Swarms of bees could unlock secrets to human brains

Scientists at the University of Sheffield believe decision making mechanisms in the human brain could mirror how swarms of bees choose new nest sites.

Striking similarities have been found in decision making systems between humans and insects in the past but now researchers believe that bees could teach us about how our brains work.

Experts say the insects even appear to have solved indecision, an often paralysing thought process in humans, with scouts who seek out any honeybees advertising rival nest sites and butt against them with their heads while producing shrill beeping sounds.

Dr James Marshall, of the University of Sheffield's Department of Computer Science, who led the UK involvement in the project and has also previously worked on similarities between how brains and insect colonies make decisions, said: "Up to now we've been asking if honeybee colonies might work in the same way as brains; now the new mathematical modelling we've done makes me think we should be asking whether our brains might work like honeybee colonies.

"Many people know about the waggle dance that honeybees use to direct hive mates to rich flower patches and new nest sites. Our research published in the journal Science (on December 9), shows that this isn't the only way that honeybees communicate with each other when they are choosing a new nest site; they also disrupt the waggle dances of bees that are advertising alternative sites."

Biologists from Cornell University, New York, University of California Riverside and the University of Bristol set up two nest boxes for a homeless honeybee swarm to choose between and recorded how bees that visited each box interacted with bees from the rival box. They found that bees that visited one site, which were marked with pink paint, tended to inhibit the dances of bees advertising the other site, which were marked with yellow paint, and vice versa.

Tom Seeley of Cornell University, author of the best-selling book Honeybee Democracy said "We were amazed to discover that the bees from one nest box would seek out bees performing waggle dances for the other nest box and butt against them with their heads while simultaneously producing shrill beeping sounds. We call this rough treatment the 'stop signal' because most bees that receive this signal will cease dancing a few seconds later."

Dr Patrick Hogan of the University of Sheffield, who constructed the mathematical model of the bees, added: "The bees target their stop signal only at rivals within the colony, preventing the colony as a whole from becoming deadlocked with indecision when choosing a new home. This remarkable behaviour emerges naturally from the very simple interactions observed between the individual bees in the colony."

Source EurekaAlert!

How dense is a cell?

Combining an ancient principle with new technology, MIT researchers have devised a way to answer that question.

MIT researchers designed this tiny microfluidic chip that can measure the mass and density of single cells.

More than 2,000 years after Archimedes found a way to determine the density of a king’s crown by measuring its mass in two different fluids, MIT scientists have used the same principle to solve an equally vexing puzzle — how to measure the density of a single cell.

“Density is such a fundamental, basic property of everything,” says William Grover, a research associate in MIT’s Department of Biological Engineering. “Every cell in your body has a density, and if you can measure it accurately enough, it opens a whole new window on the biology of that cell.”

The new method, described in the Proceedings of the National Academy of Sciences the week of June 20, involves measuring the buoyant mass of each cell in two fluids of different densities. Just as measuring the crown’s density helped Archimedes determine whether it was made of pure gold, measuring cell density could allow researchers to gain biophysical insight into fundamental cellular processes such as adaptations for survival, and might also be useful for identifying diseased cells, according to the authors.

Grover and recent MIT PhD recipient Andrea Bryan are lead authors of the paper. Both work in the lab of Scott Manalis, a professor of biological engineering, member of the David H. Koch Institute for Integrative Cancer Research and senior author of the paper.

Going with the flow

Measuring the density of living cells is tricky because it requires a tool that can weigh cells in their native fluid environment, to keep them alive, and a method to measure each cell in two different fluids.

How the lab can determine the weight and density of individual cells.

In 2007, Manalis and his students developed the first technique to measure the buoyant mass of single living cells. Their device, known as a suspended microchannel resonator, pumps cells, in fluid, through a microchannel that runs across a tiny silicon cantilever, or diving-board structure. That cantilever vibrates within a vacuum; when a cell flows through the channel, the frequency of the cantilever’s vibration changes. The cell’s buoyant mass can be calculated from the change in frequency.

To adapt the system to measure density, the researchers needed to flow each cell through the channel twice, each time in a different fluid. A cell’s buoyant mass (its mass as it floats in fluid) depends on its absolute mass and volume, so by measuring two different buoyant masses for a cell, its mass, volume and density can be calculated.

The new device rapidly exchanges the fluids in the channel without harming the cell, and the entire measurement process for one cell takes as little as five seconds.

David Weitz, professor of physics at Harvard University, says the new technique is a clever way of measuring cell density, and opens up many new avenues of research. “The very interesting thing they show is that density seems to have a more sensitive change than some of the more standard measurements. Why is that? I don’t know. But the fact that I don’t know means it’s interesting,” he says.

Changes in density

The researchers tested their system with several types of cells, including red blood cells and leukemia cells. In the leukemia study, the researchers treated the cells with an antibiotic called staurosporine, then measured their density less than an hour later. Even in that short time, a change in density was already apparent. (The cells grew denser as they started to die.) The treated leukemia cells increased their density by only about 1 percent, a change that would be difficult to detect without a highly sensitive device such as this one. Because of that rapid response and sensitivity, this method could become a good way to screen potential cancer drugs.

“It was really easy, by the density measurement, to identify cells that had responded to the drug. If we had looked at mass alone, or volume alone, we never would have seen that effect,” Bryan says.

The researchers also demonstrated that malaria-infected red blood cells lose density as their infection progresses. This density loss was already known, but this is the first time it has been observed in single cells.

Being able to detect changes in red-blood-cell density could also offer a new way to test athletes who try to cheat by “doping” their blood — that is, by removing their own blood and storing it until just before their competition, when it is transfused back into the bloodstream. This boosts the number of red blood cells, potentially enhancing athletic performance.

Storing blood can alter the blood’s physical characteristics, and if those include changes in density, this technique may be able to detect blood doping, Grover says.

Researchers in Manalis’ lab are now investigating the densities of other types of cells, and are starting to work on measuring single cells as they grow over time — specifically cancer cells, which are characterized by uncontrolled growth.

“Understanding how density of individual cancer cells relates to malignant progression could provide fundamental insights into the underlying cellular processes, as well as lead to clinical strategies for treating patients in situations where molecular markers don’t yet exist or are difficult to measure due to limited sample volumes,” Manalis says.

Other authors on the paper are MIT research scientist Monica Diez-Silva; Subra Suresh, former dean of the MIT School of Engineering; and John Higgins of Massachusetts General Hospital and Harvard Medical School.

Source MIT

Magnetic Field Sensed by Gene, Study Shows

A researcher studying how monarch butterflies navigate has picked up a strong hint that people may be able to sense the earth’s magnetic field and use it for orienting themselves. 

Many animals rely on the magnetic field for navigation, and researchers have often wondered if people, too, might be able to detect the field; that might explain how Polynesian navigators can make 3,000-mile journeys under starless skies. But after years of inconclusive experiments, interest in people’s possible magnetic sense has waned.

That may change after an experiment being reported Tuesday by Steven M. Reppert, a neurobiologist at the University of Massachusetts Medical School, and his colleagues Lauren E. Foley and Robert J. Gegear. They have been studying cryptochromes, light-sensitive proteins that help regulate the daily rhythm of the body’s cells, and how they help set the sun compass by which monarchs navigate.

But the butterflies can navigate even when the sun is obscured, so they must have a backup system. Since physical chemists had speculated the cryptochromes might be sensitive to magnetism, Dr. Reppert wondered if the monarch butterfly was using its cryptochromes to sense the earth’s magnetic field. He first studied the laboratory fruit fly, whose genes are much easier to manipulate and showed three years ago that the fly could detect magnetic fields but only when its cryptochrome gene was in good working order.
He then showed that the monarch butterfly’s two cryptochrome genes could each substitute for the fly’s gene in letting it sense magnetic fields, indicating that the butterfly uses the proteins for the same purpose.

