Study of 123 ungulate species shows males are born with smaller molars, expecting shorter lives
In the September issue of The American Naturalist, Juan Carranza (Biology and Ethology Unit, University of Extremadura, Spain) and Javier Pérez-Barbería (Macaulay Institute, United Kingdom) offer a new explanation for why males of ungulate species subjected to intense competition are born with lower survival expectancies than females. The research reveals that male ungulates have smaller molars relative to their body size – and hence less durable teeth that will wear out sooner, which might contribute to their shorter lives compared with females.
Roaring male Iberian red deer with females
(photograph by Juan Carranza)
Natural selection favors reproduction rather than survival; the cost of reproduction compromises survival. Males of species subjected to intense male-male competition for access to females are known to have shorter life expectancies than females. Earlier aging in males might be related to higher reproductive costs, especially when lifetime reproductive success in males takes place within the few years when they can win contests and maintain their dominance.
By comparing body and dental size of males and females of 123 species of ungulates, the authors offer another compelling explanation for why male ungulates lead shorter lives. They estimated the pattern of change of these traits along the evolutionary development of the group and found that for species where a single male has many females and where the males and females are different sizes, the rate of increase of dental size was lower than that of body size. As a result, smaller teeth (in comparison to body size) are produced in males. It is possible that natural selection did not produce larger, more durable teeth because there was no reproductive return from it, since males in these species do not generally increase their success by living longer after prime age.
“These findings,” the authors state, “provide us with interesting insights into how natural and sexual selection design our bodies and their longevity.”
Juan Carranza and F. Javier Pérez-Barbería, “Sexual selection and senescence: male size-dimorphic ungulates evolved relatively smaller molars than females”, The American Naturalist (2007) volume 170:370–380. DOI: 10.1086/519852
As a retired advanced weather spotter for the National Weather Service in Pontiac Michigan, I have observed numerous weather phenomon. I have “ball lightning” on video.
St. Elmo’s Fire is an electrical weather phenomenon in which visible plasma is created by a coronal discharge originating from a grounded object in an atmospheric electric field (such as those generated by thunderstorms).
St. Elmo’s fire is named after Erasmus of Formiae (also called St. Elmo), the patron saint of sailors (who sometimes held its appearance to be auspicious). Alternatively, Peter Gonzalez is said to be the St. Elmo after whom St. Elmo’s fire has its name.
Ball lightning is often erroneously identified as St. Elmo’s Fire. They are separate and distinct meteorological phenomena.(Wikipedia)
Physically, St. Elmo’s Fire is a bright blue or violet glow, appearing like fire in some circumstances, from tall, sharply pointed structures such as lightning rods, masts, spires and chimneys, and on aircraft wings. St. Elmo’s Fire can also appear on leaves, grass, and even at the tips of cattle horns. Often accompanying the glow is a distinct hissing or buzzing sound.
Benjamin Franklin correctly observed in 1749 that it is electric in nature.
Although referred to as “fire”, St. Elmo’s Fire is in fact plasma. The electric field around the object in question causes ionization of the air molecules, producing a faint glow easily visible in low-light conditions. Approximately 1,000 – 30,000 volts per centimeter is required to induce St. Elmo’s Fire; however, this number is greatly dependant on the geometry of the object in question. Sharp points tend to require lower voltage levels to produce the same result because electric fields are more concentrated in areas of high curvature, thus discharges are more intense at the end of pointed object.
The nitrogen and oxygen in earth’s atmosphere causes St. Elmo’s Fire to fluoresce with blue or violet light; this is similar to the mechanism that causes neon lights to glow.
Whole-genome transfer raises questions about evolution, sequencing
Scientists at the University of Rochester and the J. Craig Venter Institute have discovered a copy of the entire genome of a bacterial parasite residing inside the genome of its host species.
The finding, reported in today’s Science, suggests that lateral gene transfer—the movement of genes between unrelated species—may happen much more frequently between bacteria and multicellular organisms than scientists previously believed, posing dramatic implications for evolution.
Such large-scale heritable gene transfers may allow species to acquire new genes and functions extremely quickly, says Jack Werren, a principle investigator of the study.
Wolbachia in yellow with host cells in red.
The results also have serious repercussions for genome-sequencing projects. Bacterial DNA is routinely discarded when scientists are assembling invertebrate genomes, yet these genes may very well be part of the organism’s genome, and might even be responsible for functioning traits.
