Beauty For Love Beauty For Love Wed, 25 Apr 2018 03:40:34 +0000 en-US hourly 1 Rooftop sensors on U.S. embassies are warning the world about ‘crazy bad’ air pollution Wed, 25 Apr 2018 03:01:46 +0000  

The U.S. embassy’s hourly smog updates have irked Beijing officials—and spurred mitigation measures.

Kevin Frayer/Stringer/GETTY IMAGES

Rooftop sensors on U.S. embassies are warning the world about ‘crazy bad’ air pollution

In October 2010, as heavy smog hung over Beijing, the U.S. embassy’s Twitter feed said its rooftop pollution sensor had detected “crazy bad” levels of hazardous microparticles. So-called PM2.5 had shot up to about 550 micrograms per cubic meter—a level to which programmers had given the sardonic label because they thought it would never be reached. The undiplomatic language ruffled feathers in Beijing; embassy staff apologized, deleted the tweet, and replaced the label with “beyond index.”

Yet that incident and others like it spurred public complaints that eventually elicited more aggressive efforts to tame the pollution. By now, rooftop sensors like those that drew attention to Beijing’s pollution sprout from 26 diplomatic posts in 16 countries. Their immediate goal is to protect the health of U.S. diplomats. But they are raising concerns about air pollution from Sarajevo to New Delhi and supplying data to research efforts. The “little-air-monitor-that-could,” as physicist and former U.S. diplomat David Roberts calls it, has become a worldwide watchdog.

The first Beijing sensor, installed a decade ago, was meant to provide warnings of bad-air days to U.S. citizens. The fine particles it measures, mostly residues of coal burning and vehicle emissions, are linked to respiratory and heart disease. Third party apps made the readings widely available to Chinese who wanted to monitor PM2.5—and got little information from their own government.

China had been struggling to rein in air pollution ever since the late 1990s, after Beijing won the bid for the 2008 Olympics. But officials were embarrassed by the slow progress that the sensor readings highlighted, especially when the U.S. data undercut the Beijing government’s rosy pronouncements of “blue sky” days, when pollution supposedly fell. Officials demanded that the embassy stop releasing the data. “We said we couldn’t, since the data regarded the health of U.S. citizens,” recalls Gary Locke, who served as ambassador to China from 2011 to 2014.

Beijing officials also challenged the usefulness of the U.S. data, pointing out, for instance, that the embassy sensor was in only one location and therefore could be giving an incomplete picture. In response, the embassy teamed up with U.S. Environmental Protection Agency (EPA) scientists to validate the results. “Since we were being criticized, we wanted to make sure we were doing it correctly,” says Erica Thomas, a Department of State official who led air monitoring at the embassy in Beijing from 2010 to 2014.

Tensions came to a head in late 2011, when Beijing’s smog got so bad that its airport canceled hundreds of flights. Based on monitoring of larger particles, municipal authorities insisted that the air was only “slightly polluted”—provoking ridicule from bloggers citing U.S. data. “It was the straw that broke the camel’s back,” says Angel Hsu of Yale University, an expert on pollution in China. Days later, China proposed new air quality standards that included PM2.5 for the first time. It now runs the biggest PM2.5 monitoring system in the world.


The Department of State, too, expanded its PM2.5 monitoring efforts, first within China and then around the world, and is using the sensors for research as well. Drawing on PM2.5 data from five diplomatic posts in China, a 2015 study in Atmospheric Environment revealed previously unknown variations in PM2.5 levels; for instance, in Beijing the particles tended to peak around midnight and bottom out in spring, because of weather patterns. And the U.S. embassy in Sarajevo is now testing cheaper sensors with an aim of deploying them “in different pollution environments,” says Caroline D’Angelo, who runs the Department of State’s monitoring network in Washington, D.C.

