozens of known channelopathies, and more being uncovered at an increasing pace,” Sack says. “If you have electrical signaling, you have to have a potassium channel, and when that channel goes bad, the cell doesn’t work the same anymore. For example, the Kv2.1 channel that this probe binds to leads to epilepsy when it’s not functioning properly.”
In addition, the ability to better observe electrical signaling could help researchers map the brain at its most basic levels.
“Understanding the molecular mechanisms of neuronal firing is a fundamental problem in unraveling the complexities of brain function,” Cohen says.Lots of spider toxins to try
While creating a probe that can read whether the Kv2.1 channel is firing or at rest is an important proof-of-concept, there’s still a lot of work to be done. Sack and Cohen will continue to collaborate, testing other types of spider venoms that bind to different potassium channels.
“The beauty of this is the potential,” Sack says. “This is a toehold into a new way of visualizing electrical activity, and there’s a huge family of spider toxins that target different ion channels. We’ve tagged a Ford; we should be able to tag a Chevy.”
The study appears in the Proceedings of the National Academy of Sciences.
The researchers who conducted this study come from UC Davis, Marine Biological Laboratory at Woods Hole, and the Molecular Foundry, Lawrence Berkeley National Laboratory.
The NIH and the Milton L. Shifman Endowed Scholarship for the Neurobiology Course at Woods Hole supported the project. Work at the Molecular Foundry received support from the Office of Science, Office of Basic Energy Sciences, of the US Department of Energy.
Source: UC Davis
The flu virus has a clever way to trick cells into cracking open its shell and releasing its genetic code.
Until now, very little has been known about how the capsid of the flu virus is cracked open.
Scientists say they’ve uncovered the details: the virus disguises itself as a bundle of waste, called an aggresome. Cells react by activating their “waste disposal system” and tearing open the capsid.
The waste disposal system of a cell is essential for eliminating protein garbage. If the cell fails to dispose of these waste proteins (caused by stress or heat) quickly enough, the waste starts to aggregate.
To get rid of these aggregates, the cell activates its machinery, which dismantles the clumps and breaks them down into smaller pieces, so that they can be degraded. It is precisely this mechanism that the influenza virus exploits.How viruses infect
Viruses cannot multiply without cellular machinery. The pathogen infiltrates the host cells and uses their replication and protein production machinery to multiply.Related Articles On Futurity
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The virus has to overcome the initial barrier by docking on the surface of the cell membrane.
The cell engulfs the virus in a bubble and transports it towards the cell nucleus. During this journey, the solution inside the bubble becomes increasingly acidic. The acidic pH value is ultimately what causes the virus’s outer shell to melt into the membrane of the bubble.
The flu virus has to overcome a further obstacle before releasing its genetic code: the few pieces of RNA that make up the genome of the flu virus are packed into a capsid, which keeps the virus stable when moving from cell to cell. The capsid also protects the viral genes against degradation.The disguise
The virus capsid carries cellular waste “labels” on its surface. These labels, called unanchored ubiquitin, call into action an enzyme known as histone deacetylase (HDAC6), which binds to ubiquitin.
At the same time, HDAC6 also binds to scaffolding motor proteins, pulling the perceived “garbage bundle” apart so that it can be degraded. This mechanical stress causes the capsid to tear, releasing the genetic material of the virus.
The viral RNA molecules pass through the pores of the cell nucleus, again with the help of cellular transport factors. Once within the nucleus, the cell starts to reproduce the viral genome and build new virus proteins.Total infection time
The researchers were also surprised by how long the opening of the capsid takes, with the process lasting around 20 to 30 minutes. The total infection period—from docking onto the cell’s surface to the RNA entering the cell nucleus—is two hours.
“The process is gradual and more complex than we thought,” says Yohei Yamauchi, a former postdoc with ETH Zurich professor Ari Helenius, who detected HDAC6 by screening human proteins for their involvement in viral infection.
In a follow-up study, lead author Indranil Banerjee confirmed how the flu virus is programmed to trick HDAC6 into opening its capsid.
A mouse model provided encouraging proof. If the protein HDAC6 was absent, the flu infection was significantly weaker than in wild-type mice: the flu viruses did not have a central docking point for binding to the waste disposal system.Possible therapy?
Little research has previously been conducted on how an animal virus opens its capsid. This is one of the most important stages during infection.
“We did, however, underestimate the complexity associated with unpacking the capsid,” admits Helenius.
Whether there are therapeutic applications for the findings remains to be seen as an absence of HDAC6 merely moderates the infection rather than prevents it. The known HDAC6 inhibitors target its two active areas.