“This study establishes the widespread occurrence and high frequency of a process that we would have dismissed as science fiction until just a few years ago,” says W. Ford Doolittle, Canada Research Chair in Comparative Microbial Genomics at Dalhousie University, who is not connected to the study. “This is stunning evidence for increased frequency of gene transfer.”
Fruit fly ovaries showing wolbachia infection within.
“It didn’t seem possible at first,” says Werren, professor of biology at the University of Rochester and a world-leading authority on the parasite, called Wolbachia. “This parasite has implanted itself inside the cells of 70 percent of the world’s invertebrates, coevolving with them. And now, we’ve found at least one species where the parasite’s entire or nearly entire genome has been absorbed and integrated into the host’s. The host’s genes actually hold the coding information for a completely separate species.”
Wolbachia may be the most prolific parasite in the world—a “pandemic,” as Werren calls it. The bacterium invades a member of a species, most often an insect, and eventually makes its way into the host’s eggs or sperm. Once there, the Wolbachia is ensured passage to the next generation of its host, and any genetic exchanges between it and the host also are much more likely to be passed on.
Since Wolbachia typically live within the reproductive organs of their hosts, Werren reasoned that gene exchanges between the two would frequently pass on to subsequent generations. Based on this and an earlier discovery of a Wolbachia gene in a beetle by the Fukatsu team at the University of Tokyo, Japan, the researchers in Werren’s lab and collaborators at J. Craig Venter Institute (JCVI) decided to systematically screen invertebrates. Julie Dunning-Hotopp at JCVI found evidence that some of the Wolbachia genes seemed to be fused to the genes of the fruitfly, Drosophila ananassae, as if they were part of the same genome.
Michael Clark, a research associate at Rochester then brought a colony of ananassae into Werren’s lab to look into the mystery. To isolate the fly’s genome from the parasite’s, Clark fed the flies a simple antibiotic, killing the Wolbachia. To confirm the ananassae flies were indeed cured of the wolbachia, Clark tested a few samples of DNA for the presence of several Wolbachia genes.
To his dismay, he found them.
“For several months, I thought I was just failing,” says Clark. “I kept administering antibiotics, but every single Wolbachia gene I tested for was still there. I started thinking maybe the strain had grown antibiotic resistance. After months of this I finally went back and looked at the tissue again, and there was no Wolbachia there at all.”
Clark had cured the fly of the parasite, but a copy of the parasite’s genome was still present in the fly’s genome. Clark was able to see that Wolbachia genes were present on the second chromosome of the insect.
Clark confirmed that the Wolbachia genes are inherited like “normal” insect genes in the chromosomes, and Dunning-Hotopp showed that some of the genes are “transcribed” in uninfected flies, meaning that copies of the gene sequence are made in cells that could be used to make Wolbachia proteins.
Werren doesn’t believe that the Wolbachia “intentionally” insert their genes into the hosts. Rather, it is a consequence of cells routinely repairing their damaged DNA. As cells go about their regular business, they can accidentally absorb bits of DNA into their nuclei, often sewing those foreign genes into their own DNA. But integrating an entire genome was definitely an unexpected find.
Werren and Clark are now looking further into the huge insert found in the fruitfly, and whether it is providing a benefit. “The chance that a chunk of DNA of this magnitude is totally neutral, I think, is pretty small, so the implication is that it has imparted of some selective advantage to the host,” says Werren. “The question is, are these foreign genes providing new functions for the host” This is something we need to figure out.”
Evolutionary biologists will certainly take note of this discovery, but scientists conducting genome-sequencing projects around the world also may have to readjust their thinking.
Before this study, geneticists knew of examples where genes from a parasite had crossed into the host, but such an event was considered a rare anomaly except in very simple organisms. Bacterial DNA is very conspicuous in its structure, so if scientists sequencing a nematode genome, for example, come across bacterial DNA, they would likely discard it, reasonably assuming that it was merely contamination—perhaps a bit of bacteria in the gut of the animal, or on its skin.
But those genes may not be contamination. They may very well be in the host’s own genome. This is exactly what happened with the original sequencing of the genome of the anannassae fruitfly—the huge Wolbachia insert was discarded from the final assembly, despite the fact that it is part of the fly’s genome.
In the early days of the Human Genome Project, some studies appeared to show bacterial DNA residing in our own genome, but those were shown indeed to be caused by contamination. Wolbachia is not known to infect any vertebrates such as humans.