Findings are radiating into other disciplines. During a stint at the U.S. consulate in São Paulo, Brazil, Tommy Flynn, a program manager with the South Carolina Department of Health and Environmental Control, is providing technical assistance on the monitors. But he has also learned from the consulate’s practice of distributing filter masks to high-risk groups during ultra–high-pollution events. That’s a lesson, he says, that could be applied in South Carolina during forest fires. And scientists from NASA and the World Bank are using embassy PM2.5 data, now posted on EPA’s AirNOW monitoring website, to groundtruth satellite measurements of pollution, filling in gaps in the global map of reliable air quality measurements.

The U.S. sensors continue to serve as a diplomatic cudgel, as well. In India, where air pollution in New Delhi and other cities has skyrocketed, “the data has flowed from the embassy to the media and then created outcry,” says Christa Hasenkopf, a former Department of State official who now runs the air pollution nonprofit OpenAQ in Washington, D.C. As Locke says, the monitoring program “has taken on a life its own.”


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Indonesian divers have evolved bigger spleens to hunt underwater Wed, 25 Apr 2018 03:01:39 +0000  

Indonesian divers have evolved bigger spleens to hunt underwater

Some of the most exciting discoveries in evolutionary biology in recent years have shown how humans have adapted to extreme conditions, such as living at high altitude. Now, researchers have found that Indonesia’s Bajau people, who for generations have spent the majority of their days diving and hunting underwater, also have genetic adaptations for their unusual lifestyle. These “sea nomads” carry a gene variant that seems to lead to unusually large spleens that can supply an extra boost of oxygenated red blood cells on demand.

The new study suggests that people exposed to low-oxygen conditions have evolved “many pathways” for coping, says Gabriel Haddad, a physiologist at the University of California (UC), San Diego, who was not involved with the work.

The Bajau have lived for more than 1000 years on house boats in the waters around Malaysia, the Philippines, and Indonesia. Divers spend more than 60% of their 8-hour work days underwater, spearing fish, hunting sea cucumbers, and gathering black coral to fashion into jewelry. That lifestyle fascinated Melissa Ilardo, who first heard about the sea nomads as a graduate student studying corals in Southeast Asia. Intrigued by work pinpointing the genes that help Tibetans, Ethiopians, and South Americans adapt to chronic oxygen deprivation at high altitude, Ilardo—now a postdoc at the University of Utah in Salt Lake City—approached her colleagues about doing similar studies in the Bajau. “We were quite skeptical that it would be possible to find anything,” said one, Rasmus Nielsen, an evolutionary genomicist at UC Berkeley.

Physiologists know that most mammals—including humans—undergo a “diving response” when their faces hit cold water. Their heart rates slow; blood is shunted into the body’s core, and the spleen contracts, releasing some of its store of oxygenated red blood cells. In 1990, researchers learned that the spleens of Japanese pearl divers contract harder than normal, boosting blood oxygen by up to 9% during dives. Ilardo decided to see whether Bajau spleens were similarly special.

Using a portable ultrasound machine, she measured the organ in 59 Bajau and 34 people from a nearby farming community. The Bajau’s spleens were 50% larger than those of their land-based neighbors on average, she and her colleagues report today in Cell.

Ilardo then compared DNA—sequenced from saliva swabs—from the two groups. She found that the Bajau had 25 genes that differed from both the farmers and a large earlier study of Han Chinese. That makes the genes likely candidates for the evolutionary process known as natural selection. One such gene, PDE10A, has been shown to affect thyroid activity in mice, which in turn affects spleen size.

It’s often difficult to show that a gene has undergone recent evolutionary adaptations in living people, but in this case, there is strong evidence, even though the Bajau have been living the sea life for just a few thousand years, says study co-author Eske Willerslev, an evolutionary genomicist at the University of Copenhagen.

Mark Aldenderfer, an archaeologist at UC Merced who was not involved with the work, agrees: “Perhaps the biggest takeaway from this paper is that natural selection continues to work on human populations.”