Blocking the enzymatic activity does not help prevent HDAC6 from binding to ubiquitin, but rather supports the virus by stabilizing the cell’s framework.
“We would need a substance that prevents HDAC6 from binding to ubiquitin, without touching the enzyme,” says Yamauchi.
Nevertheless, the structure of HDAC6 indicates that this is possible and follow-up experiments are already planned. The researchers have filed a patent for this purpose.
Researchers from the Friedrich Miescher Institute for Biomedical Research in Basel and the Biological Research Center in Szeged (Hungary) also collaborate on the study, which is published in the journal Science.
Source: ETH Zurich
Teenagers are routinely given hearing tests at school, but those tests aren’t very good at identifying high-frequency hearing loss, which comes from headphones and loud noises.
The American Academy of Pediatrics, in partnership with the Bright Futures children’s health organization, sets standards for pediatric preventive care and recommends screening adolescents with subjective questions and then following up with objective tests for those found to be at high risk of hearing loss.Related Articles On Futurity
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But the screening questions are not specifically developed for children or adolescents, who are traditionally poor self-reporters of hearing status.
“We found that you can’t rely on the Bright Futures questions to select out teenagers at high risk for hearing loss who would warrant an objective screen,” says Deepa Sekhar, assistant professor of pediatrics at Penn State University.
A study in 2010 using data from the National Health and Nutrition Examination Survey showed that one in five adolescents aged 12 to 19 has hearing loss. Most have high-frequency hearing loss, which may be related to increasing hazardous noise exposures from such things as personal listening devices, concert-going, ATV-riding, and hunting with firearms.‘When you hear a beep’
For the new study, published in the Journal of Medical Screening, eleventh grade students at a Pennsylvania high school answered the 10 Bright Futures screening questions and additional questions assessing other potential risk factors for adolescent hearing loss.
They also took the Pennsylvania state-mandated hearing test—the familiar hearing screening where children raise their hand when they hear a tone—and a test developed by the researchers to better detect high-frequency noise-related hearing loss. Some of the children underwent additional standard hearing testing in a soundproof booth.
Neither the Bright Futures questions nor the additional questions were tailored specifically to adolescent hearing loss. In addition, the Pennsylvania school hearing test was found to have a sensitivity of 13 percent for adolescent hearing loss while the study-designed hearing test had 100 percent sensitivity.
“Although our test had more false positives, we caught 100 percent of the students with hearing loss,” Sekhar says.Subtle symptoms
School hearing tests currently used in most states screen mainly for low-frequency hearing loss, which is seen more often in younger children due to frequent ear infections and fluid in the ear.
But these tests often miss high-frequency loss. Sekhar is working to develop an objective hearing screening test specifically for adolescents with more high-frequency tones above 3,000 Hertz. These tones are typically affected by hazardous noise exposure. A testing protocol that requires adolescents to fail twice instead of once will reduce false positives.
“The onset of high-frequency hearing loss is often very insidious and the symptoms are often very subtle,” Sekhar says. “It’s important to identify hearing problems at any age because of the impact it can have on all different areas of life, including academic success, workplace advancement, and social relationships.”
Students with mild hearing loss are more likely to repeat a grade. Also, it’s estimated that people with hearing loss lose between $220,000 and $440,000 in earnings over a lifetime.
The study failed to find an association between typical adolescent noise exposures and hearing loss. The challenge in doing so may stem from the fact that genetics and duration of exposure are additional factors that affect an individual’s risk of hearing loss.
“You could be listening at a lower volume for an extended period of time, and that can be as bad as a high-volume sound for a short period of time,” Sekhar says.
Other researchers from Penn State and from Bloomsburg University contributed to the study. A grant from the Academic Pediatric Association/Maternal and Child Health Bureau Young Investigator Award provided funding.
Source: Penn State
As the 2014 midterm elections draw closer, a political scientist says that traditional conservatives and their tea party counterparts may have different concerns and motivations regarding foreign policy.
While traditional conservatives seem most motivated by concern over American security, Christopher Parker, professor of political science at University of Washington, suggests that those identifying as tea party conservatives have somewhat more mixed motivations, linked with agitation over the Obama presidency and stemming from a feeling of “losing their country” to a “decline of American ethno-cultural dominance.
“There is no such thing as ‘conservative’ foreign policy if it means that all conservatives speak with a single voice,” Parker says. “Instead, conservatives are divided on what motivates their foreign policy preferences: securing American interests, or ethno-cultural threat.”Is the US stronger since 2008?
