Born to be Big

Early exposure to common chemicals may be programming kids to be fat.
By Sharon Begley NEWSWEEK
Published Sep 11, 2009
From the magazine issue dated Sep 21, 2009

It’s easy enough to find culprits in the nation's epidemic of obesity, starting with tubs of buttered popcorn at the multiplex and McDonald's 1,220-calorie deluxe breakfasts, and moving on to the couch potatofication of America. Potent as they are, however, these causes cannot explain the ballooning of one particular segment of the population, a segment that doesn't go to movies, can't chew, and was never that much into exercise: babies. In 2006 scientists at the Harvard School of Public Health reported that the prevalence of obesity in infants under 6 months had risen 73 percent since 1980. "This epidemic of obese 6-month-olds," as endocrinologist Robert Lustig of the University of California, San Francisco, calls it, poses a problem for conventional explanations of the fattening of America. "Since they're eating only formula or breast milk, and never exactly got a lot of exercise, the obvious explanations for obesity don't work for babies," he points out. "You have to look beyond the obvious."
The search for the non-obvious has led to a familiar villain: early-life exposure to traces of chemicals in the environment. Evidence has been steadily accumulating that certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. "The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity," says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). "Exposure to environmental chemicals during development may be contributing to the obesity epidemic." They are not the cause of extra pounds in every person who is overweight—for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice—but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.
The new thinking about obesity comes at a pivotal time politically. As the debate over health care shines a light on the country's unsustainable spending on doctors, hospitals, and drugs, the obese make tempting scapegoats. About 60 percent of Americans are overweight or obese, and their health-care costs are higher: $3,400 in annual spending for a normal-weight adult versus $4,870 for an obese adult, mostly due to their higher levels of type 2 diabetes, heart disease, and other conditions. If those outsize costs inspire greater efforts to prevent and treat obesity, fine. But if they lead to demonizing the obese—caricaturing them as indolent pigs raising insurance premiums for the rest of us—that's a problem, and not only for ethical reasons: it threatens to obscure that one potent cause of weight gain may be largely beyond an individual's control.
That idea did not have a very auspicious genesis. In 2002 an unknown academic published a paper in an obscure journal. Paula Baillie-Hamilton, a doctor at Stirling University in Scotland whose only previous scientific paper, in 1997, was titled "Elimination of Firearms Would Do Little to Reduce Premature Deaths," reported a curious correlation. Obesity rates, she noted in The Journal of Alternative and Complementary Medicine, had risen in lockstep with the use of chemicals such as pesticides and plasticizers over the previous 40 years. True enough. But to suggest that the chemicals caused obesity made as much sense as blaming the rise in obesity on, say, hip-hop. After all, both of those took off in the 1970s and 1980s.
Despite that obvious hole in logic, the suggestion of a link between synthetic chemicals and obesity caught the eye of a few scientists. For one thing, there was no question that exposure in the womb to hormonelike chemicals can cause serious illness decades later. Women whose mothers took the antimiscarriage, estrogenlike drug DES during pregnancy, for instance, have a high risk of cervical and vaginal cancer. In that context, the idea that exposure to certain chemicals during fetal or infant development might "program" someone for obesity didn't seem so crazy, says Jerrold Heindel of NIEHS. In 2003 he therefore wrote a commentary, mentioning Baillie-Hamilton's idea, in a widely read toxicology journal, bringing what he called its "provocative hypothesis" more attention. He underlined one fact in particular. When many of the chemicals Baillie-Hamilton discussed had been tested for toxicity, researchers focused on whether they caused weight loss, which is considered a toxic effect. They overlooked instances when the chemicals caused weight gain. But if you go back to those old studies, Heindel pointed out, you see that a number of chemicals caused weight gain—and at low doses, akin to those that fetuses and newborns are exposed to, not the proverbial 800 cans of diet soda a day. Those results, he says, had "generally been overlooked."
Scientists in Japan, whose work Heindel focused on, were also finding that low levels of certain compounds, such as bisphenol A (the building block of hard, polycarbonate plastic, including that in baby bottles), had surprising effects on cells growing in lab dishes. Usually the cells become fibroblasts, which make up the body's connective tissue. These prefibroblasts, however, are like the kid who isn't sure what he wants to be when he grows up. With a little nudge, they can take an entirely different road. They can become adipocytes—fat cells. And that's what the Japanese team found: bisphenol A, and some other industrial compounds, pushed prefibroblasts to become fat cells. The compounds also stimulated the proliferation of existing fat cells. "The fact that an environmental chemical has the potential to stimulate growth of 'preadipocytes' has enormous implications," Heindel wrote. If this happened in living animals as it did in cells in lab dishes, "the result would be an animal [with] the tendency to become obese."
It took less than two years for Heindel's "if" to become reality. For 30 years his colleague Newbold had been studying the effects of estrogens, but she had never specifically looked for links to obesity. Now she did. Newbold gave low doses (equivalent to what people are exposed to in the environment) of hormone-mimicking compounds to newborn mice. In six months, the mice were 20 percent heavier and had 36 percent more body fat than unexposed mice. Strangely, these results seemed to contradict the first law of thermodynamics, which implies that weight gain equals calories consumed minus calories burned. "What was so odd was that the overweight mice were not eating more or moving less than the normal mice," Newbold says. "We meas-ured that very carefully, and there was no statistical difference."
On the other side of the country, Bruce Blumberg of the University of California, Irvine, had also read the 2002 Baillie-Hamilton paper. He wasn't overly impressed. "She was peddling a book with questionable claims about diets that 'detoxify' the body," he recalls. "And to find a correlation between rising levels of obesity and chemicals didn't mean much. There's a correlation between obesity and a lot of things." Nevertheless, her claim stuck in the back of his mind as he tested environmental compounds for their effects on the endocrine (hormone) system. "People were testing these compounds for all sorts of things, saying, 'Let's see what they do in my [experimental] system,' " Blumberg says. "But cells in culture are not identical to cells in the body. We had to see whether this occurred in live animals."