One of the monarch’s two cryptochrome genes is similar in its DNA sequence to the human cryptochrome gene. That prompted the idea of seeing whether the human gene, too, could restore magnetic sensing to fruit flies whose own gene had been knocked out. In the journal Nature Communications, Dr. Reppert reports that this is indeed the case. “A reassessment of human magnetosensitivity may be in order,” he and his colleagues write.

The human cryptochrome gene is highly active in the eye, raising the possibility that the magnetic field might in some sense be seen, if the cryptochromes interact with the retina.
Dr. Reppert said the focus on human use of the magnetic field for navigation might be misplaced. Following an idea proposed last year by John B. Phillips of Virginia Tech, he said the primary use of magnetic sensing might be for spatial orientation.

“It could be providing a spherical coordinate system that the animal could use for spatial positioning,” he said.
Dr. Phillips said that Dr. Reppert’s work was of interest but that he had been surprised by an experiment in which Dr. Reppert disrupted the part of the cryptochrome thought to interact with the magnetic field, yet the flies had still detected the magnetism. “It’s 50-50 whether he’s really studying what he thinks he is,” Dr. Phillips said.

Dr. Reppert replied that he had already ruled out the alternative explanation suggested by Dr. Phillips.
But both scientists agreed on the possibilities opened up by the cryptochrome system. Depending on how the proteins are aligned in the eye, insects may perceive objects as being lighter or darker as they orient themselves in relation to the magnetic field, Dr. Phillips said.
In fact, the cryptochrome system might supply a grid imposed on all the landmarks in a visual scene, helping a squirrel find a buried acorn, or a fox integrate its visual scene with what it hears. “This is the fun stage where we are not constrained by many facts,” Dr. Phillips said.

If butterflies, birds and foxes possess such a wonderful system, why would it ever have died out in the human lineage? “It may be that our electromagnetic world is interfering with our ability to do this kind of stuff,” Dr. Phillips said.
As for Dr. Reppert, he is now planning his next step, that of understanding how the cryptochrome proteins sense the magnetic field and how they convey that information to the fruit fly’s and monarch’s brain.

Source The New York Times

50-year search for calcium channel ends

Cell's power generator depends on long-sought protein.

Boston, MA (June 19, 2011)—Mitochondria, those battery-pack organelles that fuel the energy of almost every living cell, have an insatiable appetite for calcium. Whether in a dish or a living organism, the mitochondria of most organisms eagerly absorb this chemical compound. Because calcium levels link to many essential biological processes—not to mention conditions such as neurological disease and diabetes—scientists have been working for half a century to identify the molecular pathway that enables these processes.

After decades of failed effort that relied on classic biochemistry and membrane protein purification, Vamsi Mootha, HMS associate professor of systems biology, and colleagues have discovered, through a combination of digital database mining and laboratory assays, the linchpin protein that drives mitochondria's calcium machinery.
"This channel has been studied extensively using physiology and biophysics, yet its molecular identity has remained elusive," said Mootha, who also has appointments at Massachusetts General Hospital and at Broad Institute. "But thanks to the Human Genome Project, freely downloadable genomic databases, and a few tricks -- we were able to get to the bottom of it."

These findings will appear online June 19 in Nature.

The results build on work from Vamsi and his group over the past decade. In 2008, he and his team published a near-comprehensive protein inventory, or proteome, of human and mouse mitochondria. This inventory, called MitoCarta, consisted of just over 1,000 proteins, most of which had no known function.
In a September 2010 paper, Mootha's group described using the MitoCarta inventory to identify the first protein specifically required for mitochondrial calcium uptake. Their strategy was simple. They knew that mitochondria from humans and Trypanosomes (a parasitical organism), but not baker's yeast, are capable of absorbing large amounts of calcium. By simply overlapping the mitochondrial protein profiles of these three organisms, the group could spotlight roughly 50 proteins out of the 1,000 that might be involved with calcium channeling. They found that one protein, which they dubbed MICU1, is essential for calcium uptake.

"That was an significant advance for the field," says Mootha. "We showed that MICU1 was required for calcium uptake, but because it did not span the membrane, we doubted it was the central component of the channel. But what it provided us with was live bait to then go and find the bigger fish."
Traditionally, researchers used standard laboratory methods for such a fishing exhibition, such as attaching biochemical hooks to the protein, casting it into the cell's cytoplasm, then reeling it back in the hope that another, related protein will have bitten. But MICU1's function as a regulator of a membrane channel made this technically prohibitive. Instead, graduate student Joshua Baughman and postdoctoral researcher Fabiana Perocchi went fishing in publicly available genomic databases.

With MICU1 as their point of reference, they scoured those databases that measure whole genome RNA and protein expression, as well as an additional database containing genomic information for 500 species, and looked for proteins whose activity profile mirrored MICU1's. A single anonymous protein with no known function stood out. The researchers named it MCU, short for "mitochondrial calcium uniporter."
To confirm that MCU is central to mitochondria's calcium absorption, the team collaborated with Alnylam Pharmaceuticals, a company that leverages a laboratory tool called RNAi in order to selectively knock out genes in both cells and live animals. Using one of the company's platforms, the researchers deactivated MCU in the livers of mice. While the mice displayed no immediate reaction, the mitochondria in their liver tissue lost the capacity to absorb calcium.
This basic science finding may prove relevant in certain human diseases. "We've known for decades now that neurons in the brains of people suffering from neurodegenerative disease are often marked by mitochondrial calcium overload," said Mootha, an expert on rare mitochondrial diseases who sees patients at Massachusetts General Hospital when he's not in the lab.
"We also know that the secretion of many hormones, like insulin, are triggered by calcium spikes in the cell's cytoplasm. By clearing cytosolic calcium, mitochondria can shape these signals. Scientists studying the nexus of energy metabolism and cellular signaling will be particularly interested in MICU1 and MCU. It's still very early, but they could prove to be valuable drug targets for a variety of diseases – ranging from ischemic injury and neurodegeneration to diabetes."

Source EurekaAlert!

UI study examines link between teen sex and divorce rate

A University of Iowa study found that women who make their sexual debut as young teens are more likely to divorce, especially if "the first time" was unwanted, or if she had mixed feelings about it.
Published in the April issue of the Journal of Marriage and Family, the analysis found that 31 percent of women who had sex for the first time as teens divorced within five years, and 47 percent divorced within 10 years. The divorce rate for women who delayed sex until adulthood was far lower: 15 percent at five years, and 27 percent at 10 years.

Author Anthony Paik, associate professor of sociology in the UI College of Liberal Arts and Sciences, examined the responses of 3,793 ever-married women to the 2002 National Survey of Family Growth.
A first sexual experience that was unwanted or not completely wanted was strongly associated with divorce. If the young woman chose to lose her virginity as a teen, the results were more nuanced.
When the first intercourse took place early in adolescence –- before the age of 16 –- the women were more likely to divorce, even if that first sexual experience was wanted.

If the young woman waited until age 16 or 17 and the first sex was wanted, there was no direct link to dissolution down the road. But, while the sex itself did not increase the likelihood of a marital split, other factors related to sexuality -– such as a higher number of sexual partners, pregnancy, or out-of-wedlock birth -– increased the risk for some respondents.

Thirty-one percent of women who experienced adolescent sexual debut had premarital sex with multiple partners, compared to 24 percent of those who waited. Twenty-nine percent experienced premarital conceptions, versus 15 percent who waited. And, one in four women who had sex during their teenage years had a baby before they were married, compared to only one in ten who held off.
"The results are consistent with the argument that there are down sides to adolescent sexuality, including the increased likelihood of divorce," Paik said. "But there's also support for the 'more sex positive' view, because if a teen delays sex to late adolescence and it is wanted, that choice in itself doesn't necessarily lead to increased risk of divorce."