“Such transfers have happened before in the distant past” notes Werren. “In our very own cells and those of nearly all plants and animals are mitochondria, special structures responsible for generating most of our cells’ supply of chemical energy. These were once bacteria that lived inside cells, much like Wolbachia does today. Mitochondria still retain their own, albeit tiny, DNA, and most of the genes moved into the nucleus in the very distant past. Like wolbachia, they have passively exchanged DNA with their host cells. It’s possible wolbachia may follow in the path of mitochondria, eventually becoming a necessary and useful part of a cell.
“In a way, wolbachia could be the next mitochondria,” says Werren. “A hundred million years from now, everyone may have a wolbachia organelle.”
“Well, not us,” he laughs. “We’ll be long gone, but wolbachia will still be around.”
This research was funded by the National Science Foundation.
Media Contact: Ron Walli
Communications and External Relations
OAK RIDGE, Tenn., Aug. 29, 2007 — Mice that are part of the Collaborative Cross project at Oak Ridge National Laboratory are helping scientists around the world learn more about possible causes of drug abuse, diabetes, sleep disorders, stress and pain, kidney disease and a number of other conditions that affect millions of people.
The Collaborative Cross, begun in 2005 with a grant from the Ellison Medical Foundation, represents a fundamentally new way of conducting genetics research and aims to create 1,000 strains of mice that feature the genetic diversity of the world population. When completed in about five years, the research community will have access to an extremely versatile resource plus data that is the click of a mouse away. There will be other benefits as well.
“With our new facility at ORNL, we offer economies of scale for the production of populations of mice,” said Elissa Chesler, leader of the systems genetics group in the Biosciences Division. “Without having to maintain their own mouse colonies, researchers will have access to mice that will enable them to do experiments that cannot be done anywhere else.”
While conventional genetics studies have primarily involved stand-alone experiments aimed at discovering single gene variants, the Collaborative Cross represents the new approach that researchers say is necessary to develop a community resource for understanding the genetic and environmental complexity of human diseases. With this approach, using a reference population that allows for high genetic diversity and large sample size, researchers can more effectively examine combinations of genes responsible for diseases. This combination is what makes the Collaborative Cross special.
“We can stop blaming single genes for causing diseases,” Chesler said. “We now know that bad combinations of normal genes are at fault, and this mouse population will make it possible to determine complex causes and to develop drugs to treat those diseases.”
In one experiment at ORNL, William Lariviere of the University of Pittsburgh School of Medicine hopes to find genes that cause some people to be more sensitive to pain than others and to identify new drugs for treatment of different types of pain. The study involves collecting a standard set of thermal, chemical, inflammatory and mechanical sensitivity measures in groups of mice from 80 different lines in a genetic reference population called the BXD lines.
Data from Lariviere’s study will form an important foundation for integrative genomic analysis of pain. The results will be placed in the public domain through Web resource http://www.genenetwork.org.
“The BXD lines are a powerful tool for integration, but they do not have maximum precision and genetic diversity,” Lariviere said. “For that, we will collect additional trait data in the Collaborative Cross mouse population being created at ORNL.”
One area of specific interest to Lariviere is variations in the amount of messenger RNA (mRNA) produced by different individuals. This often determines how much of a particular protein is made, and that in turn might be related to biological pathways that are involved in processes such as pain perception.
“Because we will measure both the mRNA levels and the sensitivity levels in the same strains of mice, we will be able to efficiently not only study the genes that cause individual differences in pain sensitivity, but also identify the pathway of genes that make ideal targets for new pain drugs,” Lariviere said.
In another study, Michael Miles of Virginia Commonwealth University leads a team that hopes to learn more about the connection between anxiety and alcoholism. Working with Alex Putman and Chesler, the researchers have identified a region of a mouse chromosome that appears to significantly alter the effects of alcohol on anxiety.
“Understanding the basic mechanisms connecting brain events in anxiety and alcoholism could lead to better treatments for both disorders,” Miles said.
In this study, researchers used special strains of mice being raised and maintained at ORNL. Miles noted that the strains of mice used for his study are not available through any commercial source and offer a “great advantage to genetic studies of complex diseases.”
In upcoming months the researchers hope to identify the actual genes in this chromosome region that alter the response to alcohol.
In another study, Bruce O’Hara of the University of Kentucky is working to identify sleep- and wake-related genes. In addition to gaining a more thorough understanding of the sleep process, this research could lead to better drugs to help people with sleep disorders.
O’Hara’s study takes advantage of noninvasive piezoelectric sensors instead of conventional techniques that use electroencephalogram and eletromyogram recordings, which require surgical implants and cables that tether the mouse to a recording device. This limitation has made it impractical to study large numbers of animals, which is necessary in genetic screening, according to O’Hara.