In 2006 he fed pregnant mice tributyltin, a disinfectant and fungicide used in marine paints, plastics production, and other products, which enters the food chain in seafood and drinking water. "The offspring were born with more fat already stored, more fat cells, and became 5 to 20 percent fatter by adulthood," Blumberg says. Genetic tests revealed how that had happened. The tributyltin activated a receptor called PPAR gamma, which acts like a switch for cells' fate: in one position it allows cells to remain fibroblasts, in another it guides them to become fat cells. (It is because the diabetes drugs Actos and Avandia activate PPAR gamma that one of their major side effects is obesity.) The effect was so strong and so reliable that Blumberg thought compounds that reprogram cells' fate like this deserved a name of their own: obesogens. As later tests would show, tributyltin is not the only obesogen that acts on the PPAR pathway, leading to more fat cells. So do some phthalates (used to make vinyl plastics, such as those used in shower curtains and, until the 1990s, plastic food wrap), bisphenol A, and perfluoroalkyl compounds (used in stain repellents and nonstick cooking surfaces).
Programming the fetus to make more fat cells leaves an enduring physiological legacy. "The more adipocytes, the fatter you are," says UCSF's Lustig. But adipocytes are more than passive storage sites. They also fine-tune appetite, producing hormones that act on the brain to make us feel hungry or sated. With more adipocytes, an animal is doubly cursed: it is hungrier more often, and the extra food it eats has more places to go—and remain.
Within a year of Blumberg's groundbreaking work, it became clear that altering cells' fate isn't the only way obesogens can act, and that exotic pollutants aren't the only potential obesogens. In 2005 Newbold began feeding newborn rats genistein, an estrogenlike compound found in soy, at doses like those in soy milk and soy formula. By the age of 3 or 4 months, the rats had higher stores of fat and a noticeable increase in body weight. And once again, mice fed genistein did not eat significantly more—not enough more, anyway, to account for their extra avoirdupois, suggesting that the compound threw a wrench in the workings of the body's metabolic rate. "The only way to gain weight is to take in more calories than you burn," says Blumberg. "But there are lots of variables, such as how efficiently calories are used." Someone who uses calories very efficiently, and burns fewer to stay warm, has more left over to turn into fat. "One of the messages of the obesogens research is that prenatal exposure can reprogram metabolism so that you are predisposed to become fat," says Blumberg.
The jury is still out on whether soy programs babies to be overweight—some studies find that it does, other studies that it doesn't—but Newbold didn't want her new grandchild to be a guinea pig in this unintentional experiment. When her daughter mentioned that she was planning to feed the baby soy formula, as about 20 percent of American mothers do, Newbold said she would cover the cost of a year's worth of regular formula if her daughter would change her mind. (She did.) As a scientist rather than a grandmother, however, Newbold hedged her bets. "Whether our results can be extrapolated to humans," she said in 2005, "remains to be determined."
Another challenge to the simplistic calories-in/calories-out model came just this month. The time of day when mice eat, scientists reported, can greatly affect weight gain. Mice fed a high-fat diet during their normal sleeping hours gained more than twice as much weight as mice eating the same type and amount of food during their normal waking hours, Fred Turek of Northwestern University and colleagues reported in the journal Obesity. And just as Newbold found, the two groups did not differ enough in caloric intake or activity levels to account for the difference in weight gain. Turek suspects that one possible cause of the difference is the disruption in the animals' circadian rhythms. Genes that govern our daily cycle of sleeping and waking "also regulate at least 10 percent of the other genes in our cells, including metabolic genes," says Turek. "Mess up the cellular clock and you may mess up metabolic rate." That would account for why the mice that ate when they should have slept gained more weight: the disruption in their clock genes lowered their metabolic rate, so they burned fewer calories to keep their body running. Studies in people have linked eating at odd times with weight gain, too.
Mice are all well and good, but many a theory has imploded when results in lab animals failed to show up in people. Unfortunately, that is not the case with obesogens. In 2005 scientists in Spain reported that the more pesticides children were exposed to as fetuses, the greater their risk of being overweight as toddlers. And last January scientists in Belgium found that children exposed to higher levels of PCBs and DDE (the breakdown product of the pesticide DDT) before birth were fatter than those exposed to lower levels. Neither study proves causation, but they "support the findings in experimental animals," says Newbold. They "show a link between exposure to environmental chemicals … and the development of obesity."
Given the ubiquity of obesogens, traces of which are found in the blood or tissue of virtually every American, why isn't everyone overweight? For now, all scientists can say is that even a slight variation in the amounts and timing of exposures might matter, as could individual differences in physiology. "Even in genetically identical mice," notes Blumberg, "you get a range of reactions to the same chemical exposure." More problematic is the question of how to deal with this cause of obesity. If obesogens have converted more precursor cells into fat cells, or have given you a "thrifty" metabolism that husbands calories like a famine victim, you face an uphill climb. "It doesn't mean you can't work out like a demon and strictly control what you eat," says Blumberg, "but you have to work at it that much harder." He and others are quick to add that obesogens do not account for all cases of obesity, especially in adults. "I'd like to avoid the simplistic story that chemicals make you fat," says Blumberg. For instance, someone who was slim throughout adolescence and then packed on pounds in adulthood probably cannot blame it on exposure to obesogens prenatally or in infancy: if that were the cause, the extra fat cells and lower metabolic rate that obesogens cause would have shown themselves in childhood chubbiness.
This fall, scientists from NIH, the Food and Drug Administration, the Environmental Protection Agency, and academia will discuss obesogens at the largest-ever government-sponsored meeting on the topic. "The main message is that obesogens are a factor that we hadn't thought about at all before this," says Blumberg. But they're one that could clear up at least some of the mystery of why so many of us put on pounds that refuse to come off.