Parker and coauthor Rachel Blum, a doctoral student at Georgetown University, came to this view after reviewing recent literature on public attitudes toward foreign policy and examining the 2012 American National Election Study, an in-person and internet survey of about 6,000 voters by Stanford University and the University of Michigan. The Brookings Institution has published the report.Related Articles On Futurity
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The election study, they say, reveals a wide difference between traditional or “establishment” conservatives and their tea party counterparts on the question of whether America was safer than in 2008. Fully 70 percent of tea party conservatives disagreed that America had grown safer in the intervening years, compared to about 39 percent of traditional conservatives.
They note a significant but smaller difference when respondents were asked if US strength had increased since 2008: Far more tea party conservatives—about 90 percent—disagreed, compared with about 70 percent among more traditional conservatives.
“At first glance, these are fairly innocuous questions,” the researchers write. “However, upon closer inspection, 2008 coincides with the beginning of the Obama administration. This makes it likely that respondents are thinking about Obama and his administration’s leadership when they are answering these questions.”All the way back to Jackson
Asked about foreign policy toward Iran, tea partyers and traditional conservatives were in near-total agreement that invasion was not a viable option, but tea partyers more heavily favored only economic sanctions as well as the possible bombing of Iran nuclear sites.
Parker and Blum ascribe these philosophical differences to the differing motivations of the two groups. The tea party, they argue, is motivated largely by “a nationalist sentiment” that dates back to the days of President Andrew Jackson.
“Tea party conservatives, more than establishment conservatives, are motivated by fear and anxiety associated with the belief that the America to which they’ve become accustomed, in which white men have dominated from the beginning, is in rapid decline,” the researchers write.
Parker and colleague Matt Barreto examined political differences between traditional conservatives and tea partyers on domestic issues in their 2013 book, Change they Can’t Believe In: The Tea Party and the Politics of Paranoia. They found overwhelmingly more tea partyers than traditional conservatives agreeing to the statement that President Obama is “destroying the country.”
Parker and Blum argue that the same predisposition carries over to the foreign policy views of tea party conservatives.
“Because conservatives appear split on these important issues,” they conclude, “the midterms promise to pose a challenge, especially in Senate where some seats—and perhaps the balance of power in the upper chamber—may hinge on foreign policy.”
Source: University of Washington
People who pay more attention to their feelings and experiences tend to have better cardiovascular health, a new study suggests.
As reported in the International Journal of Behavioral Medicine, researchers found a significant association between self-reported “dispositional mindfulness” and better scores on four of seven cardiovascular health indicators, as well as a composite overall health score.Related Articles On Futurity
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Dispositional mindfulness is defined as someone’s awareness and attention to what they are thinking and feeling in the moment.
The study is the first to quantify such an association between mindfulness and better cardiovascular health, says study lead author Eric Loucks, assistant professor of epidemiology in the Brown University School of Public Health. It’s an encouraging link for health promotion, because mindfulness can be enhanced with training.
“Mindfulness is changeable, and standardized mindfulness interventions are available,” Loucks says. “Mostly they’ve been looked at for mental health and pain management, but increasingly they are being looked at for cardiovascular risk factors such as obesity, smoking, and blood pressure.”
The connection may come about because people who are attuned to their present feelings may be better at minding and managing the various cravings—for salty or sugary foods, cigarettes, or even some time on the couch—that undermine health, Loucks says. Mindfulness interventions, for example, have already shown efficacy in helping people to quit smoking.Comparing measurements
In the study, Loucks and his colleagues asked 382 participants in the broader New England Family Study to answer the 15 questions of the Mindful Attention Awareness Scale (MAAS).
MAAS questions, rated on a six-point scale from “almost always” to “almost never” include “I find it difficult to stay focused on what’s happening in the present” and “I tend not to notice feelings of physical tension or discomfort until they really grab my attention.”
The participants also underwent tests to determine ratings on seven indicators of cardiovascular health, as suggested by the American Heart Association: smoking avoidance, physical activity, body mass index, fruit and vegetable consumption, cholesterol, blood pressure, and fasting blood glucose.
The researchers also noted the participants’ age, race, sex, education, and scores on standardized scales of depression, and sense of control in their lives.
In their analysis of the data, Loucks and his team examined the association between the degree of self-reported mindfulness and the scores on each of the seven cardiovascular health indicators, accounting for age, sex, and race. They also calculated a composite score of the health indicators.In-the-moment benefits
Participants with high MAAS scores had an 83 percent greater prevalence of good cardiovascular health (as measured by the composite score) compared to those with relatively low MAAS scores. High vs. low MAAS scores were associated with significantly higher cardiovascular health on four of the seven individual indicators: BMI, physical activity, fasting glucose, and avoiding smoking.
