Deep-sea glow serves as bait Marine bacteria light up to get a ride elsewhere

Bioluminescent bacteria glow in the ocean for the same reason roadside eateries display neon signs: They want to attract hungry diners.
New laboratory experiments bolster the longstanding theory that marine bacteria light up to get themselves a free ride to other parts of the ocean in the digestive tracts of larger beasts, scientists from Israel and Germany report online December 27 in the Proceedings of the National Academy of Sciences.
“It’s terrific to see this experiment,” says J. Woodland Hastings, a bioluminescence expert at Harvard University who was not involved in the research. “It’s nice to see these ideas confirmed.”
Many deep-sea creatures, from bacteria to fish to squid, are bioluminescent — meaning they generate light inside their bodies through chemical reactions. Different organisms glow for different reasons; the anglerfish, for instance, can light up a lure to attract prey, while some plankton glow when disturbed to attract predators of whatever is stirring them up.
Bioluminescent bacteria live throughout the ocean, and may have several reasons to explain their built-in glow. More than three decades ago, researchers suggested that one such reason could be to mark the presence of a floating food particle, so that a passing fish would see it and eat it. But no one had tracked this idea all the way to its logical conclusion — until now.
Margarita Zarubin, a graduate student at the Interuniversity Institute for Marine Sciences in Eilat, Israel, started with a type of luminescent bacterium, Photobacterium leiognathi, found 600 meters deep in the Red Sea. She put one bag of glowing bacteria at one end of a seawater tank, and at the other end she put another bag of bacteria that had a genetic change that kept the microbes dark. Shrimp and other small animals clustered around only the glowing bacteria.
Next she let brine shrimp swim in water with the luminescent bacteria. After two and a half hours, the shrimp themselves began to glow from their microbial dinner. “We could see the luminescence from inside their guts,” says Zarubin, who did the work while at the University of Oldenburg in Germany and is now with the Hebrew University of Jerusalem.
Then she dropped both glowing and dark shrimp into a flume so they were swept past a hungry cardinalfish; the fish ate only the luminescent shrimp. Finally, the scientists tested the fish feces, and found that the bacteria had passed unscathed through the fish guts and came out intact. The whole process spreads the bacteria through the water faster than they could move otherwise, Zarubin says. 
For their part, the shrimp must balance the benefit of eating a food particle that happens to glow against the drawback of becoming luminescent themselves, thus making themselves more vulnerable to predators. But in deep dark waters where food is scarce, the advantage of getting a snack probably outweighs the disadvantage of potentially being eaten, Zarubin says.
Some animals have pigment in their guts that can block light emission as they digest glowing particles, says Michael Latz, a marine biologist at the Scripps Institution of Oceanography in La Jolla, Calif. Only when the animal pops out a glowing fecal pellet do the bacteria become visible again, signaling another creature to eat them and keep the microbes on the move.
Such deep-sea bacterial recycling could be important for more than just understanding bioluminescence, Latz says. The guts of shrimp and other small marine creatures may serve as a highway for spreading bacterial pathogens throughout the sea, like the one that causes cholera.

Molecule ties itself in a complex knot

Chemists have tangled themselves a complicated knot: a molecule whose 160 atoms loop over one another like a five-pointed star.
The molecule’s design, called a pentafoil, is the most complex knot synthesized from building blocks other than DNA. Knowing how to make a pentafoil, its discoverers say, could lead to ways to make materials lighter, stronger or more flexible than before.
“By knowing how to design types of knots, hopefully we can optimize these properties,” says David Leigh, a chemist at the University of Edinburgh. He and his colleagues report the new knot in the January issue of Nature Chemistry.
The simplest knot is the “unknot,” a loop that doesn’t cross over itself. The next simplest — a “trefoil,” with three crossing points — was first made out of a molecule in 1989. Leigh’s team decided to take things a step further and aim for the five-crossing pentafoil. 
The scientists took negatively charged chloride ions and added ingredients such as positively charged iron ions and long chains of carbon and other atoms, then chemically programmed the whole thing to assemble itself. Five of the chains looped over one another and hooked up, along with five irons, with each chloride to create the pentafoil.
This molecule turns out to be interesting for more than just its shape, Leigh says. “The pocket where the chloride ion sits turns out to be a perfect fit, and if you remove it, the molecule is desperate to bind chloride back in there,” he says. So the molecule could be used as a sensor to help detect chlorine in its surroundings, he says.
Building bigger knots could also help scientists uncover general rules of knotted molecules. Rubber, for instance, gets much of its stretchiness from knots within its polymer chains.
But given that mathematicians know of more than 6 billion kinds of knots, chemists still have a long way to go.

Face deficit holds object lesson Recognizing mugs may not be special in the brain

A brain-damaged man who can’t remember faces has nosed into a scientific debate about how people learn to recognize other complex objects. Deaf users of sign language also have a hand in this dispute.
The brain-damaged man’s facial failures are one symptom of a general inability to perceive configurations of object parts, suggests a new investigation led by psychologist Cindy Bukach of the University of Richmond in Virginia. The man thus stumbles at identifying not only people’s faces but also computer-generated, three-part objects called Greebles, even after extensive training, Bukach’s team reports online December 8 in Neuropsychologia.
Bukach and her colleagues studied LR, a man who fails to recognize his daughter when shown a picture of her but remembers distinctive facial features, such as Elvis’ sideburns. Damage in a car accident to a brain area just under the right temple caused this condition, called prosopagnosia.
“There are many ways in which face recognition can be disrupted, but our evidence shows that LR’s type of prosopagnosia impairs recognition of objects with multiple parts, with faces as the most obvious example,” Bukach says. Relative positions of the eyes, nose and mouth, as well their shapes, contribute to perceiving a face as a single entity.
In a 2006 report, her team designed a collection of eight faces using different combinations of two sets of eyes, noses and mouths. After briefly viewing a face, LR correctly selected it from all eight faces 25 percent of the time — about what would be expected if he based choices on a single facial feature, Bukach says. Further testing showed that LR homed in on the mouth.
In the new study, the researchers designed eight Greebles, using different combinations of two versions of three distinctive appendages. LR recognized Greebles he had just seen 31 percent of the time, improving little after several one-hour, weekly training sessions. Four healthy volunteers struggled at discerning Greebles at first but recognized most of them after training.
Bukach opposes an influential view that the brain evolved systems for dealing with key types of knowledge, including face recognition (SN: 7/7/01, p. 10). A proponent of that view, psychologist Bradley Duchaine of Dartmouth College, previously reported that a prosopagnosia patient named Edward — who cited lifelong problems recognizing faces — learned to discriminate Greebles but not human faces.
If face recognition depends on a general capacity for learning to recognize multi-part objects, Duchaine holds, healthy volunteers should recognize novel Greebles as poorly as prosopagnosia patients do at first but perform better than patients after seeing lots of Greebles. LR’s Greeble difficulties exceeded those of healthy volunteers from the start, a sign of fundamental object-recognition problems that make the results hard to interpret, Duchaine contends. “These new results don’t help us understand mechanisms used for face processing,” he says.
LR’s poor Greeble-detection accuracy before and after training indicates that he focused on only one Greeble appendage when trying to tell the funny-looking objects apart, Bukach responds.
Support for the idea that brains use a general mechanism to recognize complex objects comes from deaf people who communicate with American Sign Language. Just as upside-down faces look weird and often unrecognizable to healthy volunteers, so do upside-down signs shown to fluent ASL users, say psychologists David Corina of the University of California, Davis, and Michael Grosvald of the University of California, Irvine.
Because healthy individuals perceive faces as whole entities, topsy-turvy faces look bizarre, Corina says. Likewise, ASL users learn to see signs as integrated sets of movements that look peculiar when inverted, the researchers propose in a paper published online December 6 in Cognition.
Many researchers assume that people understand sign language by breaking each sign down into hand shapes, arm movements and other elements.
Corina and Grosvald also find that deaf ASL users are faster than hearing nonsigners at recognizing videos of head scratching and other common grooming actions. Sign languages exploit brain areas devoted to detecting human actions in general, they propose.
Psycholinguist Karen Emmorey of San Diego State University calls new evidence that fluent signers perceive signs as whole entities “a key insight.” Further work needs to confirm that learning a sign language modifies action-related brain areas, she adds.