Only a small percentage of women who had sex before age 18 said it was completely wanted. Just 1 percent chose to have sex at age 13 or younger, 5 percent at age 14 or 15, and 10 percent at age 16 or 17. Another 42 percent reported first sexual intercourse before age 18 that was not completely wanted, while the remaining portion of the sample waited until age 18 or older to have sex (wanted, 22 percent; unwanted, 21 percent).
Paik said there are a couple potential explanations for the link between teen sex and divorce.
"One possibility is a selection explanation, that the women who had sex as adolescents were predisposed to divorce. The attitudes that made them feel OK about having sex as teens may have also influenced the outcome of their marriage," Paik said. "The other possibility is a causal explanation –- that the early sexual experience led to the development of behaviors or beliefs that promote divorce."

In a statistical analysis, he found more evidence for the latter, suggesting that the sexual experiences as a teen affected the marriage. The results related to unwanted sex supported his hunch. Nevertheless, he cautions that it is too early to rule out the selection explanation.
"If the sex was not completely wanted or occurred in a traumatic context, it's easy to imagine how that could have a negative impact on how women might feel about relationships, or on relationship skills," Paik said. "The experience could point people on a path toward less stable relationships."

Limitations of the study included a lack of information on respondents' work status, which is often used as a control factor in divorce research, and the fact that the Centers for Disease Control and Prevention data included some imputed values. Paik arrived at the same results by excluding the imputed figures, but would like to repeat the study with the new 2006-08 data to confirm that the findings still hold.
"It's a timely topic, given the current debate over the sexualization of girls," Paik said. "This study tries to provide some answers about adolescent sexuality and the risk of marital dissolution, and the results show that both the context and early onset of first intercourse are associated with divorce."

Source University of Iowa

Beyond Condoms: The Long Quest for a Better Male Contraceptive

A joke among researchers in the field of male contraception is that a clinically approved alternative to condoms or vasectomy has been five to 10 years away for the past 40 years. The so-close-yet-so-far state of male contraceptive development has persisted in large part because of three serious hurdles: the technical challenges of keeping millions of sperm at bay, the stringent safety standards that a drug intended for long-term use in healthy people must meet, and, ultimately, the question of whether men will use it.

Any sex-ed grad can tell you: the only two effective contraceptives for men today are condoms and vasectomy. Condoms have been around for at least 300 years, with early versions made of animal intestines. Today's rubber prophylactics are relatively cheap and widely available, offer bonus protection against sexually transmitted infections, and are 98 percent effective against pregnancy if used properly. On the other hand, surgery to cut the vas deferens (sperm ducts) is nearly foolproof in pregnancy prevention but is usually considered irreversible and tantamount to sterilization. "It's appalling that besides condoms men only have a surgical nonreversible method," says Regine Sitruk-Ware, a reproductive endocrinologist at the Population Council in New York City.

For decades the promise seemed to lie in a hormonal approach—an analogue to the female birth control pill—that would adjust the hormones controlling sperm production. Inconsistent results among men and side effects associated with long-term testosterone use have, however, led some researchers lately to set their sights elsewhere. Newer, nonhormonal methods target various developmental nodes in the formation of sperm, their motility and their egg-penetrating capabilities. There is also work on a form of reversible vasectomy which involves blocking the vas deferens with a polymer gel that may later be dissolved.

Most of the new alternatives under development are geared toward men in long-term relationships who seek a dependable, reversible form of contraception. Increasingly, men want more control over their fertility, and many would like to share the burden of contraception with their female partners. For couples in which the woman cannot handle female birth control for whatever reason—in some women, hormonal contraceptives can cause significant side effects such as bleeding, reduced libido and increased cardiovascular risks; IUDs (intrauterine devices) can cause severe cramps; diaphragms can kill spontaneity and require manual insertion—male contraception may be the best or only option. "It's really an unmet need," Sitruk-Ware says.

About half of pregnancies in the U.S. are unplanned and half of these end in abortion. An effective male contraceptive might have salutary implications for population growth worldwide, but for William Bremner, who leads the Center for Research in Reproduction and Contraception at the University of Washington (U.W.) in Seattle, the goal is providing options to individual couples. "If people had effective methods and real choices, there would be fewer unwanted children and markedly fewer abortions," he says.

Worthy intentions, notwithstanding, the reality is that funding has been a continual challenge for the field. The National Institutes of Health (NIH) currently provides nearly all of the funding for male contraception research in the U.S.—and for some international studies, too. Researchers agree that for a new contraceptive to come to market, support from pharmaceutical companies is a practical necessity, but interest in the industry has been waning in recent years. A major blow came in 2006 when two major companies that had been on board, Schering AG and Organon, shut down their joint hormonal male contraceptive program soon after Schering's acquisition by Bayer. That meant the end of a major funding stream as well as the loss of any research advances that had been made by the project. "Unfortunately, the people who were working on it are under obligation to keep confidential the information, in case they ever go back to it," says Diana Blithe, director of the Male Contraceptive Development Program at the NIH.

Hobbling sperm without hormones
Although none have reached clinical trial stage, nonhormonal methods of male contraception are gaining traction. About three or four years ago, John Amory, a researcher and clinician at U.W. who has been working on hormonal methods for many years, became interested in a nonhormonal target: retinoic acid, a metabolite of vitamin A that is essential for spermatogenesis. In animal models the compound bisdichloroacetyldiamine safely and reversibly induces infertility by inhibiting an enzyme, aldehyde dehydrogenase 1a2, required for retinoic acid synthesis in the testes. Unfortunately, bisdichloroacetyldiamine also inhibits a similar enzyme, aldehyde dehydrogenase 2, required for alcohol metabolism in the liver—meaning that animals on bisdichloroacetyldiamine were unable to process alcohol. "And some would say that if it weren't for alcohol no one would need a contraceptive anyway," jokes Amory, who is working on ways to more specifically inhibit aldehyde dehydrogenase 1a2. In another approach, detailed June 1 in Endocrinology, Debra Wolgemuth's lab at Columbia University used a synthetic retinoid to block retinoid acid receptors, achieving reversible infertility in mice.

Several labs are also looking at ways to thwart sperms' ability to find and swim toward the egg. A group of proteins known as CatSpers controls hyperactivation—the frenzied flagellar beating of sperm tails after ejaculation. Two studies published in March found that progesterone and high-pH, or alkalinity, around an egg act on CatSpers to turn on hyperactivation. Because CatSpers are believed to be found only on sperm, drugs targeted specifically to these proteins would presumably have few side effects elsewhere in the body.

Other agents being investigated, including gamendazole and adjudin, target the Sertoli cells within the testes that provide crucial nourishment to growing sperm. None of these nonhormonal drugs will be tested in humans for at least another two or three years, Sitruk-Ware says. Once a contraceptive target is determined, researchers can use high-throughput screening technology to check thousands of compounds for drug potential.

The dark horse
The most tireless advocate for new male contraceptives may be Elaine Lissner, director of the one-woman operation Male Contraception Information Project, which tries to raise public awareness of nonhormonal male contraceptives. In particular, she has been trumpeting a particular method known as reversible inhibition of sperm under guidance (RISUG). Developed and currently undergoing clinical trials in India, RISUG involves a small incision in the scrotum and injection of a polymer gel into the vas deferens, the same tubes severed in vasectomy. (Vasectomy is reversible in some cases with expensive microsurgery to reconnect the vas deferens. Complications such as anti-sperm antibodies that form when sperm leaks into the body during vasectomy, however, make reversal more than a problem of plumbing.) The porous polymer does not block the flow of sperm but purportedly renders sperm inert by disrupting the chemistry of their cell membranes. Although many researchers appreciate Lissner's advocacy efforts, they do not necessarily share her enthusiasm for RISUG, which is still untested the U.S.

RISUG's fighting chance, touted by its supporters, is its potential reversibility. In nonhuman primates, reversibility has been achieved by dissolving the polymer with an injected solvent. In Amory's view, however, "until they demonstrate reversibility in humans, it's really no different than a vasectomy," although, he adds, "I'd love it if this worked."

Lissner, who is not a scientist herself, bought the international rights to RISUG last year and has created a foundation called Parsemus to develop the procedure in the U.S. That means starting from square one, with toxicology testing and small animal studies. Lissner hopes to eventually get the procedure, now re-branded as Vasalgel, approved as a medical device in the U.S. Before that happens, however, Vasalgel, like all other contenders in the male contraceptive line-up will have to catch the eye of a funding source.