That higher mindfulness did not also associate with higher scores for blood pressure or cholesterol may be because neither of those health indicators directly affect how someone feels in a typical moment, whereas smoking, obesity (and closely related fasting glucose), and physical activity are all much more explicitly evident experiences for the self.
Meanwhile, fruit and vegetable consumption, an indicator of diet quality, showed a positive association with higher MAAS scores, but with too wide a range of uncertainty to be considered statistically significant.
Loucks says the next step in his research is to begin testing whether improving mindfulness can increase cardiovascular health indicators. He says he hopes to launch randomized controlled trials with long-term follow-up (because behavioral interventions often look good in the short term but then don’t last).
The National Institutes of Health provided support for the study.
Source: Brown University
Scientists are officially debunking the myth that megalodon sharks still exist. The whale-eating monsters became extinct about 2.6 million years ago.
“I was drawn to the study of Carcharocles megalodon’s extinction because it is fundamental to know when species became extinct to then begin to understand the causes and consequences of such an event,” says Catalina Pimiento, a doctoral candidate at the Florida Museum of Natural History at University of Florida.
“I also think people who are interested in this animal deserve to know what the scientific evidence shows, especially following Discovery Channel specials that implied megalodon may still be alive.”
Published in PLOS ONE, the study represents the first phase of Pimiento’s ongoing reconstruction of megalodon’s extinction. As modern top predators, especially large sharks, are significantly declining worldwide due to the current biodiversity crisis, the study serves as the basis to better understand the consequences of these changes.
“When you remove large sharks, then small sharks are very abundant and they consume more of the invertebrates that we humans eat,” Pimiento says. “Recent estimations show that large-bodied, shallow-water species of sharks are at greatest risk among marine animals, and the overall risk of shark extinction is substantially higher than for most other vertebrates.”Megalodon mania
Pimiento plans to further investigate possible correlations between changes in megalodon’s distribution and the evolutionary trends of marine mammals, such as whales and other sharks.
“When we calculated the time of megalodon’s extinction, we noticed that the modern function and gigantic sizes of filter feeder whales became established around that time,” she says. “Future research will investigate if megalodon’s extinction played a part in the evolution of these new classes of whales.”
The slowly unraveling details of megalodon’s extinction and various aspects of its natural history have consumed Pimiento’s research for the past six years, including ongoing analysis of megalodon’s body size and a 2010 PLOS ONE study that suggested that Panama served as a nursery habitat for the species.
For the new study, researchers used databases and scientific literature of the most recent megalodon records and calculated the extinction using a novel mathematical model proven reliable in recent experimental testing by study coauthor Christopher F. Clements with the Institute of Evolutionary Biology and Environmental Studies at the University of Zurich.
The study will not only serve as a key reference for debunking the myth that megalodon still exists, but its new methods will influence the future of scientific research of extinct animals and plants, says Jorge Velez-Juarbe, a vertebrate paleontologist with the Natural History Museum of Los Angeles County.
“The methodology that the authors used had only been previously employed to determine extinction dates in historical times, such as to estimate the extinction date of the dodo bird,” he says.
“In this work, scientists applied that same methodology to determine the extinction of an organism millions of years ago, instead of hundreds. It’s a new tool that paleo-biologists didn’t have, or rather had not thought of using before.”
Source: University of Florida
The post There’s zero chance you’ll be eaten by a megalodon appeared first on Futurity.
Laboratory tests of an approved therapeutic suggest it may treat symptoms of autoimmune diseases such as type-1 diabetes and multiple sclerosis.
These diseases occur when a group of immune cells called pro-inflammatory T-effector cells become sensitized to specific cells in the body, identifying them as foreign and attacking them as if they were invading bacteria.
“IGF-1 is already an approved therapeutic and has been tested in many different settings. That means it will be much easier to start clinical trials.”
This “friendly fire” goes unchecked due to the failing of another type of immune cell: called the T-reg, which controls T-effector cells, shutting them down when they are not needed.
In laboratory work researchers created conditions that mimic type-1 diabetes and multiple sclerosis. They found that administering a molecule called insulin-like growth factor-1 (IGF-1) induced the production of T-reg cells, which in turn suppressed symptoms.