Tuberous sclerosis complex

<a href="http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Tuberous_sclerosis_complex_(TSC)?open">Tuberous sclerosis complex (TSC) - Better Health Channel</a><br/>
Tuberous sclerosis complex is a genetic disorder that affects various parts of the body to varying degrees of severity. Its common characteristic is the formation of tuber-like growths in the brain. The growths can cause seizures, delayed development and autism, however, approximately half of people with TSC are of normal intelligence. There is no cure.

Gene therapy helps counter hemophilia B

A gene therapy based on a cargo-toting virus that gravitates to liver cells might provide hemophilia B patients with long-lasting protection against bleeding, an international team of scientists reports online December 10 in the New England Journal of Medicine.
Hemophilia B is the second-most common form of hemophilia, a hereditary disorder in which blood fails to clot properly. Patients must receive preventive injections of a clotting compound called factor IX to prevent bleeding from cuts, scratches or bruises. In the new study, four of six hemophilia B patients given the gene therapy no longer need the clotting compound.
The work “is truly a landmark study, since it is the first to achieve long-term expression of a blood protein at therapeutically relevant levels,” physician Katherine Ponder of Washington University in St. Louis, who wasn’t part of the study team, wrote in the same issue of the journal. The findings were also presented December 11 in San Diego at a meeting of the American Society of Hematology.
British researchers treated six men ages 27 to 64 with the gene therapy, an innocuous virus coupled with components that induce liver cells to make factor IX. Before the study, the men had been getting intravenous infusions of factor IX two to three times a week, says study coauthor Andrew Davidoff, a surgeon at St. Jude Children’s Research Hospital in Memphis, Tenn., where the gene therapy was designed.
Each patient received a single infusion of the therapy, called serotype-8-pseudotyped, self-complementary adenovirus-associated virus vector. Scientists have now monitored the men for nine to 20 months.
Four patients who received medium or high doses of the therapy have made enough factor IX themselves to cease getting the preventive infusions of it. Two patients who were given low doses of the gene therapy are making less. While they still need factor IX infusions, they have cut back to one every 10 to 14 days, Davidoff says.
The virus used as the delivery vehicle, known as AAV-8, was chosen in part because it is unlikely that many people receiving it would have been exposed to it and already made antibodies against it, Davidoff says. The virus also targets liver cells, which naturally make factor IX. And although AAV-8 enters a cell it doesn’t integrate with material in the nucleus, greatly reducing the risk that the therapy would interfere with normal cell function.
Because of these attributes, “there’s a modest level of excitement” about this approach, says hematologist W. Keith Hoots of the National Heart, Lung, and Blood Institute in Bethesda, Md., which funded the study in part. The treatment cannot be repeated in a patient, however, because the immune system would recognize AAV-8 the second time around. Even so, the approach has promise because there are dozens of other AAVs that are still untapped, Hoots says.
Two of the patients were given a brief course of steroid drugs when they showed signs of liver inflammation, but no other side effects emerged. Earlier tests in large animals had shown that this therapy could last 10 years or longer. Further testing in people is planned, Davidoff says.

Eggs have own biological clock Aging mechanisms in worms’ reproductive cells differ compared with rest of body

DENVER — Egg cells age differently than cells in the rest of the body, a new study shows.

The finding, from experiments with roundworms presented December 5 at the annual meeting of the American Society for Cell Biology, might one day lead to ways to predict how long women will stay fertile or even to extend a woman’s fertile years.

Princeton University biologist Coleen Murphy and her colleagues study aging in the roundworm, Caenorhabditis elegans. The worms typically live for about 21 days, but fertility drops off sharply after about a week and the worms can no longer reproduce after they are about 9 days old. Even though 9-day-old worms still have plenty of eggs left, the egg cells, also called oocytes, are of such poor quality they can’t produce embryos.

Women experience a similar sharp decline in fertility starting in their late 30s. This drop-off in reproductive capability is one of the earliest signs of aging.

In earlier work, Murphy and colleagues discovered that certain mutations in biological processes regulated by insulin prolonged worms’ lives and gave them about three extra fertile days. Mutations in a different biological process, controlled by a protein called TGF-beta, extended fertility but not life span.

In the new study, the researchers examined which genes are turned on or off to prolong life and fertility in the oocytes and other body cells of the long-lived worms.

“We were really surprised to find this was a completely different mechanism” controlling aging in eggs compared with other body cells, Murphy said at the cell biology meeting. “In fact, there was almost no overlap between the genes involved in the long life of worms and those that extend fertility in the oocytes.”

Body, or somatic, cells are known to turn on stress-management genes to protect proteins and change metabolism as they age. But oocytes don’t bother with guarding proteins, Murphy and her colleagues found. Instead, eggs ramp up production of factors that protect them from or repair DNA damage and make more of proteins that help egg cells divvy up their chromosomes correctly, the researchers reported.

Because the entire job of an egg is to provide genetic information used to build a new generation, it is perhaps not so surprising that eggs devote resources to making sure the DNA stays healthy and chromosomes and are allocated properly, said Craig Blackstone, a physician and researcher at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. “It makes sense that this would happen, but it hadn’t been shown before,” he said. “It’s clever of her to study this.”

Cilia control eating signal Little hairlike appendages in brain cells control weight by sequestering an appetite hormone

A primary cilium (red) protrudes from a neuron (green). Most normal cells in healthy people have primary cilia. New research shows that the hairlike cilia help suppress appetite.

DENVER — The action of tiny hair-like appendages on cells can mean the difference between fat and thin. Now scientists have a better idea of how the little hairs, called primary cilia, control appetite.

Primary cilia — single, hairlike projections that all cells in vertebrates usually have — seem to sequester a protein that senses and responds to an appetite-stimulating hormone, Nicolas Berbari of the University of Alabama at Birmingham reported December 6 at the annual meeting of the American Society for Cell Biology. In people and mice that lack primary cilia, the appetite stimulant works overtime, leading to overeating and obesity, Berbari said.

These findings may lead to new ways to control appetite and prevent or reverse obesity.

And the study may help scientists better understand the process of eating, said Kirk Mykytyn, a cell biologist at Ohio State University in Columbus. “This work is important because it’s more thoroughly clarifying the molecular mechanism involved in obesity associated with the loss of cilia,” he said.

A mouse that lacks primary cilia in its cells becomes obese (right) compared with a normal mouse (left).

People with Bardet-Biedl syndrome have defects in genes responsible for building primary cilia. A prominent consequence of the disease is obesity. Working with mice that also lack primary cilia due to defects in the same genes, Berbari and his colleagues tried to figure out exactly how the cellular appendages are involved in appetite.

Previous research had suggested that primary cilia work like tiny antennae, helping nerve cells in an eating-control center of the brain to sense an appetite-dampening hormone called leptin. The theory was that taking away the cilia also removed leptin’s ability to put the brakes on eating.

But Berbari and colleagues found that mice lacking cilia still respond to leptin as an appetite suppressant, suggesting that sensing the hormone is not the problem.

“The original work was barking up what was the most obvious tree, but turned out to be the wrong tree,” Berbari said.

Instead, the researchers discovered that a protein called MCHR1, which senses an appetite stimulant called melanin-concentrating hormone, is normally found in primary cilia. Concentrating the sensor protein in the cilia may keep the protein from inappropriately triggering eating.

Berbari has preliminary evidence that his hypothesis may be correct. He fed peanut butter pellets containing a drug that inactivates MCHR1 to mice with intact cilia and to mice that have no cilia. The mice with intact cilia maintained their regular weight despite having unlimited access to food. Mice lacking cilia lost weight when given the drug, suggesting that turning off MCHR1’s ability to stimulate appetite corrects the appetite-control problems caused by missing cilia.

The researchers still don’t know exactly how MCHR1 activity stimulates appetite or how the cilia keep the sensor in check.

Biology’s big bang had a long fuse

A new effort to date the early history of modern animals finds a lot of evolutionary dawdling.

The last common ancestor of all living animals probably arose nearly 800 million years ago, a multidisciplinary research team reports in the Nov. 25 Science. From that common ancestry, various animal lineages diverged and evolved on their own paths. Yet the major animal groups living today didn’t arise until roughly 200 million years later, in an exuberant burst of forms preserved in fossils during what’s called the Cambrian explosion.

“There’s a deeper history that’s been missing from the fossil record,” says study coauthor Kevin Peterson of Dartmouth College. He and his colleagues have been pushing back that date for a last common ancestor, and now, he reports, the analysis has the broadest reach yet. “We show that animals evolved quite a bit before they show up in the fossil record.”