The current status of hormonal methods
The female birth control pill, which went on the market in 1960, increases levels of progesterone to suppress ovulation; similarly, a male hormonal contraceptive would increase levels of testosterone to suppress sperm production. Testosterone inhibits the release of two pituitary hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which control in the testes testosterone production and spermatogenesis, respectively. Thus, testosterone works in a negative feedback loop with LH and FSH to maintain relatively constant levels of testosterone in the blood. A male contraceptive that delivers extra testosterone into the bloodstream sends a signal to the pituitary to suppress the hormones that promote sperm production.

For women, the birth control pill replicates the body's natural state of infertility—pregnancy—and essentially fools the body into acting as if it were pregnant. "Men don't have an analogous time. After puberty they keep making sperm until they die," Amory explains.

Compared with the one-egg-per-month output of the female reproductive system, the roughly 1,000-sperm-per-heartbeat output of the male reproductive system is "a quantitatively challenging problem" for contraceptive research, Amory says. Thankfully for Amory's cohort, effective male contraception does not require complete obliteration of sperm production. Only about 5 percent of sperm are functional to begin with, Amory estimates, and very few of these high-quality sperm will survive the arduous journey to the egg. Lowering sperm count to less than one million per milliliter of ejaculate from the normal range of 20 million to 30 million per milliliter results in de facto infertility.

Though often referred to as the "male pill," male hormonal contraceptives in development are mostly synthetic testosterone delivered in the form of injections, slow-release implants or rub-on gels that absorb through the skin. (Oral ingestion of testosterone is less effective because much of the hormone is then broken down by the liver.) Adding progesterone (a female sex hormone), which also suppresses spermatogenesis, to a testosterone regimen improves contraceptive outcomes. The testosterone–progesterone combination achieves effective contraception for more than 90 percent of men—but for reasons that are still unclear, there are always some men for whom sperm production is insufficiently suppressed. For comparison, the female pill is about 98 percent effective when taken correctly.

In April a clinical trial of injections of long-acting progestin (synthetic progesterone) and testosterone was ended early due to higher than expected rates of minor side effects such as irritability and acne among the 321 participants. The trial was a collaboration between the World Health Organization and CONRAD, an Arlington, Va.–based nonprofit that supports reproductive health research. Douglas Colvard, deputy director of programs at CONRAD, expressed disappointment at the end of the trial but was optimistic there would be valuable data from the third of participants who had completed 12 months of injections.

A clinical trial of a contraceptive implant, led by the Population Council, the University of California, Los Angeles, and U.W., will begin late this year or early 2012, according to Sitruk-Ware. The implant, which is matchstick-size and placed under the skin of the upper arm, contains a modified synthetic steroid that resembles testosterone but should not have the same effect on prostate growth sometimes associated with testosterone treatments.

"The idea is a good one," Amory says of male hormonal contraception, "and it works most of the time, but not well enough for a pharmaceutical company to jump in and put some money and time into it."

Do men really want it?
When asked whether a new contraceptive will appeal to men, researchers are quick to point out that men are already responsible for 30 percent of contraception in developed countries (and 14 percent in developing countries), split about evenly between condoms and vasectomies. Even if that is the minority of sexual partners, those figures still add up to hundreds of millions of men.

A 2002 survey of 9,000 men in nine countries across four continents found that more than 55 percent of men would be willing to use a hormonal form of contraception. In a 1996 survey of nearly 2,000 women in Scotland, China and South Africa 87 percent thought that a hormonal male contraceptive was "a good idea" and 98 percent of women said they would trust their partners to use a hypothetical "male pill". "Of course, we don't really know for sure what people will do," Amory says. "All surveys have that limitation."

The risk–benefit analysis for male contraceptives is different from that of female contraceptives because at the end of the day, men are not the ones getting pregnant, Colvard says. For that reason, future male contraceptives may come with incentives other than pregnancy prevention: side benefits such as muscle gain, fat loss and even baldness prevention.

(Of course, infertility is a well-known side effect of testosterone doping in athletes. Although testosterone used for contraceptive purposes would show up on a drug test, according to Amory, the levels are far below those needed for significant muscle enhancement.)

Although many men may welcome new contraceptive options, there is not the same momentum that pushed female contraception. "We don't see groups of men going on the streets," Sitruk-Ware says. "On the other hand, when we do clinical trials in various countries the men are very interested."

For now, researchers and consumers can only assume that when presented with a full pipeline of new drugs and better data on the safety, efficacy and public acceptability of male contraceptives, pharmaceutical companies will eventually see an opportunity for their profit margins. The hope is, "If you make it, they will come," NIH's Blithe says.

Source Scientific American

Study Reveals Important Aspects of Signalling Across Cell Membranes in Plants

Plant receptors use different signalling method than do animal receptors.

Every living plant cell and animal cell is surrounded by a membrane. These cellular membranes contain receptor molecules that serve as the cell's eyes and ears, and help it communicate with other cells and with the outside world.
The receptor molecules accomplish three basic things in the communication process: 1) recognize an outside signal, 2) transport that signal across the cell's membrane and 3) initiate the reading of the signal inside the cell and then initiate the cell's response to that signal. These steps are collectively known as transmembrane signaling.

 Click on image for larger version.

 Transmembrane signaling in a plant cell aided by a steroid.

Transmembrane signaling in animal cells has been significantly more studied and observed than that in plant cells. But now, with support from the National Science Foundation, researchers from Joanne Chory's laboratory at the Salk Institute have published new observations about transmembrane signaling in plants; their paper appears in the June 12, 2011, advanced online edition of Nature.
According to the study, transmembrane signaling mechanisms used by plants differ from those used by animals. Specifically, Michael Hothorn of the Salk Institute reports that a small steroid molecule on the outside of the plant cell assists in the transmembrane signaling process. By contrast, this sort of molecule and its receptor is generally located inside the nuclei of animal cells.

While studying transmembrane signaling in plants, Hothorn and colleagues observed the steroid, shown in yellow, attach to a membrane-bound receptor, shown in blue. This attachment enabled the steroid's counterpart--a co-receptor protein, shown in orange--to bind to the blue receptor. Once bound, the orange co-receptor and the blue receptor become glued together by the yellow steroid, allowing their intracellular domains to touch and initiate communication.
In the case observed by Hothorn, transmembrane signaling initiated plant growth.

Source National Science Fundation

Teens look to parents more than friends for sexual role models

Recent adolescent sexual health study shatters stereotypes

This release is available in French. MONTREAL, June 15, 2011 – The results of a national online study show that 45% consider their parents to be their sexuality role model. Shattering stereotypes that parents and society hold about teen sexuality, the survey also revealed that only 32% looked to their friends and just 15% took inspiration from celebrities. Dr. Jean-Yves Frappier, a researcher at the University of Montreal's affiliated CHU Sainte-Justine Hospital Research Centre will be presenting the results at the Canadian Paediatric Society's 88th Annual Conference on June 18, 2011.

Importantly, the survey also revealed that many of the teenagers who look to their parents live in families where sexuality is openly discussed, and that moreover, teenagers in these families have a greater awareness of the risks and consequences of sexually transmitted infections. "Good communication within families and especially around sexual health issues is associated with more responsible behaviours," Frappier said.
However, 78% of the mothers who participated in the survey believed that their children modeled their friends' sexual behaviour, and that a lack of involvement of communication with fathers is especially detrimental. "Parents seem to underestimate their role and the impact that they have," Frappier noted. "Health professionals and the media have an important role to play in empowering parents and enabling them to increase their communications with their children with regards to sexual health issues."

The survey involved 1139 mothers of teenagers and 1171 youths between 14 and 17 years of age. The questionnaire touched on topics such as sources of sexual health information, communication about sexual health, family functioning and sexual activities. This study was financed in part by a grant from Merck Frosst Co. The University of Montreal is known officially as Université de Montréal. The Research Centre of the CHU Sainte-Justine is known officially as the Centre de recherche du Centre hospitalier universitaire Sainte-Justine.