The research confirms that IGF-1 acts directly on T-reg cells—rather than indirectly by affecting some other factor that induces T-reg cells to multiply.Related Articles On Futurity
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Lead author Nadia Rosenthal, a professor at Monash University and scientific head of the European Molecular Biology Laboratory (EMBL), says the findings, published this week in EMBO Molecular Medicine, have clinical significance.
“IGF-1 is already an approved therapeutic and has been tested in many different settings. That means it will be much easier to start clinical trials for IGF-1 in autoimmune and inflammatory diseases than it would if we were proposing a new, untested drug,” Rosenthal says.
In a separate study published earlier this year, Rosenthal and Daniel Bilbao at EMBL in found that IGF-1 also suppresses allergic contact dermatitis, an inflammatory skin disease.
Rosenthal plans to explore the role of IGF-1 in inflammation and regeneration, and its potential for treating conditions such as muscular atrophy, fibrosis, and heart disease.
Source: Monash University
Subliminal messages containing positive stereotypes about aging can improve older adults’ physical functioning for several weeks, according to a new study.
Researchers used a new intervention method to examine for the first time whether exposure to positive age stereotypes could weaken negative age stereotypes and their effects over time, and lead to healthier outcomes.Related Articles On Futurity
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The study, published online in Psychological Science, consisted of 100 older individuals (average age 81 years) who live in the greater New Haven, Connecticut area.
Some of the participants were subjected to positive age stereotypes on a computer screen that flashed words such as “spry” and “creative” at speeds that were too fast to allow for conscious awareness.
Individuals exposed to the positive messaging exhibited a range of psychological and physical improvements that were not found in control subjects. They benefited from improved physical function, such as physical balance, which continued for three weeks after the intervention ended.
Also, during the same period, positive age stereotypes and positive self-perceptions of aging got stronger, and negative age stereotypes and negative self-perceptions of aging weakened.Fighting bad stereotypes
“The challenge we had in this study was to enable the participants to overcome the negative age stereotypes which they acquire from society, as in everyday conversations and television comedies,” says lead researcher Becca Levy, associate professor and director of the Social and Behavioral Science Division of the Yale School of Public Health.
“The study’s successful outcome suggests the potential of directing subliminal processes toward the enhancement of physical function.”
While it has been previously shown by Levy that negative age stereotypes can weaken an older individual’s physical functioning, this is the first time that subliminal activation of positive age stereotypes was found to improve outcomes over time.
The study found that the intervention influenced physical function through a cascade of positive effects: It first strengthened the subjects’ positive age stereotypes, which then strengthened their positive self-perceptions, which then improved their physical function.
The study’s effect on physical function surpassed a previous study by others that involved a six-month-exercise intervention’s effect with participants of similar ages.
The National Institute on Aging; National Heart, Lung and Blood Institute; and the Patrick and Catherine Weldon Donaghue Medical Research Foundation supported the study. The research team also included Corey Pliver of the Yale School of Public Health, Martin Slade of the Yale School of Medicine, and Pil Chung of the University of California, Berkeley.
Scientists have figured out the optimal gap needed between two gold nanoparticles to turn them into optical antennae.
When the gap is optimal, the particles can concentrate light shining on them into the tiny regions between the gap. Researchers can use the light to sense molecules inside the space.Related Articles On Futurity
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“Up until now there were two competing theories surrounding what gap was required between particles to best concentrate the light but we now have the technology to test it,” says lead investigator Ken Crozier, a professor of physics and electronic engineering at the University of Melbourne.
Crozier says he and colleagues used a top-down approach to measure the gap width.
“We coated the nanoparticles with molecules, and performed spectroscopy on them with a laser-based microscope we built. We measured the signal given off by the molecules as a function of the gap width.
“We found that as the gap width decreased, the signal increased until the gap width reached the atomic scale, after which the signal began to decrease—giving us the gap width that optimizes the signal from the molecules.”
This work, published in Nature Communications, gives scientists a deeper understanding of the physics of nanotechnology.
The National Science Foundation and the Harvard Quantum Optics Center supported the project. Lead author Wenqi Zhu performed the work under Crozier’s supervision as a PhD student at Harvard University and is now with the National Institute of Standards and Technology.
Source: University of Melbourne
Buprenorphine maintenance therapy works better than detox for treating patients with prescription opioid dependence in primary care, new research shows.
Prescription opioid dependence has been increasing for the last 15 years and now surpasses heroin dependence. Doctors are also writing more prescriptions for pain management, which has led to higher experimentation and addiction rates, according to lead author David Fiellin, professor of internal medicine at Yale School of Medicine.