Gender Testing of Female Athletes

This is a REALLY interesting website from the Howard Hughes Medical Institute (HHMI) about how to verify a persons gender. Click on the link and scroll down to 'Gender Testing for Female Athletes.... find out why'.
Read the information then 'begin exploring'.
Be sure to read about male development and CAIS.

http://www.hhmi.org/biointeractive/gender/index.html

What do you think? Share your comments with the class.

Male bass in many US rivers feminized, study finds

By SETH BORENSTEIN, AP Science Writer
– Mon Sep 14, 5:54 pm ET

WASHINGTON – Government scientists figure that one out of five male black bass in American river basins have egg cells growing inside their sexual organs, a sign of how widespread fish feminizing has become.
The findings come from the U.S. Geological Survey in its first comprehensive examination of intersex fish in America, a problem linked to women's birth control pills and other hormone treatments that seep into rivers. Sporadic reports of feminized fish have been reported for a few years.
The agency looked at past data from nine river basins — covering about two-thirds of the country — and found that about 6 percent of the nearly 1,500 male fish had a bit of female in them. The study looked at 16 different species, with most not affected.
But the fish most feminized are two of the most sought-after freshwater sportfish: the largemouth and smallmouth, which are part of the black bass family. Those two species were also the most examined with nearly 500 black bass tallied.
"It's widespread," said USGS biologist Jo Ellen Hinck. She is the lead author of the study, published online this month in Aquatic Toxicology. She said 44 percent of the sites where black bass were tested had at least one male with egg cells growing inside.
Past studies have linked the problem to endocrine-disrupting hormones, such as estrogen from women's medicines. While the fish can still reproduce, studies have shown they don't reproduce as well, Hinck said.
Intersex fish are also seen as a general warning about what some experts see as a wider problem of endocrine disruptors in the environment.
The egg cells growing in the male fish's gonads can only be seen with a microscope after the fish has been caught and dissected.
The study used data from 1995 to 2004, when the government stopped funding the research. The only river basin examined that didn't show any problems was Alaska's Yukon River Basin.
The Southeast, especially the Pee Dee River Basin in North and South Carolina, had the highest rates of feminization. In Bucksport, S.C., 10 of 11 largemouth bass examined were intersex. In parts of the Mississippi River in Minnesota and the Yampa River in Colorado, 70 percent of the smallmouth bass had female signs.
Hinck said black bass seem to be more prone to the problem, but researchers don't know why. She also found one common carp that was female with bits of male testes growing inside.