This work updates the notion of a long evolutionary lag, when much of the basic biological toolkit was already in place for a later surge of new body forms, says paleontologist and study coauthor Douglas Erwin of the National Museum of Natural History in Washington, D.C., and the Santa Fe Institute.

“The Cambrian explosion is like the industrial revolution,” Erwin says. Inventions that would later be important for a major shift in technology — or, in this case, genetic novelties important for evolution — appeared long before they played a role in widespread changes that had a major impact on life.

For understanding animal origins, the new paper “is really worthwhile as it stands back and tries to make sense of the whole picture,” says James Valentine of the University of California, Berkeley, who studies animal evolution.

Just what happened with animals during that Cambrian explosion remains one of the more celebrated puzzles in the history of life. Charles Darwin mused over how diverse animal forms appear suddenly (geologically speaking) without much in the way of precursors. Darwin’s answer, as Erwin puts it, was that paleontologists just needed to look harder.

More than a century of hard looking has turned up some signs, fossils as well as traces of biological chemistry, of enigmatic animal life before the Cambrian period began about 541 million years ago. Yet the relationship to modern animals often is not clear. Theories themselves have exuberantly exploded in number and form.

For the new study, Erwin and the rock side of the team updated the scorecard on the earliest fossil occurrences with recent fossil finds and the current thinking on dates of rock layers. On the molecular side, Peterson and his colleagues expanded the family tree to cover seven genes from 118 different kinds of living animals. Fossils provided dates for a scattering of branch points in the tree, allowing researchers to estimate time from rates of change.

Combining fossil dates and the DNA analysis, Peterson, Erwin and their colleagues conclude that the basic genetic tools for fancy animal bodies arose long before a surge of evolutionary innovation around the Cambrian period gave rise to modern animal forms.

During that 200 million-year-plus run-up to the Cambrian explosion, animals did evolve more diverse cell chemistry to regulate basic genes, and the environment changed. But Peterson attributes much of the Cambrian rise of modern animal forms to changes in the interactions among organisms themselves. “You see an evolutionary explosion, if you will, because animals are eating other animals for the first time,” he says.

The paper’s discussion of toolkit genes and the diverse cell chemistry that arose to orchestrate them overlooks some possibly important complexity, objects molecular biologist Mark Q. Martindale of the University of Hawaii’s Kewalo Marine Laboratory. At least 30 percent of the genes of animals analyzed so far have no recognizable similar gene in another species. “These so-called orphan genes could have a tremendous amount to do with diversification of animal lineages, but people just pooh-pooh these differences and focus on the things that are shared,” he says.

Some of the relationships in the evolutionary tree “have been and will continue to be controversial,” says evolutionary biologist Casey Dunn of Brown University in Providence, R.I., who wasn’t involved in the research. “But the point of the tree isn’t the relationships themselves — it is some key dates.”

Neuron transplant in damaged brain fixes obesity

A neuron transplant has rewired damaged brain areas in mice, raising hopes that similar transplants might one day help to treat spinal-cord injuries, Parkinson's disease and other brain conditions.

Jeffrey Macklis at Harvard University and his colleagues took healthy neurons from mouse embryos that had been labelled with a green fluorescent protein. They used them to repair a brain circuit involved in the regulation of food intake and body weight in response to a hormone called leptin in mutant mice born with damage to that area, which become dangerously overweight as a result.

The fluorescent neurons survived the transplant, integrated into the brain circuit, and differentiated into mature neurons that could communicate with existing neurons and respond to leptin, insulin and glucose – suggesting that they had repaired the damaged circuit. The treated obese mice went on to weigh 30 per cent less than their untreated counterparts.

"These embryonic neurons were wired in with less precision than one might think, but that didn't seem to matter," says Jeffrey Flier, dean of Harvard Medical School, who was part of the team. "They are like antennas that were immediately able to pick up the leptin signal."

The next question is whether transplanted neurons could rewire other complex brain circuits involved in diseases or brain injury, which might be more dependent on signals coming from other neurons, rather than signals coming from the blood. "In these cases, can we rebuild circuitry in the mammalian brain? I suspect that we can," says Macklis.

Journal reference: Science, DOI: 10.1126/science.1209870

Exceptional memory linked to bulked-up parts of brain.....People who can recall life’s events in detail have enlarged region linked to obsessive-compulsive disorder

WASHINGTON — Like the fictional detective Carrie Wells on the TV show Unforgettable, some real-life people can remember every day of their lives in detail. Those superrememberers have more bulk in certain parts of their brains, possibly explaining the remarkable ability to recall minutiae from decades ago, researchers said November 13 at the annual meeting of the Society for Neuroscience.

One brain region involved in such incredible recall has been implicated in obsessive-compulsive disorder, hinting that OCD and superior memory might have a common architecture in the brain.

Scientists have long studied people with memory deficits, but there haven’t been many studies on people with exceptional memories. “Looking at memory from a deficit gave us a lot of insight into memory,” said study coauthor Aurora LePort of the University of California, Irvine. “Looking at memory from a superior perspective gives us a new tool. It may just broaden our knowledge and ability to know what’s going on.”

In 2006, UC Irvine neuroscientist Larry Cahill and collaborators published a report on a woman who could remember detailed accounts of her life. Cahill and colleagues then began hearing from many people who claimed to have extraordinary memories. After sifting through and eliminating the impostors, the team was left with 11 people who scored off the charts for autobiographical memory. These people could effortlessly remember, for instance, what they were doing on November 2, 1989, and could also tell you that it was a Thursday. “They’re not going home and saying ‘OK, let me write down what I did today and memorize it,’ ” LePort said.

Using brain scans, researchers found that people with supermemories had larger brain regions associated with memory, including the left temporoparietal junction and the left posterior insula. What’s more, a brain structure called the lentiform nucleus, a cone-shaped mass in the core of the brain, was bigger in people with exceptional memories. This brain area has been linked to obsessive-compulsive disorder.

The subjects haven’t been clinically evaluated for OCD, but LePort says that there are some similarities. “The ability to organize their memories by dates seems to relieve anxiety,” she says.

Researchers don’t know how the brain accomplishes this feat. These people could encode information more effectively, or have a better system of retrieving it, or both. “Right now, we can see the brain areas that are coming out and speculate about what’s going on,” LePort says.

The team hopes to do further studies examining what’s happening in the brain as these people remember.

One tantalizing lead suggests that genetics might be involved. Though no genetic tests have been performed, some of the volunteers have reported that family members share extraordinary powers of recall, LePort says.

The result “certainly pushes us beyond the boundaries of what we might normally think,” said memory expert Howard Eichenbaum of Boston University. “It violates a standard principle that most of us have, which is that normal memory is pretty damn optimized.”

The volunteers are now keeping detailed diaries, so that the scientists can test whether particular kinds of memories are better suited to recollection. People might be better at remembering emotional memories, for instance.

Radiation sickness treatment shows promise

A drug composed of an ordinary antibiotic combined with a microbe-fighting compound may be enough to protect thousands of people from the ravages of radiation sickness in the aftermath of a major nuclear accident or attack, experiments with mice suggest.

Researchers exposed mice to a heavy dose of radiation and 24 hours later gave some of them injections of an antibiotic and a protein that’s made naturally by the immune system. Thirty days later, most mice that received no treatment were dead, whereas nearly 80 percent of mice that received the treatment still appeared healthy, a team reports in the Nov. 23 Science Translational Medicine.

Follow-up studies are still needed before the combo can be used to treat people, but versions of the antibiotic and the protein have already been used in humans, so the new approach looks promising. It might even be used as a preemptive measure for first responders.

“This could potentially be very useful,” says radiobiologist Gayle Woloschak of Northwestern University in Chicago, who was not involved with the study.

Radiation exposure of levels up to 10 gray (the mice received 7 gray, about 45,000 times the dose of a chest X-ray) would usually require a bone marrow transplant and probably treatment with a compound that stimulates bone marrow growth. “During a mass casualty event you’re not going to be able to do bone marrow transplants,” says Woloschak. And while questions remain about long-term survival of mice given the new treatment, “it’s quite exciting,” she says.

When the body is exposed to intense levels of radiation, bone marrow is one of the first things to shut down. Bone marrow is where most white blood cells arise, so the body’s immune system can’t fight infection properly when compromised. And a working, fighting immune system is just what’s needed after exposure to radiation. Radiation can cause bacteria that are usually confined to the gut to leak into the blood, causing blood pressure to spike, fever, abnormal blood clotting and even organ failure.