These and other experiments are housed in ORNL’s Laboratory for Comparative Functional Genomics, a pathogen-free 36,000-square-foot facility that is home to approximately 30,000 mice. The lab, completed in 2004, boasts accommodations for 80,000 mice, cryogenic storage and other state-of-the-art features.
UT-Battelle manages Oak Ridge National Laboratory for the Department of Energy. Funding for the mouse facility is provided by DOE’s Office of Biological and Environmental Research within the Office of Science. The Ellison Medical Foundation supports basic biomedical research on aging relevant to understanding aging processes and age-related diseases and disabilities.
ANN ARBOR, Mich.— A camper who chases a grizzly but won’t risk unprotected sex. A sky diver afraid to stand up to the boss. New research shows that not all risk is created equal and people show a mixture of both risky and non-risky behaviors.
The survey also shows that men are significantly riskier than women overall.
The University of Michigan research refutes the standard theories of risk that group people as either risk-seeking or risk-avoiding, and suggests that we can have a mix of both risky and non-risky behavior depending on the type.
The study appears in the journal Evolutionary Psychology. Daniel Kruger, a research scientist at the U-M School of Public Health, and colleagues X.T. Wang, University of South Dakota, and Andreas Wilke, UCLA, identified areas of risk taking (risk domains) based on the types of challenges that our ancestors faced during many thousands of years of human evolution.
“People are complex,” said Kruger. “Just because somebody seems to be a big risk taker in one area doesn’t mean they will take risks in all areas.”
The types of risks identified include competition with other individuals; competition with other groups; mating and allocating resources for mate attraction; environmental risks (chasing a bear or skydiving); and fertility risks. The study showed that our tendencies for risk taking follow these different types of challenges.
“It is remarkable not just that we were able to identify different areas of risk taking, but also that many of the challenges faced by our ancestors are similar to challenges we face in our modern world today,” Kruger said.
People surveyed for the study were least likely to take fertility risks, and most likely to take risks related to social status in one’s group — like standing up to one’s boss. In all domains, men were significantly more risk taking than women. During human evolution, men competed for social status and resources in order to attract mates. Thus, this pattern is not surprising, Kruger said.
The risks that threaten fertility function differently than the others, Kruger said. Other types of risk have a possible benefit in terms of survival and reproduction. But with fertility risks, there is just a threat to reproduction. They can only cause harm in the evolutionary sense since they would only hurt our ability to procreate.
“Those were types of risks that weren’t attractive to other people, those risks were the least likely to be taken, and people saw those risks as unattractive in a potential mate,” Kruger said.
Although in most parts of the world, threats from predators may be limited to those making wilderness expeditions, we still live in a world with complex challenges involving other individuals and material investments. The basic elements of our social environment have not changed; we just live on a much larger scale.
The study appears in the latest issue of Evolutionary Psychology.
For more on Kruger visit: http://www.ns.umich.edu/htdocs/public/experts/ExpDisplay.php”ExpID=931
The University of Michigan School of Public Health has been working to promote health and prevent disease since 1941, and is consistently ranked among the top five schools in the country. Faculty and students in the school’s five academic departments and dozens of collaborative centers and institutes are forging new solutions to the complex health challenges of today, including chronic disease, health care quality and finance, emerging genetic technologies, climate change, socioeconomic inequalities and their impact on health, infectious disease, and the globalization of health. Whether making new discoveries in the lab or researching and educating in the field, our faculty, students, and alumni are deployed around the globe to promote and protect our health. For more on the School of Public Health, see: http://www.sph.umich.edu/
Contact: Laura Bailey
University of Michigan
WINSTON-SALEM, N.C. – New findings that one in 20 North Carolina men who have sex with men (MSM) reported using crystal methamphetamine during the previous month suggests increased risk for spreading HIV and other sexually transmitted diseases (STD), according to researchers from Wake Forest University School of Medicine and colleagues.
The rate of methamphetamine use among 1,189 MSM was 30 times higher than levels reported in the general U.S. population over the same period. Methampehtamine, or “meth,” is a highly addictive stimulant that has been found to impair judgment, decrease inhibition, increase impulsivity and enhance sexual sensitivity – which can all increase the potential for transmitting HIV.
The study’s authors found that participants who reported using methamphetamines were more likely to report inconsistent condom use during anal sex within the past three months, a history of STD infection, being HIV-positive and using medications designed to treat erectile dysfunction.