A Spineless Solution

Sep 3rd 2009

From The Economist print edition

http://www.economist.com/sciencetechnology/displaystory.cfm?story_id=14350129

A better way to find novel antibiotics

Science Photo Library Wriggle for the camera, please
NEW antibiotics are always welcome. Natural selection means the existing ones are in constant danger that pathogens will evolve resistance to them. But winnowing the few chemicals that have antibiotic effects from the myriad that might do, but don’t, is tedious. So a technique invented recently by Frederick Ausubel of Harvard University and his colleagues, which should help to speed things up, is welcome.
Dr Ausubel’s method, the details of which have just been published in ACS Chemical Biology, employs nematode worms of a species called C. elegans as its sacrificial victims. C. elegans is one of the most intensively studied animals on Earth (it was the first to have its genome read completely). It is a mere millimetre long, and can be mass produced to order, so it is ideal for this sort of work.
Dr Ausubel set out to make an automated system that could infect worms with bacteria, treat them with chemical compounds that might have antibiotic effects, and then record the results. The device he has built starts by laying the worms on a “lawn” of pathogenic bacteria for 15 hours and then mixing them with water to create a sort of worm soup. It then places the infected worms into individual enclosures, using a machine called a particle sorter that is able to drop a precise number of worms (in this case 15) into each of 384 tiny wells arrayed on a single plate. These wells have, in turn, each been pre-loaded with a different chemical that is being tested for possible antibiotic properties. Once in place, the worms are left alone for five days.
Until now, researchers engaging in this sort of work have had to monitor each wellful of worms by eye (assisted by a microscope) to determine whether the inmates were alive or dead. To avoid this time-consuming process, Dr Ausubel and his team exposed their worms to an orange stain once the five days were over. The stain in question enters dead cells easily, but cannot enter living ones. They were thus able to distinguish the quick from the dead by colour, rather than propensity to wriggle.
Moreover, using a stain in this way meant they could automate the process by attaching a camera to the microscope, taking photographs of all 384 wells, and feeding the images into a computer that had been programmed to measure the area of orange in a well and contrast that with the total area occupied by worms. When they compared this automated mechanism for identifying dead worms with manual methods that depended upon human eyes, they found it was every bit as effective.
So far Dr Ausubel and his colleagues have managed to test around 37,000 compounds using their new method, and they have found 28 that have antibiotic properties. Their most exciting discovery is that some of these substances work in completely different ways from existing antibiotics. That means entirely new types of resistance mechanism would have to evolve in order for bacteria to escape their effects.
Mass screening of this sort is not, itself, a new idea in the search for drugs, but extending it so that it can study effects on entire animals rather than just isolated cells should make it even more productive. And worms, unlike, say, white mice, have few sentimental supporters in the outside world.

Liposuction Fat Turned Into Stem Cells, Study Says

John Roach for National Geographic News
September 8, 2009

The research appears online today in the journal Proceedings of the National Academy of Sciences.