Source  EurekaAlert!

Mother-to-daughter womb transplant maybe next year

Has a successful womb transplant actually been done?
No, but a team led by Mats Brännström of the University of Gothenburg's Sahlgrenska Hospital in Sweden is preparing to try early next year. He told New Scientist that his team is reviewing 10 potential patients, and hoping to transplant wombs into maybe five or six who are most suitable.

So why all the fuss now?
One of the potential donors, a British 56-year-old called Eva Ottosson, told journalists about a proposal to donate her womb to her 25-year-old daughter, Sara, who lives in Stockholm, Sweden. Sara has a condition called Mayer-Rokitansky-Kuster-Hauser syndrome, which means she has no uterus herself, and is also missing parts of her vagina. If Sara is chosen for the procedure and it works, her eggs will be fertilised by her partner's sperm and implanted in the same womb from which she herself was born.

Has a womb transplant been attempted before?
Yes. In 2000, Saudi Arabian surgeons implanted a womb into a 26-year-old woman who had had her own uterus removed at age 20 because of serious bleeding following a caesarean section. But they had to remove it 99 days later because of blood clots in associated blood vessels. The donor was a 46-year-old who had been advised to have a hysterectomy because of ovarian cysts. The news came to light in 2002 at a scientific meeting.

How successful has the procedure been in animals?
Brännström's group has done a series of experiments in progressively larger animals. In 2002, mice with transplanted wombs successfully gave birth to pups, and a year later Brännström revealed that the pups were healthy and able to breed normally. Brännström told New Scientist today that since then, he has successfully transplanted wombs into sheep and baboons, always from related donors. In much more recent, unpublished research, however, he demonstrated in rats that it's possible to transplant wombs from unrelated females.

When it comes to people, what will the procedure involve?
Brännström says he will transplant the womb itself, plus all uterine arteries and veins to supply and drain blood from the organ. No nerves will be transplanted. Then the recipient will receive low doses of immunosuppressive drugs to prevent rejection. He expects the organ will be accepted more easily than most transplants because pregnancy itself is an immunoprivileged condition, in which foreign material from the father is accepted by the body's immune system. An immediate pregnancy "will probably help the uterus to be accepted", he says.

What are the major hurdles?
Brännström says that the surgery itself will be the most difficult step. Compared to other, relatively isolated organs, such as the kidneys, the uterus is deeply embedded and hard to get at, and so may be technically difficult to transplant. "But we've overcome it in all animal models," he says.

And the risks?
Rejection is the main worry. And as with all pregnancies, there are risks of hypertension, diabetes and many other complications.

If a woman has no womb at all, or one that's damaged, wouldn't it be simpler just to fertilise her eggs and implant them in the womb of a surrogate mother?
"That would be a reasonable alternative," says Brännström. But in many countries, including Sweden, surrogacy is illegal, he says. Also, there may be extra physical strain and risks for older women, such as Sara's mother, in carrying babies – although Brännström acknowledges that surgery to remove the organ is also risky for older donors.

Is anyone else attempting this?
Other groups investigating the possibility include one led by Richard Smith of the Chelsea and Westminster Hospital in London, and another led by Giuseppe Del Priore at the New York Downtown Hospital.

So will it be an unseemly race to be first?
Brännström says not. He says the teams all know each other and cooperate, and all are keen for the procedure to work, whoever does it first.

Finally, will scientists ever develop an artificial womb?
Far fetched. Forget Brave New World for now – although in 1992, Japanese researchers did successfully sustain a goat fetus to term in a tank of nutrients, the nearest thing yet to an artificial womb. The fetus had been removed from the mother about three-quarters of the way through pregnancy.

Source New Scientist

Two isolates from E. coli outbreak available

An outbreak of Escherichia coli causing a severe illness called hemolytic-uremic syndrome (HUS) began in Germany on May 2, 2011 and has killed more than 20 people and sickened more than 2,000. The organism causing the outbreak has been identified as a strain of E. coli O104:H4 that produces a Shiga toxin and causes an illness similar to infection with E. coli O157:H7. Two isolates from this outbreak have been sequenced. Both strains, TY-2482 and LB226692, have been annotated and are now available from Virginia Bioinformatics Institute's (VBI's) Pathosystems Resource Integration Center (PATRIC, patricbrc.org), which is funded by the National Institute of Allergy and Infectious Diseases.

 Escherichia coli

In the rush to save lives, many laboratories are analyzing these genomes and providing data to the research community. Bruno Sobral, PATRIC's principal investigator, commented, "The PATRIC team is working around the clock to help the scientific community address this emergency. Analyses such as these provide insights into the origin of highly pathogenic strains and potential response strategies."

The two genomes have been annotated with Rapid Annotation using Subsystem Technology (RAST), making them consistent with the 184 E. coli genomes and the total 2,865 bacterial genomes available at PATRIC. The proteins conserved across all E. coli have been used to generate a preliminary phylogenetic tree that is based on 166640 characters across 527 genes in 354 taxa. This tree shows that the two new strains are most closely related to the pathogenic, enteroaggregative strain 559899, which may give additional insight into its origin. The tree is available in interactive form on the PATRIC website (http://patricbrc.org/portal/portal/patric/Phylogeny?cType=taxon&cId=561). For a comparison of the RAST annotations with the other publicized annotations, visit http://theseed.org/ecoli/.

As can be seen in the PATRIC Protein Family Sorter (http://patricbrc.org/portal/portal/patric/FIGfamSorterB?cType=taxon&cId=561&dm=result), the proteins from these two new pathogenic strains have several unique islands as compared to other E. coli genomes. Further investigation of these islands and unique proteins may yield clues as to virulence or intervention strategies for the new strains. The "heatmap" tab of the Protein Family Sorter presents a graphical view presence and absence of the proteins across the E. coli genomes.

Much of the information in PATRIC is updated on an ongoing basis including:

• An interactive Disease Map with outbreak information. Visit http://patricbrc.org/portal/portal/patric/DiseaseOverview?cType=taxon&cId=562 and then select the Disease Map tab.
• The PATRIC Google news search for countermeasures and other information (http://patricbrc.org/portal/portal/patric/GSearch?dm=countermeasure&kw=Escherichia+coli+TY-2482).

PATRIC is performing additional analyses, including collecting a list of the important genes identified, and will be providing gene trees and multiple sequence alignments of the genes with their closest homologs. Updates will be posted at http://enews.patricbrc.org/

Source EurekaAlert!

Canine telepathy?

Can dogs read our minds? How do they learn to beg for food or behave badly primarily when we're not looking? According to Monique Udell and her team, from the University of Florida in the US, the way that dogs come to respond to the level of people’s attentiveness tells us something about the ways dogs think and learn about human behavior. Their research, published online in Springer's journal Learning & Behavior, suggests it is down to a combination of specific cues, context and previous experience.

Recent work has identified a remarkable range of human-like social behaviors in the domestic dog, including their ability to respond to human body language, verbal commands, and to attentional states. The question is, how do they do it? Do dogs infer humans' mental states by observing their appearance and behavior under various circumstances and then respond accordingly? Or do they learn from experience by responding to environmental cues, the presence or absence of certain stimuli, or even human behavioral cues?

Udell and colleagues' work sheds some light on these questions.Udell and team carried out two experiments comparing the performance of pet domestic dogs, shelter dogs and wolves given the oportunity to beg for food, from either an attentive person or from a person unable to see the animal. They wanted to know whether the rearing and living envi-ronment of the animal (shelter or human home), or the species itself (dog or wolf), had the greater impact on the animal's performance.They showed, for the first time that wolves, like domestic dogs, are capable of begging successfully for food by approaching the attentive human. This demonstrates that both species - domesticated and non-domesticated - have the capacity to behave in accordance with a human's attentional state. In addition, both wolves and pet dogs were able to rapidly improve their performance with practice.