“Primary care physicians lack evidence-based guidelines to decide between detoxification or providing patients with ongoing maintenance therapy,” says Fiellin.Related Articles On Futurity
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Fiellin and his colleagues conducted a 14-week randomized clinical study of 113 patients with prescription opioid dependence. Patients randomly received either buprenorphine detoxification or ongoing buprenorphine maintenance therapy.
Buprenorphine is a medication used to treat addiction. Study participants in the detoxification group received six weeks of stable doses of buprenorphine followed by three weeks of tapering doses. All patients received physician and nurse support and drug counseling for all 14 weeks.
The team found that patients in the detoxification group tested positive for illicit opioid use more often than those in the maintenance group. Patients who received ongoing buprenorphine were less likely to use illicit opiates. Few of the patients in the detoxification group stayed in treatment or were able to abstain after the medication was discontinued.
“For prescription opioid dependence, buprenorphine detoxification is less effective than ongoing maintenance treatment, and increases the risk of overdose and other adverse events,” says Fiellin.
“We found that a number of providers were offering patients buprenorphine detoxification. This is not consistent with how the disease process works.
“It is very common for patients seeking treatment to request detoxification,” says Fiellin. “They want to be off of everything as soon as possible as opposed to considering long-term treatment, but unfortunately there’s no quick fix for the disease. The majority of patients will do better if they receive ongoing maintenance treatment.”
The National Institute on Drug Abuse funded the study, which appears in JAMA Internal Medicine.
The 1918 influenza virus killed 50 million people worldwide, and now scientists are hoping to apply the lessons learned to fight diseases like Ebola.
The pandemic, also known as the “Spanish flu,” claimed 675,000 lives in nine months in the United States alone. Of the total killed, as many as 20 million were in India.Related Articles On Futurity
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“If we get another flu pandemic and it infects tens of millions in the US, killing half a million people, that’s going to be worse than anything that’s happened to us in at least the last 50 to 100 years,” says Siddharth Chandra, director of the Asian Studies Center at Michigan State University.
Chandra and Eva Kassens-Noor, assistant professor of urban and transport planning, studied weekly death rates in 213 districts from nine provinces in India, information contained in reports from the sanitary commissioner’s office.
They found that the virus entered India in Bombay, which experienced a three-week flu wave and a peak death rate of 54.9 people per 1,000. As it spread east, the flu epidemic lengthened to eight weeks and fewer people died.
Simply put: when the flu hit, it hit hard and fast.Will Ebola get worse?
“This has all sorts of implications for pandemics that are happening now or might be threatening to happen,” Chandra says. “In scenarios resembling the 1918 pandemic as it unfolded in India, locations close to an entry point will have extremely short windows of time to deal with a virulent pathogen, placing emphasis on the emergency management of a short and severe wave of illness.”
Possibly a severe wave like the Ebola virus in West Africa, he says.
According to the World Health Organization, there have been 9,216 confirmed, probable, and suspected cases of Ebola in seven countries and 4,555 deaths. While Ebola is far less contagious than the flu and it’s not moving as quickly, if there had been 9,000 cases of the 1918 flu, there would’ve been fewer than 900 deaths, Chandra says.
“One of the things this research could shed light on: are viruses like the Ebola virus going to get less virulent or more virulent as they move on?”
Find the full study in the journal BMC Infectious Diseases.
Source: Michigan State University
You may want to think twice about handling a cash register receipt, especially if you’ve just slathered on some hand sanitizer or lotion.
Most receipts contain high levels of the chemical BPA (Bisphenol A), which acts like a hormone and can cause birth defects and cancer.
“Store and fast food receipts, airline tickets, ATM receipts, and other thermal papers all use massive amounts of BPA on the surface of the paper as a print developer.”
Researchers found a rapid increase of BPA in the blood of people who used a skin care product and then touched a store receipt with BPA.
“BPA first was developed by a biochemist and tested as an artificial estrogen supplement,” says Frederick vom Saal, professor of biological sciences at University of Missouri.
“As an endocrine-disrupting chemical, BPA has been demonstrated to alter signaling mechanisms involving estrogen and other hormones. Store and fast food receipts, airline tickets, ATM receipts, and other thermal papers all use massive amounts of BPA on the surface of the paper as a print developer.
“The problem is, we as consumers have hand sanitizers, hand creams, soaps, and sunscreens on our hands that drastically alter the absorption rate of the BPA found on these receipts.”Receipts and French fries
People in the study cleaned their hands with hand sanitizer, held thermal paper receipts, and then ate French fries with their hands. BPA was absorbed very rapidly, vom Saal says.Related Articles On Futurity
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“Our research found that large amounts of BPA can be transferred to your hands and then to the food you hold and eat as well as be absorbed through your skin.