The new treatment goes after these marauding bacteria. The fluoroquinolone antibiotic, a mouse version of Cipro, aims to kill any bacteria it comes across. And the protein, called BPI, mops up and latches onto bacterial endotoxin, a nasty molecule on the coats of many bacteria.

“We think we have a combination here that is multifunctional,” says stem cell transplant doctor Eva Guinan of the Dana-Farber Cancer Institute and Harvard Medical School, who led the work with Ofer Levy, also of Harvard and Children’s Hospital Boston. “We still have a lot more to explore in detail, but the results are really encouraging.”

Immune cells function beyond battle

The immune system isn’t just about defense; it works in partnership with other cells to regulate body functions.

A new study shows that immune cells called B cells carry on a three-way conversation with gut microbes and cells lining the intestines to control fat uptake. The finding, reported online November 20 in Nature Medicine, challenges conventional wisdom that the immune system’s only job is to fight bad guys. The new knowledge also may shed some light on why people with HIV and other chronic infections become malnourished, and it might suggest ways to treat malnutrition.

The study grew out of a comment that systems biologist Andrey Morgun, now a researcher at Oregon State University in Corvallis, once heard at an immunology conference. “A speaker mentioned that the immune system isn’t just a war machine,” Morgun says.

For Morgun and his wife and research partner, Natalia Shulzhenko, also now at Oregon State, the idea was intriguing. Both had training in clinical immunology, where the immune system is thought of as a protective mechanism, not something involved in daily life outside the disease process, Morgun says. While working at the National Institute of Allergy and Infectious Diseases in Bethesda, Md., the couple convinced their research adviser there, immunologist Polly Matzinger, that the idea was worth testing.

Other researchers have noted that mice lacking antibody-producing B cells have abnormal digestive systems. In particular, the mice have difficulty absorbing fat from the diet and become malnourished. In the new study, Morgun and Shulzhenko discovered that B cells’ ability to make a type of antibody called immunoglobulin A, or IgA, is important for fat uptake. IgA is secreted in tears, saliva, milk and mucus, and helps cells lining the intestine maintain a healthy relationship with friendly bacteria.

The researchers reared mice without B cells in a sterile environment so the mice also lacked gut bacteria. The mice didn’t have a problem absorbing fat, despite their lack of immune cells. That told the researchers that intestinal microbes are involved in the process, but exactly what the microbes do to change fat uptake is still unknown.

A closer look at cells lining the intestine, called epithelial cells, showed that those cells have two jobs — self-defense and metabolism, including absorbing fat. Somehow, IgA antibodies produced by B cells trigger gut microbes to send a signal to the epithelial cells. Those cells then determine whether to devote more resources to protecting themselves, by making antimicrobial compounds, or to carry on absorbing fat and other nutrients from food.

Andrew Gewirtz, an immunologist at Georgia State University in Atlanta, draws a comparison between this newly identified role for the immune system and community services such as crowd control performed by the police: “The police don’t just show up when there’s a crime.”

Intestinal epithelial cells taken from people who have immune defects, such as those caused by HIV or a genetic condition called common variable immunodeficiency, behave similarly to those from mice lacking B cells, the researchers found. That raises the possibility that those people might be treated for malnutrition by giving them IgA antibodies.

CSI: Fleming reveals true identity of penicillin

The discovery of penicillin kick-started the antibiotic revolution. But a forensic-style investigation of the lab in which Alexander Fleming discovered the world-famous fungus suggests the Nobel prizewinner's find has been misunderstood for 80 years.

Fleming returned from a family vacation in August 1928 to find that a fungus had contaminated the samples of bacteria he had left in his lab, and that it was evidently a bacteria killer. Figuring that the fungus was secreting something that could be useful in treating human bacterial infections, Fleming sent his samples off to researchers in the US. They identified the fungus as Penicillium chrysogenum and looked for similar strains to find the one that would yield the largest antibiotic secretions. The hero strain came from a mouldy cantaloupe melon, and was tweaked to produce the penicillin used today.

Daniel Henk, Matthew Fisher and their colleagues at Imperial College London took a closer look at the fungal samples still preserved in Fleming's lab in London, now a museum. They even swabbed his old notebook. They then compared them with fungal samples collected by 300 volunteers around the world.

Henk and Fisher's team investigated the genetics of all the samples by studying certain easily recognised chunks of the genome: these don't tend to code for specific proteins, but are characterised by particular repeating patterns of short DNA sequences.
Not one, not two, not three

In the samples that would originally have been classed as P. chrysogenum, the team identified four distinct species – the original species and three brand new ones. "There is so much diversity within what we thought was a single species," says Henk.

Fleming's fungus – one of the previously unknown species – appears to be the most common of the four. "It's likely amongst the most common multicellular organisms on the planet," says Fisher.

The investigation also revealed that the fungus has two sexes and that its genome carries hallmarks of recombination, suggesting that the organism has been having sex even though it has not be seen doing so. "They're having what's known as cryptic sex – sneaky sex," says Fisher. "We can't make it happen in the lab – we can only see evidence that it has happened."

The team hope their work will help others find new antibiotics. "When the US Department of Agriculture was looking for fungi with antimicrobial properties, it was sampling randomly," says Henk. He says the new analysis suggests that doing so will simply throw up Fleming's species most of the time. In future it will be possible to use the DNA sequences to confirm that wild samples carry something truly new and worth investigating.

Henk and Fisher hope Fleming's species will be named Penicillium flemingii, but before it is, they'll have to convince the rest of the community that the fungus truly is new. Jens Frisvad at the Technical University of Denmark in Kongens Lyngby has some doubts. Based on his research, he suspects that the species might in fact have already been named P. rubens – five years before Fleming's auspicious holiday.

Journal reference: Molecular Ecology, DOI: 10.1111/j.1365-294X.2011.05244.x

Babies may benefit from moms’ lasting melancholy

A double dose of mom’s depression may do a baby good.

Infants generally thrive physically and mentally if their mothers’ emotional condition, whether healthy or depressed, remains stable before and after birth, say psychologist Curt Sandman of the University of California, Irvine, and his colleagues. Kids whose mothers stayed depressed from the fourth month of pregnancy on displayed first-year mental and physical development comparable to that of youngsters whose mothers stayed emotionally healthy for the same stretch, Sandman’s team will report in Psychological Science.

In contrast, babies’ first-year physical and mental development lagged if their mothers’ emotional state during pregnancy changed after giving birth. That pattern held whether depression during pregnancy resolved after giving birth or depression first appeared after delivering a child.

“A human fetus that prepares for inadequate care after birth based on biological messages from a depressed mother will have a survival advantage,” Sandman says. A fetus that gets thrown a caretaking curve upon leaving the womb — whether biologically primed to expect sufficient or deficient treatment — tends to struggle developmentally, at least for the first year, he suggests.

Related investigations have found that people whose mothers nearly starved during pregnancy eventually developed higher rates of diabetes and other metabolic disorders if they received enough food after birth, but not if they too got inadequate nutrition. Until now, no one has reported a health advantage for babies exposed to maternal depression before and after birth.

University of California, Davis, psychologist Jay Belsky calls the new findings “surprising, if not astonishing.” He awaits confirmation of Sandman’s results by other researchers before concluding that babies benefit from a womb with a view of upcoming hardships.

Babies may respond to maternal depression differently based on their genetic makeup, Belsky suggests (SN Online: 4/6/11). In the March 15 Biological Psychiatry, he and his colleagues reported that infants carrying two copies of a particular serotonin transporter gene variant frequently became scared and agitated if their mothers experienced intense anxiety during pregnancy.

For the new study, Sandman’s team studied 221 women at five points during their pregnancies. The women and their babies were then assessed at three-month intervals for one year. Experimenters used play tasks to measure infants’ physical and mental development.

Kids whose mothers displayed consistent emotional health or depression scored higher than those exposed to inconsistent maternal moods on physical tasks at age three months, on both physical and mental tasks at age six months, and on mental tasks at age 1. The researchers plan to see if that mental advantage lasts longer or if maternal depression eventually undermines mental development.

Results so far underscore the need to rapidly treat pregnant women’s depression so that their children experience positive maternal health before and after birth, Sandman suggests. But antidepressant medication presents health risks for fetuses, and the new findings indicate that women who attain emotional health shortly after giving birth create conditions that slow their babies’ development.