“Until now, there has been little data on meth use in the Southeast,” said lead author Scott D. Rhodes, Ph.D. M.P.H., associate professor in the Department of Social Sciences and Health Policy. “Our findings, including that meth users were more likely to be HIV-positive, suggest that prevention, intervention and treatment efforts are urgently needed.”
Rhodes noted that some of the men reported having sex with both men and women, which means the risk of HIV extends to both sexes.
The study’s results will be published on Aug. 20 in AIDS Patient Care and STDs, a leading AIDS journal that provides the latest research for clinicians and researchers. It is among the first to document meth use among MSM in the South, which carries a disproportionate HIV, AIDS, and STD burden, with 46 percent of newly identified cases.
“The findings underscore the need for further research and intervention,” said Rhodes. “The HIV/AIDS epidemic is clearly not over. We must develop innovative intervention approaches designed to reach communities at highest risk. Men who have sex with men, whether or not they identify themselves as gay, who use drugs like methamphetamines are clearly at higher risk. Yet currently nothing is being done in the Southeast.”
Participants were recruited in 2005 in five gay bars and in five geographically defined internet chat rooms in central North Carolina (primarily rural/suburban areas) and were asked to complete a brief assessment of drug use and other risk behaviors. Of the 1,189 MSM, two-thirds self-identified as black or other minorities, and 25 percent as bisexual. The mean age was 29 years.
In addition to being more inclined to risky sexual behaviors, the study participants who said they used methamphetamines were also more likely to report having higher education and health insurance coverage.
“Because users of methamphetamines were more likely to have higher educational levels and report having health insurance, we must change the way we think about meth users and develop sophisticated prevention strategies that are appropriate for these types of users,” noted Rhodes. “In addition, the link between meth use and the use of drugs for sexual dysfunction among a young population deserves attention. Meth use in combination with one of these medications may be having an even more profound impact on the HIV and STD disease epidemics in the South.”
Rhodes is also affiliated with the Maya Angelou Research Center on Minority Health at Wake Forest. In 2006, Rhodes won the New Investigator Award in Clinical Sciences at Wake Forest.
The study’s co-authors include Emily Knipper and Aimee M. Wilkin, M.D., M.P.H., both with Wake Forest, Kenneth C. Hergenrather, Ph.D., M.S.Ed., M.R.C., of George Washington University, Leland J. Yee, Ph.D., M.P.H., of the University of Pittsburgh, and Morrow R. Omli, M.A.Ed., of the University of Florida.
Media Contacts: Karen Richardson, email@example.com, or Shannon Koontz, firstname.lastname@example.org, 336-716-4587.
Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university’s School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in family medicine, 20th in geriatrics, 25th in primary care and 41st in research among the nation’s medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.
Contact: Karen Richardson
Wake Forest University Baptist Medical Center
Using virtual reality goggles to mix up the sensory signals reaching the brain, scientists have induced out-of-body-like experiences in healthy people, suggesting a scientific explanation for a phenomenon often thought to be a figment of the imagination.
The sight of their bodies located somewhere else — thanks to the goggles — plus the feel of their real bodies being touched simultaneously made volunteers sense that they had moved outside of their physical bodies, according to a pair of studies in the 24 August 2007 issue of the journal Science, published by AAAS, the nonprofit science society.
A disconnect between the brain circuits that process both these types of sensory information may thus be responsible for some out-of-body experiences, the researchers say.
Out-of-body experiences, which generally involve the feeling of disembodiment and seeing one’s own body from a location outside the body, can occur in part through drug use, epileptic seizures and other types of brain disturbances.
By projecting a person’s awareness into a virtual body, the techniques used in these studies may be useful for training people to do delicate “teleoperating” tasks, such as performing surgeries remotely. The findings may also remove some of the stigma that patients with neurological disorders may feel about having these experiences, which are frequently attributed to an active imagination or some sort of paranormal phenomenon.
The studies also help solve the age-old question of how we perceive our own bodies.
“I’m interested in why we feel that our selves are inside our bodies — why we have an ‘in-body experience,’ if you like. This has been discussed for centuries in philosophy, but it’s hard to tackle experimentally,” said Science Brevium author Henrik Ehrsson of University College London, in London, and the Karolinska Institute in Stockholm.
Both Ehrsson and another research team, led by Olaf Blanke of the Ecole Polytechique Fédérale de Lausanne (EPFL) and the University Hospital in Geneva, Switzerland, used video cameras and virtual reality goggles to show volunteers images of their own bodies from the perspective of someone behind them. The researchers also touched the volunteers’ bodies, both physically and virtually.
The volunteers in Ehrsson’s study viewed images recorded by the cameras through their headsets. In Blanke and colleagues’ study, the video was converted into holograph-like computer simulations.