The authors also found that dogs were not sensitive to all visual cues of a human's attention in the same way. In particular, dogs from a home environment rather than a shelter were more sensitive to stimuli predicting attentive humans. Those dogs with less regular exposure to humans performed badly on the begging task. According to the researchers, "These results suggest that dogs' ability to follow human actions stems from a willingness to accept humans as social companions, combined with conditioning to follow the limbs and actions of humans to acquire reinforcement. The type of attentional cues, the context in which the command is presented, and previous experience are all important."

Source Springer

How killer immune cells avoid killing themselves

After eight years of work, researchers have unearthed what has been a well-kept secret of our immune system's success. The findings published online on June 9th in Immunity, a Cell Press publication, offer an explanation for how specialized immune cells are able to kill infected or cancerous cells without killing themselves in the process.

The focus of the study is a molecule known as perforin, whose job it is to open up a pore in cells targeted for destruction. With that pore in place, proteases known as granzymes can enter target cells and destroy them.
Perforin is one of the most critical ingredients for a functional immune system. Without it, mice succumb to viral illness and lymphoma. Humans born without a working perforin gene develop an aggressive immunoregulatory disorder in the first few months of life and usually die unless treated with cytoxic drugs or a bone marrow transplant.

But perforin itself is an incredibly destructive molecule. "Perforin forms a massive pore," said Ilia Voskoboinik of the Peter MacCallum Cancer Centre in Australia. "It allows almost any protein to diffuse into a target cell. A few hundred molecules of perforin is sufficient to obliterate any cell."
When the immune cells known as cytotoxic lymphocytes (including cytotoxic T lymphocytes and natural killer cells) are activated, "they produce a massive amount of perforin, yet the cells are fine," Voskoboinik said. The question was: how do our immune cells manage such toxic cargo without endangering themselves?
Before perforin is released, the cells that produce it have to transport it from one part of the cell to another. That transport chain starts in a component of the cell known as the endoplasmic reticulum (ER). From there, it moves to the Golgi and into secretory granules where it is packaged together with granzymes. It is those secretory granules that ultimately fuse with the plasma membrane of the cytotoxic cell and allow its release into the junctions between the immune cell and the cell it aims to kill.

Scientists used to think perforin had an inhibitory domain within its structure that was only removed once they were safely stored in the secretory granules. (The acidic environment within secretory granules keeps perforin inactive until its release.) But Voskoboinik's team purified perforin and found that the protein was always active regardless of whether they had removed the supposed inhibitory domain or not.
"It seeded doubt about how perforin is inhibited," he says. "It was a puzzle. Perforin was fully functional but for some reason it couldn't kill the cell [in which it was synthesized]."
The real danger zone for the cell when it comes to perforin is the ER, Voskoboinik explained. Conditions there should be ideal for perforin to work, but something keeps it from doing so. The new study links that protection to a single amino acid at one end of the perforin protein. When that amino acid is substituted with another, perforin doesn't make it to the Golgi compartment, it builds up in the ER, and the cell dies.
"Perforin goes from zero to extremely high levels within 24 hours and it has everything it needs to be functional," Voskoboinik said. "The cell relies on a really efficient transport system to move perforin away from the danger zone and as a result the cell is absolutely protected."

The findings "close a chapter" in our understanding of the immune system that has existed in the field since perforin was discovered almost 25 years ago, Voskoboinik says. "It was one of those things that was out there on Olympus untouched. Everyone would just stare at it. That's what got us interested."

Source  EurekaAlert!

Why animals don't have infrared vision

Johns Hopkins researchers uncover the source of the visual system's 'false alarms'.

On rare occasion, the light-sensing photoreceptor cells in the eye misfire and signal to the brain as if they have captured photons, when in reality they haven't. For years this phenomenon remained a mystery. Reporting in the June 10 issue of Science, neuroscientists at the Johns Hopkins University School of Medicine have discovered that a light-capturing pigment molecule in photoreceptors can be triggered by heat, as well, giving rise to these false alarms.

"A photon, the unit of light, is just energy, which, when captured by the pigment rhodopsin, most of the time causes the molecule to change shape, then triggering the cell to send an electrical signal to the brain to inform about light absorption," explains King-Wai Yau, Ph.D., professor of neuroscience at Johns Hopkins and member of its Center for Sensory Biology. "If rhodopsin can be triggered by light energy," says Yau, "it may also be occasionally triggered by other types of energy, such as heat, producing false alarms. These fake signals compromise our ability to see objects on a moonless night. So we tried to figure it out; namely, how the pigment is tripped by accident."

"Thermal energy is everywhere, as long as the temperature is above absolute zero," says neuroscience research associate Dong-Gen Luo, Ph.D. "The question is: How much heat energy would it take to trigger rhodopsin and enable it to fire off a signal, even without capturing light?" says Johns Hopkins Biochemistry, Cellular and Molecular Biology graduate student Wendy Yue.
For 30 years, the assumption was that heat could trigger a pigment molecule to send a false signal, but through a mechanism different from that of light, says Yau, because it seemed, based on theoretical calculations: that very little thermal energy was required compared to light energy.

But the theory, according to Yau, was based mainly on the pigment rhodopsin. However, rhodopsin is mainly responsible for seeing in dim light and is not the only pigment in the eye; other pigments are present in red-, green- and blue-sensitive cone photoreceptors that are used for color and bright-light vision. Although researchers are able to measure the false events of rhodopsin from a single rhodopsin-containing cell, a long-standing challenge has been to take measurements of the other pigments. "The electrical signal from a single cone pigment molecule is so small in a cone cell that it is simply not measurable," says Luo. "So we had to figure out a new way to measure these false signals from cone pigments."
By engineering a rod cell to make human red cone pigment, which is usually only found in cone cells, Yau's team was able to measure the electrical output from an individual cell and calculate this pigment's false signals by taking advantage of the large and detectable signals sent out from the cell.

As for blue cone pigment, "Nature did the experiment for us," says Yau. "In many amphibians, one type of rod cells called green rods naturally express a blue cone pigment, as do blue cones." So to determine whether heat can cause pigment cells to misfire, the team, working in the dark, first cooled the cells, and then slowly returned the cells to room temperature, measuring the electrical activity of the cells as they warmed up. They found that red-sensing pigment triggers false alarms most frequently, rhodopsin (bluish-green-sensing pigment) triggers falsely less frequently, and blue-sensing pigment does so even less.

"This validates the 60-year-old Barlow's hypothesis that suggested the longer wavelength the pigment senses—meaning the closer to the red end of the spectrum—the noisier it is," says Yau. And this finding led the team to develop and test a new theory: that heat can trigger pigments to misfire, by the same mechanism as light.
Pivotal to this theory is that visual pigment molecules are large, complex molecules containing many chemical bonds. And since each chemical bond has the potential to contain some small amount of thermal energy, the total amount of energy a pigment molecule could contain can, in theory, be enough to trigger the false alarm.
"For a long time, people assumed that light and heat had to trigger via different mechanisms, but now we think that both types of energy, in fact, trigger identical changes in the pigment molecules," says Yau. Moreover, since longer wavelength pigments have higher rates of false alarms, Yau says this may explain why animals never evolved to have infrared-sensing pigments.

"Apart from putting to rest a long-standing debate, it's a wake-up call for researchers to realize that biomolecules in general have more potential thermal energy than previously thought," says Luo.

Source  EurekaAlert!

Bacterial roundabouts determine cell shape. Max Planck scientists decipher important mechanisms of bacterial cell wall synthesis

June 03, 2011 Almost all bacteria owe their structure to an outer cell wall that interacts closely with the supporting MreB protein inside the cell. As scientists at the Max Planck Institute for Biochemistry and at the French INRA now show, MreB molecules assemble into larger units, but not - as previously believed – into continuous helical structures. The circular movement of these units along the inside of the bacterial envelope is mediated by cell wall synthesis, which in turn requires the support of MreB. This mutual interaction may be a widespread phenomenon among bacteria and opens up new avenues for therapeutic intervention. The bacterial cell wall is already a major target for antibiotics. (Science, June 3, 2011)

Bacillus subtilis cell with several patches of Mbl (MreB-like protein) fused to the green fluorescent protein. Colors represent overlay of images taken by total internal reflection fluorescence microscopy (TIRFM, red), epifluorescence (green) and transmitted light (blue, indicates cell outline).