“What is best for the mother may not be best for the fetus or infant,” Sandman says.

Plastic isn’t over yet Tough new form could extend applications of the 20th century material

A tough new plastic that’s easily healed if scratched or damaged could find use in products prone to getting beat up, such as paints or parts for cars and sailboats. What’s more, it can be ground up and recycled into completely new products like plastic molding for electronic devices or optical lenses.

By adding some extra ingredients to traditional epoxy resins and a dash of a zinc compound to help move the chemistry along, researchers made a material whose chemical bonds continually break and reform. At really high temperatures, the bonding switcheroo makes the material malleable, but the reactions are so sluggish at ordinary temperatures that the material’s shape is essentially fixed, resisting deformation, the researchers report in the Nov. 18 Science.

“They developed a unique and very powerful approach that will have a great deal of applications,” says polymer chemist Christopher Bowman of the University of Colorado at Boulder. “It’s quite exciting.”

Most plastics that are super durable — such as those used for kitchenware and some car parts — are molded into shape and then “cured,” turning them into one giant cross-linked molecule. The molecules of softer plastics, like those used in soda bottles, typically aren’t held together with these strong bonds and can be melted and reshaped. To get an in-between material, scientists led by Ludwik Leibler of France’s National Center for Scientific Research in Paris made a regular epoxy resin, the sort available at your local hardware store. Then the researchers added acids to the mix and used a zinc-based compound to help them interact. .

The resulting material consists of a network of molecules, each holding hands with four others. These molecules are constantly switching up who they are holding hands with, but the number of bonded hands in the material always stays the same. When heated, this molecular hand swap speeds up; the number of switches that would take 100 years to complete at room temperature happen in a few seconds at 200 degrees Celsius, says Leibler.

The molecular flexibility means that at high temperatures the material can easily be remolded. Full-scale injection molding works, but so does shaping or repairing it with a hand-held hot air blower. And depending on the amount of hardeners and other ingredients, the chemistry can yield very hard plastics or ones with a more rubbery feel.

“You can do anything you want,” Leibler says. “You can work it like wood, you can make big parts if you want, and the beauty of it is all of the ingredients are things that are already used in composites.”

Busting blood clots with a nanoparticle

Nanosized gobs containing a blood clot–dissolving drug can seek out trouble spots in the body and break down blockages responsible for heart attacks, Japanese researchers reported November 14 at a meeting of the American Heart Association. The microscopic packaging seems to improve the drug’s potency and might limit its main drawback — a risk of internal bleeding — by focusing its effect at the clot.

Although the technology has been tested only in pigs, some doctors find the early results intriguing. “This could be a tremendous step forward,” said Roger Blumenthal, a cardiologist at the Johns Hopkins University School of Medicine in Baltimore. If it tests well in people, he said, this controllable form of the clot-busting drug, called tPA, might be a boon for heart attack patients in remote areas that lack hospitals equipped to deliver the highest standard of care for heart attacks.

About half of people for whom heart attacks are fatal die before reaching a hospital and getting angioplasty, in which doctors thread a balloon-tipped catheter up to the heart to prop open blocked coronary arteries with mesh cylinders called stents. With every minute that passes after a heart attack begins, part of the heart muscle is damaged by lack of blood. “It’s one thing to have a heart attack in a metropolitan area,” Blumenthal said. “But sometimes a catheterization lab may be four hours away.” A safer form of tPA, a drug that has largely gone out of use for heart attacks in the United States because of its internal bleeding risk, could play a role In such rural areas, he said.

The Japanese team, led by cardiologist Yoshihiko Saito of Nara Medical University in Kashihara, tested a form of tPA made safer by packaging it in a coating of gelatin-based nanoparticles that prevent tPA from releasing in the blood stream.

Tests in mice showed that the nanoparticles were three times more likely than regular tPA to attach to clots, because the tiny blobs stick to a common clotting compound in the body that standard tPA doesn’t bind.

The researchers then injected either the nanoparticle drug or standard tPA into 30 pigs in which the scientists had induced blood clots. Once the nanoparticles had arrived at the clot, the researchers burst the tiny blobs with ultrasound waves and released the tPA cargo at the clot.

After 30 minutes, blood flow through obstructed vessels improved by 90 percent in pigs getting the nanoparticle drug but by only 10 percent in pigs getting standard tPA. There was also less stray tPA in the bloodstream afterward with the nanoparticles.

The new technology might expand the range of people who could administer tPA, said Robert Bonow, a cardiologist at Northwestern University School of Medicine in Chicago. Paramedics typically don’t give tPA in the United States, even to heart attack patients, because of the bleeding risk. “In theory, this would be safer,” he said.

People with pulmonary embolisms might also benefit from the nanotechnology if it succeeds in further tests, said cardiologist Vincent Bufalino of Midwest Heart Specialists in Naperville, Ill., a cardiology practice. In those patients a clot obstructs blood flow to the lungs.

Doctors use tPA for some strokes that arise when a clot jams an artery supplying the brain with blood. But that medical scenario wasn’t tested in this study.

Magic trick reveals unconscious knowledge

Magic tricks prey on people’s subpar powers of perception, but new work finds that the brain has tricks of its own up its sleeve: People notice more than they think.

In the research, presented November 12 at the annual meeting of the Society for Neuroscience, Luis Martinez of CSIC- Miguel Hernandez University in Spain and colleagues amazingly “read minds” with the Princess Card Trick, invented by magician Henry Hardin in 1905. Volunteers mentally chose a playing card from a panel of six cards, which then disappeared. When a second group of cards appeared, the researchers had miraculously figured out which card a person had in mind and removed it. Few people caught the trick: All the cards in the second set were different, not just the card people had chosen.

A few seconds after viewing the two panels of cards, participants were asked which of two new cards was present in the first panel. None of the volunteers could consciously recall which card was present. Despite these avowals of ignorance, when forced to choose, people got the right answer about 80 percent of the time. “People say they don’t know, but they do,” Martinez said. “The information is still there, and we can use it unconsciously if we are forced to.”

To see whether this unconscious knowledge works for objects other than cards, Martinez and his colleagues performed a similar experiment with pictures of men’s faces. A similar kind of visual short-term memory helped people choose which face they had seen before, even when volunteers didn’t perceive that they knew the correct answer.

These unconscious, short-term memories are finicky, Martinez and his colleagues found. If the researchers talked to the volunteers while performing the trick, the ability to identify the card that had been present worsened. (Magicians may deploy a steady stream of patter for this very reason.) And if the researchers revealed the secret of the trick, participants performed no better than chance at identifying the card.

Exceptional memory linked to bulked-up parts of brain

Like the fictional detective Carrie Wells on the TV show Unforgettable, some real-life people can remember every day of their lives in detail. Those superrememberers have more bulk in certain parts of their brains, possibly explaining the remarkable ability to recall minutiae from decades ago, researchers said November 13 at the annual meeting of the Society for Neuroscience.

One brain region involved in such incredible recall has been implicated in obsessive-compulsive disorder, hinting that OCD and superior memory might have a common architecture in the brain.

Scientists have long studied people with memory deficits, but there haven’t been many studies on people with exceptional memories. “Looking at memory from a deficit gave us a lot of insight into memory,” said study coauthor Aurora LePort of the University of California, Irvine. “Looking at memory from a superior perspective gives us a new tool. It may just broaden our knowledge and ability to know what’s going on.”

In 2006, UC Irvine neuroscientist Larry Cahill and collaborators published a report on a woman who could remember detailed accounts of her life. Cahill and colleagues then began hearing from many people who claimed to have extraordinary memories. After sifting through and eliminating the impostors, the team was left with 11 people who scored off the charts for autobiographical memory. These people could effortlessly remember, for instance, what they were doing on November 2, 1989, and could also tell you that it was a Thursday. “They’re not going home and saying ‘OK, let me write down what I did today and memorize it,’ ” LePort said.

Using brain scans, researchers found that people with supermemories had larger brain regions associated with memory, including the left temporoparietal junction and the left posterior insula. What’s more, a brain structure called the lentiform nucleus, a cone-shaped mass in the core of the brain, was bigger in people with exceptional memories. This brain area has been linked to obsessive-compulsive disorder.

The subjects haven’t been clinically evaluated for OCD, but LePort says that there are some similarities. “The ability to organize their memories by dates seems to relieve anxiety,” she says.