Ehrsson had the volunteers watch a plastic rod moving toward a location just below the cameras while their real chests were simultaneously touched in the corresponding spot. Questionnaire responses afterwards indicated that the volunteers felt they were located back where the cameras were placed, watching a dummy or a body that belonged to someone else.
“This experiment suggests that the first-person visual perspective is critically important for the in-body experience. In other words, we feel that our self is located where the eyes are,” Ehrsson said.
Ehrsson also had the volunteers watch a hammer swing down to a point below the camera, as though it were going to “hurt” an unseen portion of the virtual body. Measurements of skin conductance, which reflects emotional responses such as fear, indicated that the volunteers sensed their “selves” had left their physical bodies and moved to the virtual bodies.
Blanke’s team used a similar setup to create out-of-body-like experiences (which they cautioned lacked some aspects of full-blown out-of-body experiences).
After the virtual reality exercise, a researcher would blindfold the volunteers and guide them backward. When the volunteers were asked to return to their original position, they tended to drift toward where they had seen their virtual bodies standing.
Both studies conclude that “multisensory conflict” is a key mechanism underlying out-of-body experiences.
“Brain dysfunctions that interfere with interpreting sensory signals may be responsible for some clinical cases of out-of-body experiences,” Ehrsson said. “Though, whether all out-of-body experiences arise from the same causes is still an open question.”
Bodily self-consciousness may also involve a cognitive dimension – the ability to distinguish between one’s own body and other objects – in addition to sensory signals, Blanke and his coauthors propose.
Supporting this idea, Blanke’s team reports that when the volunteers viewed a human-sized block instead of an image of a human body, they successfully returned to their original standing place, indicating that no out-of-body-like illusion had occurred.
“Full-body consciousness seems to require not just the ‘bottom up’ process of correlating sensory information but also the ‘top down’ knowledge about human bodies,” Blanke said.
Some of the out-of-body experiences that have previously eluded scientific explanation may be related to distorted “full-body perception,” according to Blanke. Virtual reality systems may provide further answers.
“We have decades of intense research on visual perception, but not very much yet on body perception. But that may change, now virtual reality offers a way to manipulate full body perception more systematically and probe out-of-body experiences and bodily self consciousness in a new way,” Blanke said.
“The Experimental Induction of Out-of-Body Experiences,” by H. Henrik Ehrsson of University College London, in London, UK and Karolinska Institute in Stockholm, Sweden. This research was supported by the Wellcome Trust, the PRESENCCIA project, an EU-funded project under the IST programme, the Human Frontier Science Program, the Swedish Medical Research Council and the Swedish Foundation for Strategic Research.
“Video Ergo Sum: Manipulating Bodily Self-Consciousness,” by Bigna Lenggenhager and Tej Tadi at Ecole Polytechique Fédérale de Lausanne (EPFL), Switzerland; Thomas Metzinger at Johannes Gutenberg-Universität Mainz in Mainz, Germany; and Olaf Blanke at Ecole Polytechique Fédérale de Lausanne (EPFL), Switzerland and University Hospital in Geneva, Switzerland. This research was supported by the Cogito Foundation, the Fondation de Famille Shandoz, the Fondation Odier and the Swiss National Science Foundation.
The American Association for the Advancement of Science (AAAS) is the world’s largest general scientific society, and publisher of the journal Science (www.sciencemag.org). AAAS was founded in 1848, and serves 262 affiliated societies and academies of science, reaching 10 million individuals. Science has the largest paid circulation of any peer-reviewed general science journal in the world, with an estimated total readership of 1 million. The nonprofit AAAS (www.aaas.org) is open to all and fulfills its mission to “advance science and serve society” through initiatives in science policy; international programs; science education; and more. For the latest research news, log onto EurekAlert!, http://www.eurekalert.org, the premier science-news Web site, a service of AAAS.
Contact: Natasha Pinol
American Association for the Advancement of Science
Australian and French scientists have made another breakthrough in the technology that will drive next generation computers and teleportation.
The researchers have successfully superposed light beams, which produces a state that appears to be both on and off at once.
Light beams that are simultaneously on and off are vital for the next-generation super computers which should be faster than current computers based on bits, that are either on or off.
Previously, only smaller light particles had been superposed and the group has also proved a quantum physics theory known as Schrödinger’s cat.
This theory, named after an Austrian physicist Erwin Schrödinger, proposed that a large object such as a cat could be simultaneously alive and dead.