Even single cells have to maintain their shape: In higher organisms, the supporting structures of the cytoskeleton, which include filament networks made of the protein actin, take care of this job. The much smaller bacterial cells possess similar cytoskeletal structures, such as the actin related protein MreB. Up to now, scientists believed that this molecule forms spiral structures on the inside of the cell membrane in non-spherical bacteria, which serve as a scaffold for the assembly of the comparatively rigid cell wall.

Using innovative imaging technologies based on fluorescent microscopy, the scientists in the laboratory of Roland Wedlich-Söldner have now been able to show that MreB proteins do not form such highly ordered structures – and yet are organized in more complex ways than they had previously assumed. “MreB molecules assemble into larger units, or patches. They move in circular paths along the inside of the cell membrane, but without following a preferred direction”, explains Julia Domínguez-Escobar, PhD student at the Max Planck Institute of Biochemistry.

A highly unexpected finding of the study was that the movement of MreB patches relies on a functioning cell wall. MreB structures cannot move on their own but are pulled along the bacterial envelope by the newly synthesized cell wall material. The MreB patches are located at the inside, the cell wall at the outside of the cell membrane. Thus, interaction is likely mediated by molecules that span the cell membrane. These molecular adapters link the incorporation of newly synthesized cellular material with the MreB units, which thereby follow the permanently growing cell wall structures.

Many parts of the cell wall are almost universally conserved in bacteria, making it likely that the newly discovered mechanism is widespread. Hence, the results could play an important role for the further investigation of bacterial cells, but also for medicine: “Cell wall synthesis already is a key target for antibiotics. New insights into the structure of the cell wall could open up urgently needed therapeutic alternatives”, hopes Wedlich-Söldner.

Source Max Planck Gesellschaft

Treasure Is Found Deep in a Gold Mine: A New Worm

Single-cell organisms have been known to live deep in the earth, more than 9,000 feet below the surface.

 Halicephalobus mephisto, a new species of bacteria feeding nematode, was discovered in a South African gold mine more than 9,000 feet below the surface. 

But until now, it was thought that the temperature, energy, oxygen and space constraints of the subsurface biosphere were too extreme for multicellular organisms.
Now, Tullis Onstott, a geoscientist at Princeton University, and colleagues from Belgium, South Africa and the
Netherlands report their discovery of a small multicellular worm that dwells at these depths.

The worm, known as Halicephalobus mephisto, is tiny — two hundredths of an inch at the longest — and belongs to the vast and diverse phylum of nematodes. Its discovery, in a shaft of the Beatrix gold mine in South Africa, is reported in the journal Nature.

The worm appears to tolerate temperatures exceeding 100 degrees Fahrenheit and feeds on subsurface bacteria.
The researchers studied soil and water samples from the mines to determine that the newly identified nematodes are uniquely subsurface organisms. The samples indicated that while the nematodes live in the deep fracture water of the mines, they do not inhabit the surface-level mining water.

The researchers say their findings should be considered as scientists search for life in other extreme conditions — like those on Mars and other planets in the solar system.

Source The New York Times

Why caffeine can reduce fertility in women

Caffeine reduces muscle activity in the Fallopian tubes that carry eggs from a woman's ovaries to her womb. "Our experiments were conducted in mice, but this finding goes a long way towards explaining why drinking caffeinated drinks can reduce a woman's chance of becoming pregnant," says Professor Sean Ward from the University of Nevada School of Medicine, Reno, USA. Ward's study is published today in the British Journal of Pharmacology.

Human eggs are microscopically small, but need to travel to a woman's womb if she is going to have a successful pregnancy. Although the process is essential for a successful pregnancy, scientists know little about how eggs move through the muscular Fallopian tubes. It was generally assumed that tiny hair-like projections, called cilia, in the lining of the tubes, waft eggs along assisted by muscle contractions in the tube walls.
By studying tubes from mice, Professor Ward and his team discovered that caffeine stops the actions of specialised pacemaker cells in the wall of the tubes. These cells coordinate tube contractions so that when they are inhibited, eggs can't move down the tubes. In fact these muscle contractions play a bigger role than the beating cilia in moving the egg towards the womb. "This provides an intriguing explanation as to why women with high caffeine consumption often take longer to conceive than women who do not consume caffeine," says Professor Ward.

Discovering the link between caffeine consumption and reduced fertility has benefits. "As well as potentially helping women who are finding it difficult to get pregnant, a better understanding of the way Fallopian tubes work will help doctors treat pelvic inflammation and sexually-transmitted disease more successfully," says Professor Ward. It could also increase our understanding of what causes ectopic pregnancy, an extremely painful and potentially life-threatening situation in which embryos get stuck and start developing inside a woman's Fallopian tube.

Source EurekaAlert!

The role of bacteria in weather events

NEW ORLEANS, LA – May 24, 2011 -- Researchers have discovered a high concentration of bacteria in the center of hailstones, suggesting that airborne microorganisms may be responsible for that and other weather events. They report their findings today at the 111th General Meeting of the American Society for Microbiology in New Orleans.

"Bacteria have been found within the embryo, the first part of a hailstone to develop. The embryo is a snapshot of what was involved with the event that initiated growth of the hailstone," says Alexander Michaud of Montana State University in Bozeman, who presented the research.
Michaud and his colleagues analyzed hailstones over 5 centimeters in diameter that were collected on the University campus after a storm in June 2010. The large hailstones were seperated into 4 layers and the meltwater from each layer was analyzed. The number of culturable bacteria was found to be highest in the inner cores of the hailstone.

"In order for precipitation to occur, a nucleating particle must be present to allow for aggregation of water molecules," says Michaud. "There is growing evidence that these nuclei can be bacteria or other biological particles."
Michaud's research is part of a growing field of study focusing on bioprecipitation, a concept where bacteria may initiate rainfall and other forms of precipitation including snow and hail. The formation of ice in clouds, which is necessary for snow and most rainfall events, requires ice nuclei (IN), particles that the ice crystals can grow around.

"Aerosols in clouds play key roles in the processes leading to precipitation due to their ability to serve as sites for ice nucleation. At temperatures warmer than -40 degrees Celsius ice formation is not spontaneous and requires an IN," says Brent Christner of Louisiana State University, also presenting at the meeting.
A diverse range of particles are capable of serving as IN, but the most active naturally occurring IN are biological in origin, capable of catalyzing ice formations at temperatures near -2 degrees Celsius. The most well-studied biological IN is the plant pathogen Psuedomonas syringae.
"Ice nucleating strains of P. syringae possess a gene that encodes a protein in their outer membrane that binds water molecules in an ordered arrangement, providing a very efficient nucleating template that enhances ice crystal formation," says Christner.

Aerosol-cloud simulation models imply that high concentrations of biological IN may influence the average concentration and size of ice crystals in clouds, horizontal cloud coverage in the free troposphere, precipitation levels at the ground and even insulation of the earth from solar radiation.
"Evidence for the distribution of biological IN in the atmosphere coupled with the warm temperatures at which they function as IN has implied that biological IN may play a role in the Earth's hydrological cycle and radiative balance," says Christner.

Sour ce EurekaAlert!

Happy guys finish last, says new study on sexual attractiveness

Women find happy guys significantly less sexually attractive than swaggering or brooding men, according to a new University of British Columbia study that helps to explain the enduring allure of "bad boys" and other iconic gender types.