Researchers don’t know how the brain accomplishes this feat. These people could encode information more effectively, or have a better system of retrieving it, or both. “Right now, we can see the brain areas that are coming out and speculate about what’s going on,” LePort says.

The team hopes to do further studies examining what’s happening in the brain as these people remember.

One tantalizing lead suggests that genetics might be involved. Though no genetic tests have been performed, some of the volunteers have reported that family members share extraordinary powers of recall, LePort says.

The result “certainly pushes us beyond the boundaries of what we might normally think,” said memory expert Howard Eichenbaum of Boston University. “It violates a standard principle that most of us have, which is that normal memory is pretty damn optimized.”

The volunteers are now keeping detailed diaries, so that the scientists can test whether particular kinds of memories are better suited to recollection. People might be better at remembering emotional memories, for instance.

Prompt liver transplant boosts survival in heavy drinkers

Heavy drinkers who have severe liver inflammation are much more likely to survive if they get a prompt liver transplant than if they wait a few months, new research finds. Allowing some alcoholics with a potentially lethal form of liver disease to move up the waiting list for a transplant — a controversial area of transplant policy — would save lives, researchers suggest in the Nov. 10 New England Journal of Medicine.
About 10 to 15 percent of donor livers go to people whose liver disease stems directly from alcohol, says Robert Brown, a hepatologist at Columbia University in New York City who wasn’t involved in the new study. But the number is an estimate at best since many people who qualify for a transplant because of liver damage from other causes might also drink, he says.
In the United States, transplant guidelines require that alcoholics stay sober for six months before they can be placed on the waiting list for a liver transplant. Six months of abstinence and medication improve the health of many people with alcohol-related liver disease, but the delay can be fatal for those with a form of alcohol-induced liver inflammation that doesn’t respond to routine medication. About 70 to 80 percent of people with this condition, called severe alcoholic hepatitis, die within six months.
For the new study, physician Philippe Mathurin of the Claude Huriez Hospital in Lille, France, and his colleagues chose 26 patients to get a liver transplant within a few weeks of being diagnosed with alcoholic hepatitis. The patients had failed to respond to medication such as steroids, the typical treatment for the condition. The researchers also monitored 26 similar patients who didn’t receive transplants.
Six months after surgery, six of the 26 transplant patients had died, compared with 20 of the 26 who didn’t get a liver transplant.
These findings challenge the notion that transplant eligibility for all alcoholism-related liver patients must be linked to a prescribed abstinence period, Mathurin argues. But changing transplant guidelines takes years, he acknowledges, and the new data will need to be reproduced by other scientists. Ultimately, he says, patients on the waiting list for donor organs “need to be ranked by sickest-first and according to the severity of their disease, regardless of the cause.”
Underlying the U.S.’s six-months-sober policy is the assumption that alcohol-related liver disease is a self-inflicted problem, Brown says. “There is an inherent bias against alcohol as a reason for transplant.” He acknowledges that consuming alcohol is a deliberate act but notes that other factors that contribute to liver disease — obesity, smoking, sedentary lifestyle, hepatitis C — could also be seen as self-inflicted. In the study, three of the 26 transplant patients reported drinking at some point during the two years after the operation.
Surgeons have to make difficult assessments when determining how urgently a patient needs a transplant, Brown says, and the new data should be factored in. “When the likelihood of dying is 70 percent, the default has to be to transplant,” he says. Patients with severe alcoholic hepatitis who don’t respond to medication would constitute only a few percent of total liver transplants, he estimates.
The true prevalence of alcoholic hepatitis is unknown, but by some estimates it comprises 10 to 35 percent of all alcohol-related liver disease.

Hands off and on in schizophrenia

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HAND-Y SWITCHSimultaneous stroking of a visible rubber hand (left) and the unseen actual hand (right) of this graduate student caused him to perceive the fake appendage as his own. Schizophrenia patients experience a rubber-hand illusion especially easily and intensely, denoting a disturbance in their sense of body and self.People with schizophrenia rapidly and intensely perceive phony replicas of hands as their own, possibly contributing to this mental ailment’s signature hallucinations, a new study suggests.
In a series of tests, people with schizophrenia believed a rubber hand placed in front of them was theirs if the visible fake hand and the patient’s hidden, corresponding hand were simultaneously stroked with a paintbrush.
Mentally healthy people took longer to experience a less dramatic version of this rubber-hand illusion than schizophrenia patients did, but the effect’s vividness increased among healthy volunteers who reported magical beliefs, severe social anxiety and other characteristics linked to a tendency to psychosis, psychologist Sohee Park of Vanderbilt University in Nashville and her colleagues report online October 31 in PLoS ONE.
“Schizophrenia patients may have a more flexible internal representation of their bodies and a weakened sense of self,” Park says. “Even without psychosis, the rubber-hand illusion can be more pronounced in certain personality types.”
Mental health clinicians have written for several decades about a disturbed sense of self in schizophrenia. A team led by psychiatrist Avi Peled of Sha’ar Menashe Mental Health Center in Hadera, Israel, first reported a powerful rubber-hand illusion in the illness in 2000.
In further support of disturbed body perception in schizophrenia, Park — who directed the new study with graduate student Katharine Thakkar — notes that patients thought that their stationary, unseen hands moved an average of 2 centimeters closer to the rubber hand as they felt and watched brush strokes. Healthy participants reported a weaker version of this effect.
One patient, a 55-year-old man, felt that he floated above his own body and looked down on himself during the three-minute stroking procedure. In a follow-up session, this man had another out-of-body experience, in which he and the experimenter hovered above a lab table for several minutes.
An inability to perceive one’s body as one’s own in schizophrenia prompts heightened reactions to the sight of detached body parts, such as the rubber hand, proposes neurologist Peter Brugger of University Hospital Zurich in Switzerland. That would explain why simply looking at the fake appendage evoked a rubber-hand illusion in several patients in the new study, he says.
Park’s team studied 24 schizophrenia patients and 21 volunteers who had no mental disorders. Patients lived by themselves or in group homes and received antipsychotic medication and other services at an outpatient clinic.
A right-brain region previously linked to out-of-body experiences and representation of one’s body goes awry in schizophrenia, Park hypothesizes. Yoga or other body-awareness exercises may weaken this portion of schizophrenia’s grip, she suggests.
Peled proposes that a communication breakdown among sensory and association networks throughout the brain underlies schizophrenia. This can undermine a sense of body ownership, but patients more often hear tormenting voices and retreat from social life, he says.

Headache tree is a pain in the brain

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Scientists have deciphered how an ingredient in the bay laurel tree (Umbellularia californica) triggers headaches in some people.Dlanglois/Wikimedia Commons

One whiff of a plant known as the headache tree can spur intense, excruciating pain — and now scientists know why.  An ingredient in the tree sets off a chain of events that eventually amps up blood flow to the brain’s outer membrane.
Other headache triggers, such as chlorine, cigarette smoke and formaldehyde, interact with some of the same cellular machinery, suggesting they all work via the same pain-inducing mechanism.
In the new study, an international group of researchers extracted the plant compound umbellulone from dried bay laurel leaves and then exposed various mouse and rat cells to the compound.  Umbellulone tickles the same cellular detector that responds to painfully cold stimuli and the sinus-clearing scent of wasabi and mustard oil, the researchers report online October 27 in Brain.
Stimulating this chemical detector ultimately triggers the release of a particular protein implicated in migraine headaches, the researchers found. This protein prompts blood vessels to swell, and scientists think this swelling puts pressure on the skull and nerves, causing pain.
The new research is solid, says neuroscientist Peter Goadsby, director of the headache center at the University of California, San Francisco. Other irritants linked to headaches interact with the same chemical detector, and it may be a good target for therapy, Goadsby says.
The scent of the bay laurel tree, Umbellularia californica, had been anecdotally implicated as a headache trigger, but it took a self-experimenting headache-sufferer to bring the plant to the attention of researchers in the Headache Center at the University of Florence. Pierangelo Geppetti, who led the study, heard from a friend about a man who was trimming trees on his property and suddenly experienced a cold sensation in his left nostril and then excruciating pain around his left eye. In his youth, the man had regularly gotten cluster headaches, which are one-sided, intense bouts of exceptional pain that often recur in people who suffer from them.
Unlike a full-bore cluster headache, the man’s symptoms quickly faded, and he forgot about the episode. But a few months later when he was again working with bay laurel, the headache struck again.  This prompted him to experiment, intentionally sniffing the crushed leaves of the tree. The intense pain resumed and not long after, Geppetti heard the headache story from their mutual friend.  Intrigued, he began investigating the chemical compounds that might be responsible.