Researchers from The University of Queensland and University of Paris South have published the latest breakthrough in the international journal NATURE.
UQ Centre for Quantum Computer Technology researcher Dr Hyunseok Jeong devised the scheme to generate and superpose the beams which was tested and proved by his French collaborators.
Dr Jeong said his group used special lasers, crystals, photon detectors, half-mirrors and other optical devices to generate and measure the superposition of light beams.
“It has been known to be extremely hard to generate Schrödinger cat states, particularly with traveling light,” Dr Jeong said.
“Even though one could generate such Schrodinger cat states, it would be extremely hard to observe them because in a very short time, they would be reduced to either alive or dead states.”
He said his group’s research findings would help speed up the development of quantum information technologies such as quantum computers, quantum cryptography and quantum teleportation.
“Using Schrödinger cat states, quantum teleportation may be performed with nearly 100 percent success probability.”
Contact: Dr. Jeong
Loss is linked to common lung cancer
Little-known bits of RNA help master tumor-suppressor gene do its job, U-M cancer researchers find
Three micro RNA genes appear to be key partners of protective gene p53; their loss is linked to common type of lung cancer
ANN ARBOR, Mich. — Scientists have shown in literally thousands of studies that the p53 gene deserves its reputation as “the guardian of the genome.” It calls to action an army of other genes in the setting of varied cell stresses, permitting repair of damaged DNA or promoting cell death when the cell damage is too great. A key net effect of p53’s action is to prevent development of cancerous cells.
Now, University of Michigan Medical School scientists provide the most thorough evidence yet that p53 also regulates a trio of genes from the realm of so-called “junk” genes — the roughly 97 percent of a cell’s genetic material whose function is only beginning to be understood.
The study shows that “in the ‘junk’ lies treasure, in terms of critical knowledge about how normal cells stifle cancer or succumb to it,” says Guido Bommer, M.D., the lead author of results, published in a recent issue of the journal Current Biology.
“The findings in the study offer new insights into specific mechanisms by which the expression of hundreds to thousands of genes and proteins is altered in the roughly 50 percent of cancers that carry mutations in the p53 tumor suppressor gene,” says Eric Fearon, M.D., Ph.D., senior author of the study and deputy director of the U-M Comprehensive Cancer Center. Scientists continue to mine for details of what goes wrong when p53 is defective and cannot perform its tumor-fighting duties.
The U-M study is one of four recent studies from labs around the world showing that p53 normally gets support from members of a small family of micro RNA genes. The studies are part of a larger effort to understand the function of micro RNA (miRNA for short).
Scientists have long known the importance of messenger RNA (mRNA), which carries protein-making instructions. However, until recently, little was known about micro RNA genes. It is now well recognized that miRNAs regulate the levels of mRNAs, and/or the levels of the proteins produced from mRNAs.
The U-M research team studied the roles of the three genes that make up the miRNA34 family. They showed that the miRNA34 genes work in concert with p53, then went on to explore which other genes the family regulates. They found the miRNA34 genes showed pronounced effects on other genes that control the timing of cell proliferation and division. They also found that the miRNA34 gene family regulated the levels of the Bcl-2 protein, a key factor that enhances a cell’s resistance to death-inducing stimuli.
The team went on to determine if expression of the miRNA34 genes was compromised in human lung cancer cells.
“We found that expression of two of the miRNA34 genes was lost in almost two-thirds of lung adenocarcinomas,” says Bommer.
Adenocarcinomas represent the most common type of non-small cell lung cancer, which is the most frequently diagnosed type of lung cancer. When expression of the miRNA34 genes was restored in lung cancer cells, some of the aberrant growth properties were inhibited.
The discoveries of the role of micro RNAs in tumor suppression could have implications for future cancer therapies.
It’s important to note that micro RNAs alone are not likely to offer new cancer treatment or prevention agents, says Fearon, who is the Emanual N Maisel Professor of Oncology, Professor of Internal Medicine, Professor of Pathology and Professor of Human Genetics at the U-M Medical School.
“However, because of the small size of mature miRNAs, there is optimism that it may be possible to deliver modified nucleic acids that might mimic the effect of the miRNAs,” he says. If modified nucleic acids were to prove effective in more laboratory studies, he adds, they might be pursued further in clinical trials as anti-cancer agents, either alone or more likely in combination with other anti-cancer agents.