Anthropologist Cynthia Beall from Case Western Reserve University in Cleveland, Ohio, isn’t yet convinced Ilardo and her colleagues fully understand what’s happened with the Bajau. She points out that although the Bajau dive more frequently than most people, they are not necessarily under the water longer for any given dive. Also, a larger spleen doesn’t necessarily mean a bigger expulsion of red blood cells, which is what actually helps the divers, she notes. And Edward Gilbert-Kawai, a physician-physiologist at the University of London, notes also “it is highly unlikely that spleen size is controlled by only one gene.”

Still, Ilardo is hopeful the Bajau can offer some help to people experiencing temporary oxygen deficits, like those with sleep apnea or brain injuries. By finding out what makes the Bajau so adept at dealing with no air, she suggests, physicians may one day learn how to better treat those conditions in their patients.


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Pioneering autism researcher cooperated with Nazis, new evidence suggests Wed, 25 Apr 2018 03:01:28 +0000  

This memorial in Vienna remembers Nazi-era victims of the children’s psychiatric facility Am Spiegelgrund, where children and adolescents were systematically killed and their brains removed for scientific research. A new book and journal article alleges that Hans Asperger, a pioneer of autism research, referred dozens of children to the clinic.


Caro/Christoph Eckelt/Newscom

Pioneering autism researcher cooperated with Nazis, new evidence suggests

Originally published on Spectrum

The Austrian doctor Hans Asperger cooperated extensively with the Nazi regime and may have sent dozens of children to their deaths.

Horrific details of his involvement were revealed yesterday in the journal Molecular Autism and will be detailed in a forthcoming book called Asperger’s Children: The Origins of Autism in Nazi Vienna.

Asperger was among the first researchers to describe autism, and his decades of work with children later informed the concept of an autism “spectrum.”

Scholars have raised questions about his associations with the Nazi Party and his involvement in Nazi efforts to euthanize children with certain health conditions or disabilities.

The new book and paper suggest that Asperger referred dozens of children to a clinic called Am Spiegelgrund in Vienna, where doctors experimented on children or killed them. Nearly 800 children, many of whom were disabled or sick, were killed there. The clinic’s staff gave the children barbiturates, which often led to their death by pneumonia.

Reacting to this news, some experts say the eponymous medical term “Asperger syndrome” should be discarded.

The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) has already dispensed with Asperger syndrome for other reasons, notes David Mandell, professor of psychiatry at the University of Pennsylvania.

“Asperger [syndrome] was put in a coffin with the DSM-5, and maybe this information will be the final nail in terms of preventing it from coming back,” he says.

Others are more cautious, saying the stain on Asperger’s name shouldn’t erase his contributions to the understanding of autism.

“I don’t think erasing history is an answer,” says Herwig Czech, a medical historian at the Medical University of Vienna and author of the new paper. “I think we also have to part ways with the idea that an eponym is an unmitigated honor of the person. It is simply a historical acknowledgment that can be, in some cases, troubling or problematic.”

Revising history

Asperger syndrome officially entered the medical lexicon in 1981, when British psychiatrist Lorna Wing found Asperger’s 1944 thesis and popularized his work.

In 1992, the International Classification of Diseases (ICD) included the syndrome and, 2 years later, the DSM did the same.

The term is still listed in the ICD-10, that manual’s current version. But the ICD-11, expected to debut in May, will subsume the syndrome into the autism diagnosis, just as the DSM-5 does.

Yet the term is still widely used to refer to someone on the milder end of the autism spectrum.

Asperger was never a member of the Nazi Party. And for decades, books and academic articles portrayed him as a benevolent figure who saved children with autism from the killing centers.

But in 2005, a medical historian named Michael Hubenstorf revealed that Asperger had had a close relationship with the prominent Nazi physician Franz Hamburger. In the 2015 book Neurotribes: The Legacy of Autism and the Future of Neurodiversity, journalist Steve Silberman also connected Asperger to Hamburger, but he didn’t find a link to Nazi eugenics.

It wasn’t until historians dug up Asperger’s clinical records that the truth came to light.