The Ultimate Remote Physiological Monitoring Biosensor Chip

With advancement in medical technologies and the idea to bring less complicated into the picture, the biomedical industry is seeing new innovations on daily basis.

Electric Potential Integrated Circuit (EPIC) is a latest biosensor by Plessey Semiconductors of Roborough, England which contactlessly measures minute changes in voltage levels of patient’s body with …
No electrical contact and gels.
No wires, leads, or medical tape.
No any need to remove the patient’s clothes.
This has to be an ultimate remote physiological monitoring sensor.

Electric Potential Integrated Circuit (EPIC)

Its a very sensitive, contactless digital voltmeter capable of measuring millivolt changes in electric fields, like a magnetometer detects changes in a magnetic field. The sensor has a huge input impedance (10s of gigaohms), so this enables to measure extremely low powered biomedical signals such as ECGs, EOGs etc.
Furthermore, the filtering technology does not allow the noise to obscure the signal of interest. So while monitoring ECG from a subject, the output doesn’t allow the electromyographic signals (due to respiration and body movements etc.) to obscure the ECG trace.

Download Electric Potential Integrated Circuit (EPIC) Sensor Press Release

You can also view the block diagram and technical specifications from here.

Advantages & Applications

• Senses the electrical activity of skeletal muscles including those that control the eyes (EOGs).
• Assisting the disabled, quadriplegics can get the ability to control a cursor on a computer screen or operate a motorized wheelchair with a series of eye movements.
• In prosthetics, it could benefit amputees, who can be employed with a myoelectric hand working on the EMG signals from the residual limb.
• It can pick up minute changes in electric fields through walls. For example, it would allow a firefighter to tell whether someone is inside a smoke-filled room.

Hope, you like this article, keep sharing your views in the comments…

Sources:
IEEE Spectrum
Plessey Semiconductors Official Website

A particulate threat to diabetics

In a new study of people with diabetes, blood pressure rose in rough lockstep with short-term increases in soot and other microscopic air pollutant particles. Such transient increases in blood pressure can place the health of the heart, arteries, brain and kidneys at risk, particularly in people with chronic disease.
In contrast, when ozone levels climbed, blood pressure tended to fall among these people, independent of particulate levels. "And that was certainly not what we expected," notes study coauthor Barbara Hoffmann of the Leibniz Research Institute for Environmental Medicine in Düsseldorf, Germany.
Temperature also had an independent effect: A five-day average increase of 11.5 degrees Celsius, for instance, was associated with a small drop in blood pressure, Hoffmann and her colleagues report online October 21 in Environmental Health Perspectives.
Earlier studies suggested that particulates of the size measured in this study — just 2.5 micrometers in diameter — can hike blood pressure, particularly in people with diabetes.
To further investigate, Hoffman and her colleagues followed 70 Boston-area men and women, ages 40 to 85, with long-standing type 2 diabetes. All lived within 25 kilometers of a major air pollution monitoring station. Each participant submitted to repeated health tests at intervals of several weeks, which the researchers matched up with air pollution values from the preceding five days.
The team found pollution-related changes primarily in systolic blood pressure, the pressure exerted by the pumping action of each heartbeat. Systolic pressure is the top number in a blood pressure reading.
Since levels of particulates and ozone don’t necessarily track, one type of air pollutant cannot be expected to cancel out blood pressure alterations posed by the other, the researchers say. And ozone-associated drops in blood pressure aren’t necessarily beneficial. In fact, Hoffmann says, they offer additional evidence of a diabetes-related impairment in the ability of blood vessels to quickly adjust to changing environmental conditions by relaxing or constricting.
Changes in ozone and air pollution levels had no effect on people whose blood sugar was well controlled. Similarly, people with healthy baseline blood pressure readings exhibited little vulnerability to pollution.
"So especially if you want to positively influence your risk from air pollution," Hoffmann says, "it seems a very good idea to tightly control your blood pressure and your blood sugar."
The fact that a rise in concentrations of near-nanoscale particulates as small as 3.5 micrograms per cubic meter of air could raise systolic blood pressure “corroborates that current levels of particulate matter disrupt blood pressure control,” says physician Robert Brook of the Division of Cardiovascular Medicine at the University of Michigan Medical School in Ann Arbor. The new data, he maintains, confirm that short-term inhalation of fine airborne particulates at ambient levels — and perhaps traffic-related soot in particular — "have small but potentially clinically meaningful effects."

The sound of screech

In a study that borders on painful, people who listened to the sounds of nails and squeaky chalk dragged across a chalkboard have helped scientists pinpoint which frequencies cause people to cringe.
Two scientists who study icky sounds have figured out why fingernails dragged across a chalkboard make people’s skin crawl. It’s not the highest or lowest sounds in the squeak that are so annoying, but rather tones that lie in the range of a piano keyboard.
This makes sense because the human ear has evolved to be sensitive to these frequencies, says Christoph Reuter of the University of Vienna’s Musicological Institute. His colleague, Michael Oehler of the Macromedia University for Media and Communication in Cologne, Germany, will present the findings in San Diego November 3 at a meeting of the Acoustical Society of America.
But sound waves alone can’t account for the excruciating experience. Knowing that a screech comes from a chalkboard instead of a piece of contemporary music increases a listener’s discomfort, the researchers found.
“I’m also convinced that watching somebody scrape their nails on a chalkboard will make the experience even more unpleasant,” says Randolph Blake, a vision scientist at Vanderbilt University in Nashville. More than a quarter of a century ago, he and his colleagues first showed that filtering out the highest frequencies doesn’t make the fingernail-scraping sound any less chilling.
To pinpoint which frequencies are to blame, Reuter and Oehler played six different chalkboard squeaks to 104 unfortunate people who rated their discomfort. The researchers measured changes in 24 listeners’ vital signs and skin conductivity — indicators of stress — while replaying the two most annoying clips.
The shrill sounds contained frequencies ranging all the way to 12,000 hertz and beyond. Cutting out the lowest or highest frequencies didn’t change the listeners’ desire to gouge out their own eyes. But removing all tones between 2,000 and 4,000 hertz did make the experience a little more pleasant — or at least a little less hellish.
It may be that the ear canal naturally resonates with these frequencies, the researchers suggest. This amplifies many of the important sounds people pay attention to every day, including the human voice.
Josh McDermott, a hearing scientist at New York University who has studied other annoying noises like metal being dragged across glass, agrees with this explanation. He says this sensitivity is why people with noisy jobs tend to lose hearing in this frequency range first. McDermott himself has trouble hearing these frequencies — a fact he blames on his former career as a radio DJ.
“We’re learning that’s where some of these really annoying sounds pack most of their punch,” he says.