In addition to Bommer and Fearon, other U-M authors include: Isabelle Gerin, Ph.D.; Ying Feng, Ph.D.; Andrew J Kaczorowski, B.S.; Rork Kuick, Ph.D.; Robert E Love , B.S.; Yali Zhai, M.D., Ph.D.; Thomas J Giordano, M.D., Ph.D.; Zhaohui S Qin, Ph.D.; Bethany B Moore, Ph.D.; Ormond A MacDougald, Ph.D.; and Kathleen R Cho, M..D., Ph.D.
This research was funded by the National Institutes of Health.
Citation: Current Biology 17, 1298–1307, August 7, 2007
Contact: Anne Rueter
University of Michigan Health System
McMaster University researchers have first insight into how Huntington’s disease is triggered
McMaster University researchers have first insight into how Huntington’s disease (HD) is triggered. The research will be published online in the British Journal, Human Molecular Genetics, on Monday, August 20.
“These are exciting results by the McMaster team,” said Dr. Rémi Quirion, Scientific Director at the Canadian Institutes of Health Research, Institute of Neuroscience, Mental Health and Addiction. Even if the huntingtin protein has been known for almost 20 years, the cause of Huntington’s disease is still not clear. Data reported here shed new lights on this aspect and possibly leading to new therapeutic potential in the future.”
Ray Truant, professor in the Department of Biochemistry and Biomedical Sciences, has been studying the biological role of the huntingtin protein and the sequences in the protein that tell it where to go within a brain cell.
Huntington disease (HD) is a neurological disorder resulting from degeneration of brain cells. The degeneration causes uncontrolled limb movements and loss of intellectual faculties, eventually leading to death. There is no treatment. HD is a familial disease, passed from parent to child through a mutation in the normal gene. The disorder is estimated to affect about one in every 10,000 persons.
Truant and PhD candidate graduate student, Randy Singh Atwal, have discovered a small protein sequence in huntingtin that allows it to locate to the part of the cell critical for protein quality control. Similar findings have been seen to be very important for other neurodegenerative diseases such as Parkinson’s and Alzheimer’s diseases.
Huntingtin protein is essential for normal development in all mammals, and is found in all cells, yet its function was unknown. It appears that huntingtin is crucial for a brain cell’s response to stress, and moves from the endoplasmic reticulum into the nucleus, the control centre of the cell. When mutant huntingtin is expressed however, it enters the nucleus as it should in response to stress, but it cannot exit properly, piling up in the nucleus and leading to brain cell death in HD.
“What is important to Huntington disease research is that in the learning of the basic cell biology of this protein, we have also uncovered a new drug target for the disease,” says Atwal.
Atwal additionally found that huntingtin can be sent to the nucleus by protein modifying enzymes called kinases, and he has determined the three-dimensional shape of this sequence.
Truant and Atwal’s work indicates that if mutant huntingtin is prevented from entering the nucleus, it cannot kill a brain cell. This means that a kinase inhibitor drug may be effective for Huntington’s disease. Kinase inhibitors form the largest number of successful new generation drugs that are coming to market for a plethora of diseases including stroke, arthritis and cancer.
“This is most exciting to us, because we immediately have all the tools and support in hand at McMaster to quickly hunt this kinase down, and find potential new drugs for Huntington’s disease in ways that are similar or better than a large pharmaceutical company”, says Truant. Truant’s lab is also collaborating in the US with the Cure Huntington’s Disease Initiative (CHDI) a novel, non-profit virtual pharmaceutical company focused on HD.
A large portion of this work was completed in the new McMaster biophotonics facility (www.macbiophotonics.ca), and additional research will be done in McMaster’s unique high throughput screening lab (hts.mcmaster.ca) and other new labs being established at the University.
“We can actually watch huntingtin protein move inside of a single live brain cell in real time in response to stress, and we can watch mutant huntingtin kill that cell, even over days,” says Truant. “Using molecular tools, computer software and sophisticated laser microscopy techniques which we’ve been developing at McMaster over the last seven years, researchers can now use these methods to hopefully watch a drug stop this from happening.”
Truant’s laboratory is supported by grants from the United States High Q Foundation, the Canadian Institutes of Health Research, the Huntington Society of Canada and the Canada Foundation for Innovation.
“This discovery reflects Dr. Truant’s growing contribution to the international campaign to create a world free from Huntington disease,” says Don Lamont, CEO & Executive Director of the Huntington Society of Canada – Canada’s only organization focused on research, education and support in the HD field.
“Our families live on a ‘tightrope’ waiting for an effective treatment or a cure for HD”, says Lamont. “The discovery provides hope for the Huntington community – most of all, hope that their children will not have to suffer the devastation of this inherited disease.”
Contact: Veronica McGuire
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