New revelations

The children’s clinic where Asperger worked was bombed by Allied troops, and for decades many people believed the clinical records had been destroyed.

In 2009, Czech was asked to speak at a 2010 symposium commemorating Asperger’s death. That inspired him to start digging into the government archives in Vienna for details about the pediatrician—where he discovered the well-preserved clinical records.

Czech found a Nazi Party file that vouched for Asperger’s loyalty even though he was not a member. He also found talks Asperger gave, as well as his medical case files and notes.

Two years later, historian Edith Sheffer visited the same Vienna archives. Sheffer has a son with autism and had long been curious about Asperger, who she had thought had a “heroic” reputation.

“From the very first file I found in the archives, I saw that he was implicated in the Nazi program that actually killed disabled children,” says Sheffer, a senior fellow at the University of California, Berkeley’s Institute for European Studies. She is the author of the new book, which is expected to be released in May.

Asperger described the behavior of children with autism as being in opposition to Nazi Party values. For instance, a typical child interacts with others as an “integrated member of his community,” he wrote, but one with autism follows his own interests “without considering restrictions or prescriptions imposed from outside.”

Asperger’s clinical files describe children with disabilities and psychiatric conditions in far more negative terms than his colleagues did. For instance, Am Spiegelgrund physicians described a boy named Leo as “very well developed in every respect.” Asperger described him as a “very difficult, psychopathic boy of a kind which is not frequent among small children.”

Asperger’s closest colleagues and mentors were the architects of Am Spiegelgrund’s eugenics program. “He was traveling at the highest echelons of the killing system, and so I really see him as more than just a passive follower,” Sheffer says.

Czech found evidence suggesting Asperger personally transferred at least two children to Am Spiegelgrund and served on a committee that referred dozens of others; the children died there. There is no evidence that Asperger saved children from the clinic.

“Could he have sent more children to Spiegelgrund? Yes, of course,” Czech says. “But did he refrain in all cases? No.”

Greater organism

The archives also reveal an arc in Asperger’s descriptions of children in his clinic. In 1937, before World War II, Asperger was circumspect in classifying children. But within months of Germany’s annexation of Austria in 1938, he began describing children with autism as a “well-characterized group of children,” Sheffer says. Within 3 years, he began calling them “abnormal children.” And by 1944, he described them as outside “the greater organism” of the Nazi ideal.

“Why did he adopt the writing style that he did? I think because he was up for promotion,” Sheffer says of his evolving approach.

She says Asperger’s career soared during the war years. As his Jewish colleagues were removed from their positions, he rose through the ranks.

After the war, however, he described himself in interviews as a resister of Nazi ideology and called the euthanasia program “totally inhuman,” according to Sheffer.

As disturbing as the revelations are, they are an important part of autism research, experts say.

Information on Asperger’s life was “scant” in the 1990s, when Ami Klin, director of the Marcus Autism Center in Atlanta, tried to track it down. “There was no historical scholarship invested in that,” he says. Klin is on the board of Molecular Autism.

Now that the details are out, however, people are divided on the appropriate way forward.

Even the two historians disagree: Unlike Czech, Sheffer says people should stop using the word “Asperger.” Ending the term’s usage would “honor the children killed in his name as well as those still labeled with it,” she wrote in The New York Times.

Some people who received a diagnosis of Asperger syndrome say it’s time to bury the term, but urge caution. “I would be very upset if there was some sort of consensus that the findings themselves were tainted and needed to be set aside because of the nature of the person who contributed them,” says Phil Schwarz, a software engineer in Massachusetts who is on the spectrum.

At the very least, others say, keeping the name may help us remember the lessons of this dark past.

This article was reprinted with permission from Spectrum, the home of autism research news and analysis.


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Autistic children may inherit DNA mutations from their fathers Wed, 25 Apr 2018 03:01:23 +0000

Based on the new findings, researchers propose a more complex model of how autism arises.