Using leftovers from liposuction patients, scientists have turned human fat into stem cells, a new study says.
The discovery may also help avoid the controversy spawned by the use of stem cells from human embryos.
Human fat is "an abundant natural resource and a renewable one," said Stanford University plastic surgeon Michael Longaker, whose liposuction patients donated the fat for the study.
Longaker envisions a future in which doctors will be able to use fat from a patient to grow, in a lab, new tissues and organs for that patient.
The opportunity wouldn't be limited to the obese.
"Even if you're in great shape, there is still enough fat to be harvested from the vast majority of patients," added Longaker, who co-authored the study.
From Fat to Stem Cells to New Organs?
The reprogrammed cells, called induced pluripotent stem cells, or iPS cells, are capable of turning into most types of cells in the body.
Scientists are keen to obtain these cells to study disease and, one day, use them to grow new tissue and replacement organs.
Previously, researchers had shown that they could derive this type of stem cell from ordinary skin cells.
But the fat technique is about twice as fast and 20 times more efficient, said Joseph Wu, the study's senior author.
"We can get iPS-like colonies, basically, in about 16 days, compared to 28 days to 32 days using [skin]," said Wu, a Stanford stem cell expert. "And if you count the number of colonies in [skin] versus fat ... we get about 20 times more the number of iPS colonies."
Reprogramming Cells
To create the stem cells, the scientists injected Trojan horse-like viruses into smooth muscle cells found in fat that surrounds blood vessels. Once inside, the viruses introduced genes that reprogrammed the cells, spurring them to grow into new forms.
Previously, this process had required growing the stem cells in a culture dish with nutrients from mouse cells. This had raised alarms about the potential for contamination from mouse proteins—a potential obstacle to government approval, Longaker, the plastic surgeon, said.
That the new method works at all is "somewhat surprising" and remains something of a mystery, Longaker said.
Sidestepping Stem Cell Controversy
The fat and skin methods allow researchers to sidestep the ethical controversy over the use of embryonic stem cells from cell lines originally harvested from unused human embryos from in vitro fertilization clinics.
In addition, Longaker noted, tissue or organs grown from a patient's own stem cells should be less likely to be rejected by the body.
The speediness of the fat method, in particular, could be lifesaving, he added.
For example, if a surgeon wanted to implant new heart tissue—derived from a heart attack victim's own fat—into a patient, the doctor might have only a short time before scar tissue would compromise the operation.
If he or she were able to generate the tissue within a few weeks, Longaker said, that "would be a big deal."

Strange jellies of the icy depths

Matt Walker
September 1, 2009
Editor, Earth News


http://news.bbc.co.uk/earth/hi/earth_news/newsid_8231000/8231367.stm

Crossota millsae, a brilliant red and purple jellyfish found at a depth of 2000m in the Arctic Ocean, is also found off California and Hawaii.

New details are emerging about the life-forms that survive in one of the world's most inaccessible places.
Scientists have published descriptions of a range of jelly-like animals that inhabit the deep oceans of the Arctic.
The animals were originally filmed and photographed during a series of submersible dives in 2005.

The small blue jelly, a type of Narcomedusae, is new to science.

One of the biggest surprises is that one of the most common animals in the Arctic deep sea is a type of jellyfish that is completely new to science.
The deep Arctic ocean is isolated from much of the water elsewhere on the globe. One area, known as the Canadian Basin, is particularly cut off by deep-sea ridges. These huge barriers can isolate any species there from other deep-water animals.
So in 2005, an international team of scientists, funded primarily by the US National Oceanic and Atmospheric Administration's Office of Ocean Exploration and Research, conducted a series of deep-sea dives using a remote operated vehicle (ROV).

The large bright orange Aulacoctena species may get its colour from worms that it eats

Details of what they found have now been published in the journal Deep Sea Research Part II.
"There were a lot of surprises," says biologist Dr Kevin Raskoff of Monterey Peninsula College in California, US, a leading member of the dive team.
"One thing was just how many different jellies there were, and the sizes of their populations."
"Some were somewhat well known from other oceans, but had not previously been found in the Arctic. That caused us to rethink our ideas about what the typical habitat would be for the species. We also discovered a number of new species that had not been found before."

Chrysaora melanaster is one of the largest Arctic jellies, living in the top layer of water at depths of between 20m and 40m, where the temperature remains nearly constant.

During a series of dives to depths of 3000m, the ROV filmed over 50 different types of gelatinous or jelly-like animal.
The majority of animals recorded were Medusae, a particular type of jellyfish that tend to be bell or disc shaped.

This red-lipped cydippid ctenophore was a common deep-water species between 1,300 to 2,400m. It still awaits description

Other jelly-like creatures seen included ctenophores, an unusual group that can look like jellyfish, but are not able to sting, siphonophores, which are actually colonies of smaller animals living together in a structure that looks like a single, larger animal, and larvaceans, plankton-like creatures unrelated to jellyfish.
Of all the Medusae observed, two species dominated at most locations visited by the ROV.
The first was a species called Sminthea arctica, which lived at depths ranging from 100m to 2,100m. This jellyfish has been recorded before by scientific expeditions.