“BPA exhibits hormone-like properties and has been proven to cause reproductive defects in fetuses, infants, children, and adults as well as cancer and metabolic and immune problems in rodents.
“BPA from thermal papers will be absorbed into your blood rapidly. At those levels, many diseases such as diabetes and disorders such as obesity increase as well. Use of BPA or other similar chemicals that are being used to replace BPA in thermal paper pose a threat to human health.”
Read the full study in the journal PLOS ONE.
Source: University of Missouri
Astronomers and geneticists are good at sharing, report researchers, who say ecologists may need a brush-up on the concept.
A study in the current issue of Bioscience explores the paradox that although ecologists share findings via scientific journals, they do not share the data on which the studies are built, says Patricia Soranno, a fisheries and wildlife professor at Michigan State University and coauthor of the paper.
“One reason for not sharing data is the fear of being scooped by another scientist; but if all data are available, then everyone is on the same playing field, there are more people to collaborate with, and you will have a bigger impact on science,” says Soranno.
“Think of the advances being made in genomics, for example, due to the human genome project and the free-flowing findings and data. Genomics is advancing at an unprecedented rate, and it’s having an impact on many other fields as well.”Good intentions
While many environmental scientists support the notion of sharing, the vast majority of them do not carry out their good intentions, according to a recent survey.Related Articles On Futurity
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Even with calls from funding organizations, scientific journals, and even the White House, it’s still yet to instill sharing as a matter of practice, says historian Georgina Montgomery.
“If you advocate for inclusion in science, if you believe scientists should be engaged with the public and decision makers in policy, then you should walk the walk and share your data,” she says. “Collaboration, rather than competition, is the best way to continue to advance science.”
To improve the current culture, the team argues that increased data sharing will allow more diverse people to actively participate in research, such as early-career scientists and those from underrepresented groups; scientists from smaller or historically less-influential institutions; citizen-scientists; and scientists from the Global South, scientists from Africa, South and Central America, and much of Asia who are often excluded from leading research.Ethics, not force
The culture is beginning to change, but now it’s time to find ways to implement it, adds Kendra Cheruvelil of fisheries and wildlife.
“We’ll still need to work through the best way to make this the norm,” she says. “We’re not saying to share data as soon as it’s gathered, and we understand that there’s not a one-size-fits-all policy. Our hope is that scientists will change their practice because they are compelled by the argument that they are ethically obliged to, not because they are forced to share data.”
Future research will focus on scientist-driven approaches to making data more shareable and increasing incentives at an institutional level. Universities offer few, if any, motivations to share data. It would help to offer credit for sharing rather than for solely emphasizing published papers, Cheruvelil adds.
Outside of universities, sharing data is key because there are many efforts to include community-based monitoring groups to help inform decisions and policies about the environment.
“If environmental scientists truly espouse the ethical value of inclusivity, including diverse groups of people at the tables of research, decision making, policy, and public debate, it is not only necessary to share scientific data, it is ethically obligatory,” says Kevin Elliott, a philosopher in fisheries and wildlife.
Source: Michigan State University
While more and more US hospitals are consolidating medical groups and physician practices to be more efficient, a new study finds the practice often backfires and increases the cost of patient care.
“This consolidation is meant to better coordinate care and to have a stronger bargaining position with insurance plans,” says lead author James Robinson, professor and head of health policy and management at University of California, Berkeley’s School of Public Health.
“The movement also aligns with the goals of the Affordable Care Act, since physicians and hospitals working together in ‘accountable care organizations’ can provide care better than the traditional fee-for-service and solo practice models.
“The intent of consolidation is to reduce costs and improve quality, but the problem with all this is that hospitals are very expensive and complex organizations, and they are not known for their efficiency and low prices.”Per patient costs
For the study, published in the Journal of the American Medical Association, Robinson and study coauthor Kelly Miller, a program analyst at Integrated Healthcare Association, analyzed four years of data (2009 to 2012) on 158 major medical groups and 4.5 million patients in California.
Groups were put into three categories: owned by physicians, owned by a local hospital or hospital system, or owned by a large hospital system that spans multiple geographic markets in the state.
The measure of costs included physician visits, inpatient hospital admissions, outpatient surgery, and diagnostic procedures, drugs, and all other forms of medical care except for mental health services. Researchers did not have data on mental health services since they are paid for separately.