Nearness key in microbe DNA swaps

Bacteria are more likely to exchange genetic information with their neighbors than with their relatives, a new study shows.
Researchers also found that bacteria living in and on humans are more likely to swap genes than are bacteria that live in soil, oceans or other environments. Exceptions to the neighborhood-only swap-meet rule are genes that confer an evolutionary advantage, such as the ones that make bacteria resistant to antibiotics.
Unlike animals, which can share genes only within species, bacteria readily exchange bits of DNA with other kinds of microbes. Previous evidence had indicated that gene swapping (which scientists call horizontal gene transfer) was mostly limited to closely related bacteria. The new finding that environment plays a bigger role than relatedness in determining swapping partners may be important for tracking antibiotic resistance and disease-causing genes among microbes.
“It’s quite intuitive that bacteria living together would have more chance to exchange,” says Gurvan Michel, a biochemist at the French National Center for Scientific Research marine biological station in Roscoff. “But nobody has really proven this idea before.”
That doesn’t mean relatedness has no importance. “This is not an either-or story,” says David Relman, a microbiologist and infectious disease specialist at Stanford University and the Veteran’s Affairs Palo Alto Health Care System. It could be that closely related species living in the same ecological niche are even more likely to swap genes than nonrelated organisms are, he says.
Inspired by a study Michel and his colleagues published last year showing that genes for digesting seaweed could be transferred from marine algae to bacteria in the intestines of sushi eaters (SN: 5/8/10, p.13), MIT evolutionary biologist Eric Alm set one of his students the task of finding other examples of genes recently swapped between unrelated bacteria.
“We were looking for five to 10, but he came back within a week and said there were 8,000 or something. We thought it was a mistake,” Alm says.
In the end, Alm and his colleagues scoured the genetic blueprints of 2,235 types of bacteria and found 10,770 recently swapped genes. Bacteria that live in or on humans were 25 times more likely to swap genes than ocean or soil bacteria, the researchers report online October 30 in Nature. And bacteria living on the gums were more likely to exchange genes with other gum bacteria than with those in the nose or vagina. The more the researchers subdivided the niches that bacteria inhabit, the more likely the gene transfer, Alm says. The pattern holds even down to how much oxygen bacteria can tolerate. Bacteria with low oxygen tolerance swap more often with other oxygen-averse bacteria than with oxygen lovers.
Disease-causing bacteria are more likely to exchange genes with other pathogenic bacteria than with friendly bacteria. The team found 13 genes shared among bacteria that cause meningitis, even though those bacteria are not otherwise related to each other. The finding suggests that researchers looking for new disease-control strategies may be able to look for swapped genes in unrelated microbes that cause similar ailments, Alm says.
Genes that did make the leap between environments were likely to be ones that make microbes resistant to antibiotics. The team uncovered 42 antibiotic-resistance genes that had recently been transferred between farm animal microbes and human-associated bacteria.
“Which is kind of scary,” Alm says, “because it means that antibiotic-resistant strains don’t have to make it into humans. They can just transfer genes to human bacteria.”
Concrete evidence of gene swapping between microbes from farm animals and humans has been hard to find, says Gautam Dantas, a microbial genomicist at Washington University School of Medicine in St. Louis who studies antibiotic resistance. “To the scientist in the field there has not been much doubt that the abuse of antibiotics in agriculture has exacerbated antibiotic resistance in humans,” he says. “We’ve basically been choosing cheap meat over human health.”

Biomarker for Huntington’s disease identified

Scientists on the trail of treatments for Huntington’s disease may have found a way to track their success. A new study reports that patients with Huntington’s disease have higher levels of expression of a gene called H2AFY in their blood compared with healthy people. What’s more, patients treated with a drug that slows the effects of the disease had reduced levels of H2AFY activity compared with people given a placebo.
The results suggest that H2AFY could serve as a tool for monitoring the progression of the disease and an indicator of whether prospective treatments are working, researchers report online October 3 in the Proceedings of the National Academy of Sciences.
“Biomarker identification for Huntington’s disease is critically important for clinical trials,” says Leslie Thompson, director of the Interdepartmental Neuroscience Program at the University of California, Irvine, who was not involved in the study.
Huntington’s disease is a hereditary movement disorder marked by involuntary bodily twitches and jerks. The damage the disorder does to nerve cells also causes severe depression and impairs a patient’s ability to reason clearly. “It’s a devastating disease,” and one for which there is no cure, says neurologist Clemens Scherzer of Brigham and Women’s Hospital in Boston, who led the new study.
Although some promising treatments are now being tested in clinical trials, one roadblock in their development has been sorting out whether candidate drugs actually halt progression of the disease. To address this problem, Scherzer and colleagues sought a biomarker — a biological indicator they could easily measure — that would provide them with a snapshot of the state of a patient’s disease.
Casting a wide net, the research team analyzed expression data from every gene in the blood cells of more than 100 people. Eight people had Huntington’s disease, and more than 80 had other neurological conditions. Compared with the other participants, the Huntington’s patients had elevated levels of H2AFY expression — levels that were as much as two times higher compared with those of healthy people.
To further study the gene as a candidate biomarker, Scherzer began collaborating with Steven Hersch and colleagues at Massachusetts General Hospital, who were conducting a clinical trial of a compound called sodium phenylbutyrate as a potential therapeutic drug for Huntington’s.
The collaborators measured H2AFY activity in blood cells of trial participants before and after they began taking sodium phenylbutyrate. As patients continued to take the compound, the researchers found decreasing H2AFY activity — a sign that the druglike compound might be slowing the nerve-cell damage inflicted by the disease.
Scherzer says he hopes that H2AFY and other biomarkers like it will help speed the development of new treatments for the disease. “The key is to make clinical trials for Huntington’s disease more efficient,” he says.

Brain gene activity changes through life

Human brains all work pretty much the same and use roughly the same genes in the same way to build and maintain the infrastructure that makes people who they are, two new studies show. And by charting the brain’s genetic activity from before birth to old age, the studies reveal that the brain continually remodels itself in predictable ways throughout life.
In addition to uncovering details of how the brain grows and ages, the results may help scientists better understand what goes awry in brain disorders such as schizophrenia and autism.
“The complexity is mind-numbing,” says neuroscientist Stephen Ginsberg of the Nathan Kline Institute and New York University Langone Medical Center, who wasn’t involved in the studies. “It puts the brain in rarefied air.”
In the studies, published in the Oct. 27 Nature, researchers focused not on DNA — virtually every cell’s raw genetic material is identical — but on when, where and for how long each gene is turned on over the course of a person’s life. To do this, the researchers measured levels of mRNA, a molecule whose appearance marks one of the first steps in executing the orders contained in a gene, in postmortem samples of donated brains that ranged in age from weeks after conception to old age.

These different patterns of mRNA levels distinguish the brain from a heart, for instance, and a human from a mouse, too, says Nenad Šestan of Yale University School of Medicine and coauthor of one of the studies. “Essentially, we carry the same genes as mice,” he says. “However, in us, these genes are up to something quite different.”
To see what those genes were up to, Šestan’s study examined mRNA levels of different genes in 57 brain samples. The team divided the brain tissue up by region, so they were also able to get an idea of genes’ behavior in different parts of the brain. A parallel study, headed by Joel Kleinman of the National Institute of Mental Health in Bethesda, looked at gene behavior in 269 brain samples from a single region called the prefrontal cortex that also spanned the lifetime.
This approach allowed the researchers to get access to the brain that had previously been impossible.
“One of the limitations in studying human brain development is that you cannot do experiments,” Šestan says. “It’s very hard to understand when things happen.”
Both studies found lots of variation in gene behavior at different life stages, but one particular period stood out: The prenatal brain had massive changes in gene activity. Many genes there were pumping out big quantities of mRNA, and this production abruptly slowed after birth. “Prenatally, things are changing faster than they change at any other time,” says Carlo Colantuoni of the Lieber Institute for Brain Development at Johns Hopkins University Medical Center, and coauthor on one paper. “Things are happening fast in there.” 
Kleinman and his colleagues turned up a curious finding: Many of the genes that slow down right after birth show a surge of activity as a person gets older. “The biggest changes that are going on occur fetally,” he says. “And then they drop off until mid-life, and then in the 50s to 70s, expression changes pick up again and become quite dramatic.”

Researchers don’t yet know what to make of this reversal, says Colantuoni. “We have just scratched the surface of what it means.”
Genes involved with building new brain cells were highly active early on, and then this activity quickly fell after birth. As these genes grew less active, genes involved in linking up nerve cells took on a greater role and became busier.
What’s more, the differences in gene behavior between male and female brains were greatest at early stages of development. Some of the genes found to be busier in male brains have been linked to schizophrenia, autism and other disorders that are known to be more prevalent among males, the researchers report. These disease-associated genes are very active early on in development and less so as a person ages, the researchers found, suggesting that something goes wrong very early in these conditions.
The scientists don’t know exactly which cells are responsible for these gene behavior differences. Figuring out whether gene behavior changes in all kinds of cells in the brain — neurons and glia, for instance — is the next step, says Ginsberg. “That’s going to be really important, especially for neuropsychiatric disorders.”
Although gene behavior is incredibly dynamic, the results suggest that brains are more alike than different. Despite millions of differences in DNA, brains have a common biochemical shape, Kleinman says. Two people who have very different DNA make-up don’t necessarily have very different gene behavior in the brain. “These individual genetic variations, they do matter — no question,” he says. But overall, genes behave similarly from person to person. “And that’s a really cool thing. It means that we’re much more alike than we are different.”
Many more studies are needed before scientists fully understand how the brain is built. Both teams plan on boosting the number of brain samples and studying the brains of people with disorders such as schizophrenia and autism. But the work is a major step forward, says geneticist Christopher Mason of Weill Cornell Medical College of Cornell University in New York City. “This is extraordinary work,” he says. “This is the beginning of telling us what the whole brain looks like.”