Crossota millsae is a brilliant red and purple jellyfish also found off California and Hawaii. This specimen was collected near the bottom of the Arctic Ocean in 2,000m of water.

However, the other common jelly was a species new to science.
"Probably the single most interesting discovery was a new species of a small blue jellyfish, from a group called the Narcomedusae," says Dr Raskoff.
"This group has several interesting features that set them apart from typical jellyfish, such as the fact that they hold their tentacles over their bell as they swim."
Most jellyfish let their tentacles drift in the water behind them, but the new species holds its tentacles out in front, perhaps enabling it to better catch prey.
The new species is so unusual that it has been classified within its own genus, and will be formally described later this year.
"It was also the third most common jellyfish found on the cruise, which is really surprising when you think about the fact that even the most common species in the area can be totally new and unexpected species," says Dr Raskoff.
Another striking find was a type of ctenophore called Aulacoctena, which is one of the most spectacular examples of its kind.
At over 15cm long, its tentacles can grip almost anything underwater, yet little is known about its lifestyle.
However, one of the specimens collected by the ROV ejected its stomach contents, which revealed it may had fed on a bright orange animal.
The researchers suspect it feeds on bright orange worms that also live in the Arctic deep, and it gets it colour from its prey.
The scientists are now keen to find out much more about how these strange and enigmatic creatures interact with their environment, and how they influence or underpin the ecology of the deep ocean in which they live.
They also hope to raise funds to explore other little-visited regions of the deep Arctic ocean, as well as exploring the Aleutian trench off the coast of Alaska.
"You don't have to go too far to find interesting areas to study, you just have to dive deep," says Dr Raskoff.

Genetic test detects infections before symptoms appear

By Steve Sternberg, USA TODAY
8/6/2009

Flu sufferers of the future may not have to wait until their fever spikes to learn they're ill, scientists said Thursday.
Geoffrey Ginsburg of Duke University and his colleagues say that they've developed an experimental genetic test that can detect infections before any symptoms appear.
Although the test cannot yet distinguish one virus from another, it can tell the difference between a bacterial and a viral illness, Ginsburg says.
Most diagnostic tests detect the germ itself or antibodies produced by the immune system to wipe out a virus or bacteria once the symptoms begin. The new approach works differently, by detecting genetic signs of infection in people who aren't sick yet.
The test betrays the activation of genes that govern an immune response. It is carried out using a silicon chip much like those used in computers and requires no more than the 10 microliters of blood from a finger-prick.
"This is the first major step in using a person's individual response to a viral or bacterial infection to lead to better diagnostics for infectious disease," Ginsburg says.
The goal of the research, sponsored by the U.S. military's Defense Advanced Research Projects Agency (DARPA), is to develop a device that can identify troops who are getting sick, in time to get them treated and to prevent them from infecting others. Ultimately, Ginsberg says, the method could also become a valuable diagnostic tool in emergency rooms and doctors' offices, where a simple test could tell the difference between the worried well and the genuinely sick.
"The true market for this may be in doctors' offices around the world, where kids are coming in with fevers and doctors have to make decisions about giving them an antibiotic," he says, noting that antibiotics can be expensive, have side effects and promote the spread of drug-resistant germs.
Arnold Monto, of the University of Michigan School of Public Health, says a test that could accurately identify viral illness, especially influenza, would be a critically important advance. "A chip like this would be great," Monto says. Not only would it help doctors more accurately diagnose people who are ill, but it would also provide public health officials with information critical to their efforts to fight epidemics.
The accuracy of the rapid tests that are currently available is inconsistent, ranging from 30% to 80%, and prompting public health officials to caution against their use. An accurate genetic test would serve multiple purposes, Monto says.
"If we could identify people before they get sick — say, in household studies — we could get a better idea of how the virus is transmitting," he says. "How influenza is transmitted affects (predictions of an epidemic's spread), control measures and personal protective measures," shedding light on how best to keep from getting infected.
Ginsburg and his team tried out the method in volunteers they infected with cold viruses, flu viruses and a less well-known cause of upper airway disease called respiratory syncytial virus. The study appears today in the journal Cell, Host & Microbe.
The study involved 57 volunteers. Their blood was drawn before and after they were infected so that each one could serve as a healthy control.
Researchers were able to tell the difference someone who was infected and someone who wasn't with 95% accuracy. The test could also distinguish between people who were infected with viruses and those with bacteria more than 93% of the time.
The researchers are trying to determine whether the test will work in patients infected with H1N1, or swine, flu.