After controlling for such factors as the mix of severely ill patients and geographic differences in cost, the researchers found that per patient expenditures were 19.8 percent higher for physician groups in multi-hospital systems compared with physician-owned organizations. Groups owned by local hospitals were better, but per patient costs still ran 10.3 percent higher compared with physician-owned groups.High-priced hospitals
Why would consolidation lead to increased costs? It could be that once a medical group has been acquired, physicians in those groups are expected to admit their patients to the high-priced hospital, Robinson says.
“Hospital-owned medical groups usually are expected to conduct ambulatory surgery and diagnostic procedures in the outpatient departments of their parent hospital, but hospital outpatient departments are much more costly and charge much higher prices than freestanding, non-hospital ambulatory centers.”
Public policy should not encourage mergers and acquisitions as a means of promoting collaboration. Instead, policymakers should consider supporting the use of bundled payments for hospitals and physicians to improve coordination of care, Robinson says.
“Hospitals are an essential part of the health care system, but they should not be the center of the delivery system. Rather, physician-led organizations based in ambulatory and community settings are likely to be more efficient and provide cheaper care.”
The findings are limited to California, the authors say, and further studies should be done using data from other states.
“Nevertheless, these findings are important since California is the nation’s leader in terms of having physicians participate in large medical groups that already perform the functions ascribed to ‘accountable care organizations’ by the Obama administration,” Robinson says.
The Robert Wood Johnson Foundation provided support for this research.
Source: UC Berkeley
The post When hospitals merge, patients often pay the price appeared first on Futurity.
Children exposed to certain types of air pollution during pregnancy and early in life are more likely to develop autism, according to a study of families living in Pennsylvania.
“Autism spectrum disorders are a major public health problem, and their prevalence has increased dramatically,” says Evelyn Talbott, professor of epidemiology at University of Pittsburgh Public Health.
“Despite its serious social impact, the causes of autism are poorly understood. Very few studies of autism have included environmental exposures while taking into account other personal and behavioral risk factors. Our analysis is an addition to the small but growing body of research that considers air toxics as one of the risk factors for ASD.”
Researchers performed a population-based study of families with and without ASD living in six southwestern Pennsylvania counties. Results show links between increased levels of chromium and styrene and childhood autism spectrum disorder, a condition that affects one in 68 children.
Talbot presented the preliminary findings at the American Association for Aerosol Research annual meeting.30 pollutants
Autism spectrum disorders (ASDs) are a range of conditions characterized by social deficits and communication difficulties that typically become apparent early in childhood. Reported cases of ASD have risen nearly eight-fold in the last two decades.Related Articles On Futurity
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While previous studies have shown the increase to be partially due to changes in diagnostic practices and greater public awareness of autism, this doesn’t fully explain the increased prevalence. Both genetic and environmental factors are believed to be partially responsible.
Researchers interviewed 217 families of children with ASD and compared these findings with information from two separate sets of comparison families of children without ASD born during the same time period within the six-county area. The families lived in Allegheny, Armstrong, Beaver, Butler, Washington, and Westmoreland counties, and the children were born between 2005 and 2009.
One of the strengths of the study was that it had “two types of controls, which provided a comparison of representative air toxics in neighborhoods of those children with and without ASD,” Talbott says.
For each family, the team used the National Air Toxics Assessment (NATA) to estimate the exposure to 30 pollutants known to cause endocrine disruption or neurodevelopmental issues. NATA is the Environmental Protection Agency’s (EPA) ongoing comprehensive evaluation of air toxics in the US, most recently conducted in 2005.Styrene and chromium
Based on the child’s exposure to concentrations of air toxics during the mother’s pregnancy and the first two years of life, the researchers note that children who fell into higher exposure groups to styrene and chromium were at a 1.4- to two-fold greater risk of ASD, after accounting for the age of the mother, maternal cigarette smoking, race, and education.
Other NATA compounds associated with increased risk included cyanide, methylene chloride, methanol, and arsenic. As these compounds often are found in combination with each other, further study is needed.
Styrene is used in the production of plastics and paints, but also is one of the products of combustion when burning gasoline in vehicles. Chromium is a heavy metal, and air pollution containing it typically is the result of industrial processes and the hardening of steel, but it also can come from power plants. Cyanide, methylene chloride, methanol, and arsenic are all used in a number of industries or can be found in vehicle exhaust.
“Our results add to the growing body of evidence linking environmental exposures, such as air pollution, to ASD,” Talbott says. “The next step will be confirming our findings with studies that measure the specific exposure to air pollutants at an individual level to verify these EPA-modeled estimates.”
Source: University of Pittsburgh