Megapress/Alamy Stock Photo

Autistic children may inherit DNA mutations from their fathers

There is no one gene that, when mutated, causes autism. But over the past decade, researchers have identified hundreds of gene variations that seem to affect brain development in ways that increase the risk of autism. However, these scientists mainly searched for variants in the DNA that directly encodes the building blocks of proteins. Now, a new study probing so-called noncoding DNA has found that alterations in regions that regulate gene activity may also contribute to autism. And surprisingly, these variations tended to be inherited from fathers who aren’t autistic.

“This is a really good article—it’s somewhat provocative and it makes us think about [autism genetics in a] different way,” says Lucia Peixoto, a neuroscientist and computational biologist at Washington State University in Spokane, who was not involved in the research. “I think it’s a great contribution to the field.”

Research into the genetic risk for autism has mainly focused on how mutations that arise spontaneously in an individual’s genome—rather than being inherited from a parent—disrupt protein-coding regions and lead to the condition. That’s because these sporadic mutations have relatively large effects and studies have shown that such mutations, although individually rare, together contribute to about 25% to 30% of cases, says Jonathan Sebat, a geneticist at the University of California, San Diego. But only about 2% of the genome consists of protein-coding areas. Sebat says the large noncoding portion of our DNA—often previously referred to as  “junk DNA”—has so far been ignored in autism research.

Sebat’s team was especially interested in the parts of noncoding DNA that regulate gene expression. They looked at whole-genome sequences from 829 families that included autistic individuals, their nonautistic siblings, and their parents. Assessing the influence of individual DNA base changes is particularly difficult in noncoding regions, so they instead identified bigger alterations, so-called structural variants, in which large sequences of DNA are inverted, duplicated, or deleted.

Each individual has thousands of structural variants in their genome, so the researchers narrowed down their analysis to examine just a handful of regulatory regions where genetic variation seemed most likely to cause disruption. They chose these by finding regions where the general population has less variation than expected, suggesting that genetic changes there could be detrimental. These included sites involved in regulating gene activity during brain development and initiating the transcription of genes.

The scientists then examined whether structural variants in these regions were associated with autism by examining the pattern of transmission from parents to their autistic and nonautistic children. Researchers have assumed that mothers are more likely to pass on autism-promoting gene variants. That’s because the rate of autism in women is much lower than that in men, and it is thought that women can carry the same genetic risk factors without having any signs of autism. But when a mother passes these genes to her sons, they are not protected in the same way and thus will be affected.

The team found that mothers passed only half of their structural variants on to their autistic children—a frequency that would be expected by chance alone—suggesting that variants inherited from mothers were not associated with autism. But surprisingly, fathers did pass on substantially more than 50% of their variants. This suggests that autistic children might have inherited risk variants in regulatory regions from their fathers but not their mothers, the researchers report today in Science.

To check that this result held up, Sebat’s team then tested a second, larger sample of 1771 families. Once again, autistic children received more structural variants from their fathers but not mothers—though the size of the effect wasn’t quite as large in this second sample.

“This is completely opposite to … what we had previously assumed,” Sebat says. Peixoto finds the paternal bias surprising as well, although she already suspected that the inherited component of autism would be more apparent in noncoding regions. Compared with mutations in protein-coding regions, variants in regulatory regions usually have “smaller but additive effects. And when you have a smaller effect, you are much more likely to pass [it] along from generation to generation.”

Based on these results, Sebat proposes a more complex model of how autism arises, in which mothers pass on mutations affecting coding regions, which have large effects that women are protected from, while fathers pass on variants affecting noncoding regions; their effects are much more moderate and may only cause symptoms when combined with risk variants from mothers.

Dalila Pinto, a molecular geneticist at the Icahn School of Medicine at Mount Sinai in New York City, says the study provides “very insightful preliminary findings.” She said she will be interested to see whether the results are replicated in even larger genome databases—and whether additional variants will be identified. Peixoto agrees: Although the research is still at an early stage, she says, it “open[s] a door in a different direction.”