The study – which may cause men to smile less on dates, and inspire online daters to update their profile photos – finds dramatic gender differences in how men and women rank the sexual attractiveness of non-verbal expressions of commonly displayed emotions, including happiness, pride, and shame.
Very few studies have explored the relationship between emotions and attraction, and this is the first to report a significant gender difference in the attractiveness of smiles. The study, published online today in the American Psychological Association journal Emotion, is also the first to investigate the attractiveness of displays of pride and shame.

"While showing a happy face is considered essential to friendly social interactions, including those involving sexual attraction – few studies have actually examined whether a smile is, in fact, attractive," says Prof. Jessica Tracy of UBC's Dept. of Psychology. "This study finds that men and women respond very differently to displays of emotion, including smiles."

In a series of studies, more than 1,000 adult participants rated the sexual attractiveness of hundreds of images of the opposite sex engaged in universal displays of happiness (broad smiles), pride (raised heads, puffed-up chests) and shame (lowered heads, averted eyes).

The study found that women were least attracted to smiling, happy men, preferring those who looked proud and powerful or moody and ashamed. In contrast, male participants were most sexually attracted to women who looked happy, and least attracted to women who appeared proud and confident.

"It is important to remember that this study explored first-impressions of sexual attraction to images of the opposite sex," says Alec Beall, a UBC psychology graduate student and study co-author. "We were not asking participants if they thought these targets would make a good boyfriend or wife – we wanted their gut reactions on carnal, sexual attraction." He says previous studies have found positive emotional traits and a nice personality to be highly desirable in a relationship partners.

Tracy and Beall say that other studies suggest that what people find attractive has been shaped by centuries of evolutionary and cultural forces. For example, evolutionary theories suggest females are attracted to male displays of pride because they imply status, competence and an ability to provide for a partner and offspring.
According to Beall, the pride expression accentuates typically masculine physical features, such as upper body size and muscularity. "Previous research has shown that these features are among the most attractive male physical characteristics, as judged by women," he says.

The researchers say more work is needed to understand the differing responses to happiness, but suggest the phenomenon can also be understood according to principles of evolutionary psychology, as well as socio-cultural gender norms.

For example, past research has associated smiling with a lack of dominance, which is consistent with traditional gender norms of the "submissive and vulnerable" woman, but inconsistent with "strong, silent" man, the researchers say. "Previous research has also suggested that happiness is a particularly feminine-appearing expression," Beall adds.

"Generally, the results appear to reflect some very traditional gender norms and cultural values that have emerged, developed and been reinforced through history, at least in Western cultures," Tracy says. "These include norms and values that many would consider old-fashioned and perhaps hoped that we've moved beyond."

Displays of shame, Tracy says, have been associated with an awareness of social norms and appeasement behaviors, which elicits trust in others. This may explain shame's surprising attractiveness to both genders, she says, given that both men and women prefer a partner they can trust.

While this study focused on sexual attraction between heterosexual men and women in North America, the researchers say future studies will be required to explore the relationship between emotions and sexual attractiveness among homosexuals and non-Western cultures.

Overall, the researchers found that men ranked women more attractive than women ranked men.

Source  EurekaAlert!

Clone army steals genes from other species

Species: Corbicula fluminea

Habitat: originally from south-east Asia, this un-frisky mollusc has spread round the world

Anyone who thinks that invading clone armies are the preserve of science fiction should think again. One is marching across Europe and north America at this very moment.

 This seemingly celibate clam has sex on occasion

The clones in question are Asian clams, or Corbicula fluminea, a species of freshwater mollusc that originated in China and Taiwan. They aren't popular in their new homes, clogging up water intake pipes and outcompeting native clams. But they have some remarkable sexual talents.

Each clam is a hermaphrodite with both male and female sexual organs – by fertilising its own eggs, it can clone itself. It is also a parasite that commandeers the eggs of other clams for its own purposes and, every so often, it steals their genes too.

The trouble with celibacy

By not having sex, C. fluminea avoids the risks of finding a mate – just ask female cowpea weevils or male spiders why that's a good idea. But if all individuals of a species go without sex, over time harmful mutations build up and the species can go extinct.

"There are almost certainly systems where strict asexuality arises, and the lineages go extinct over evolutionary time – thousands or tens of thousands of years," says David Hillis of the University of Texas at Austin. For an asexual species to survive in the long run, it must refresh its genes every so often.

The poster children for asexuality are bdelloid rotifers, tiny animals that have gone without sex for 80 million years. But they cheat: they steal swathes of genes from bacteria, fungi and plants.

Other asexual animals have similar tricks, but until now it was thought C. fluminea had no way to get new genes. Now Hillis has figured out how they do it.

No girl genes, please

When a clam wants to reproduce, it uses its own sperm to fertilise its own egg. At this point the embryo isn't on course to be a clone, because the genes from the sperm and egg could get jumbled up – in effect, the clam would have sex with itself. But the embryo ejects all the genes that came from the egg, so only the genes from the sperm make it into the developing clone.

Sometimes the clams pull the same trick with eggs from other clams of the same species, fertilising them and then dumping their genes. In effect, they parasitise each other's eggs.

That isn't so bad: at least everyone parasitises everyone else. But it's horribly bad luck for clams of a sexual clam species if an Asian clam parasitises their eggs as they have no comeback.

It's this commandeering of other species' eggs that Hillis thinks is at the root of the clams' survival. He and his colleagues compared the DNA from 10 Corbicula species, some of which were sexual and some asexual. They found that some genes in the clams' nuclear DNA were the same in both sexual and asexual species. That wouldn't happen if the asexual species were strict cloners.

An injection of genes

Hillis thinks this can be explained if the asexual clams sometimes fertilise eggs from another species and retain some or all of their genes, rather than ejecting them. That would give their offspring an injection of fresh genes. He says this sort of genetic theft may be much more common in the animal kingdom than anyone realises.

He points to cases where two asexual species of Corbicula were introduced to north America, and over time one species captured mitochondrial genes from the other. Capturing nuclear genes is much rarer, but the clams' DNA suggests it does happen.

The lesson is clear: everyone is at it, and it's for their own good. Even C. fluminea and their seemingly celibate cousins have sex on the odd occasion.

Journal reference: Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.1106742108

Source New Scientist

Gulf currents primed bacteria to degrade oil spill

A new computer model of the Gulf of Mexico in the period after the oil spill provides insights into how underwater currents may have primed marine microorganisms to degrade the oil.

"It is called dynamic auto-inoculation. Parcels of water move over the ruptured well, picking up hydrocarbons. When these parcels come back around and cross back over the well, the bacteria have already been activated, are more abundant than before, and degrade hydrocarbons far more quickly," says David Valentine of the University of California, Santa Barbara, speaking today at the 111th General Meeting of the American Society for Microbiology.

Valentine has been studying microbial communities and the fate of chemicals 4000 feet below the surface from the Deepwater Horizon oil spill since June of 2010. Valentine and his colleagues at UC Santa Barbara, the University of Rijeka in Croatia, and the Naval Research Laboratory recently developed a computer simulation by coupling the Naval Research Laboratory's physical oceanographic model with their own discoveries and knowledge of the microbes responsible for breaking down the chemicals.

"We took the physical model of the deep Gulf of Mexico, added the hydrocarbons and bacteria, set reasonable guidelines for metabolism, and let them eat starting at day 1 of the spill," says Valentine.
To confirm that the model was providing them with an accurate picture of what had happened they compared the model to spot measurements they and others had previously made in the Gulf.
"The model predicts the kinds of distributions observed at different times and locations. The assumptions that went into the model appear to be reasonable," says Valentine.

The most interesting observation they found using the model was dynamic auto-inoculation. Many parcels of water circulated in and out of the source area. Each iteration allowed the bacterial populations to increase in number and degrade the chemicals more rapidly.

"The more recirculation you have, the more quickly the hydrocarbons will be consumed," says Valentine. "We have developed a model that combines the large-scale movement of the water with the metabolism of the microbes. From that we are observing a phenomenon that molded the distribution of the bacteria over time and space, and that are consistent with real-world observations in the Gulf of Mexico."

Source EurekaAlert!