Wednesday, February 3, 2010

NEW VISIBLE LIGHT PHOTOCATALYST KILLS BACTERIA, EVEN AFTER LIGHT TURNED OFF

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In the battle against bacteria, researchers at the University of Illinois have developed a powerful new weapon – an enhanced photocatalytic disinfection process that uses visible light to destroy harmful bacteria and viruses, even in the dark.

Based upon a new catalyst, the disinfection process can be used to purify drinking water, sanitize surgical instruments and remove unwanted fingerprints from delicate electrical and optical components.

“The new catalyst also has a unique catalytic memory effect that continues to kill deadly pathogens for up to 24 hours after the light is turned off,” said Jian Ku Shang, a professor of materials science and engineering at the U. of I.

Shang is corresponding author of a paper that is scheduled to appear in the Journal of Materials Chemistry, and posted on the journal’s Web site.

Shang’s research group had previously developed a catalytic material that worked with visible light, instead of the ultraviolet light required by other catalysts. This advance, which was made by doping a titanium-oxide matrix with nitrogen, meant the disinfection process could be activated with sunlight or with standard indoor lighting.

“When visible light strikes this catalyst, electron-hole pairs are produced in the matrix,” Shang said. “Many of these electrons and holes quickly recombine, however, severely limiting the effectiveness of the catalyst.”

To improve the efficiency of the catalyst, Shang and collaborators at the U. of I. and at the Chinese Academy of Sciences added palladium nanoparticles to the matrix. The palladium nanoparticles trap the electrons, allowing the holes to react with water to produce oxidizing agents, primarily hydroxyl radicals, which kill bacteria and viruses.

When the light is turned off, the palladium nanoparticles slowly release the trapped electrons, which can then react with water to produce additional oxidizing agents.

“In a sense, the material remembers that it was radiated with light,” Shang said. “This ‘memory effect’ can last up to 24 hours.”

Although the disinfection efficiency in the dark is not as high as it is in visible light, it enables the continuous operation of a unique, robust catalytic disinfection system driven by solar or other visible light illumination.

In addition to environmental applications, the new catalyst could also be used to remove messy, oily fingerprints from optical surfaces, computer displays and cellphone screens, Shang said.

(Photo: L. Brian Stauffer)

University of Illinois

IOWA STATE UNIVERSITY RESEARCHER DISCOVERS EBOLA’S DEADLY SECRET

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Research at Iowa State University has led scientists to uncover how the deadly Zaire Ebola virus decoys cells and eventually kills them.

A research team led by Gaya Amarasinghe, an assistant professor of biochemistry, biophysics and molecular biology, had previously solved the structure of a critical part of an Ebola protein known as VP35, which is involved in host immune suppression.

Amarasinghe and his research team now know how VP35 is able to do it.

When most viruses invade a cell, they start to make RNA in order to replicate.

When the healthy host cell senses the replicating RNA, the host cell starts to activate anti-viral defenses that halt replication and eventually help clear the viral infections.

What Amarasinghe and his group have discovered is that Ebola virus encoded VP35 protein actually masks the replicating viral ribonucleic acid (RNA), so the cell doesn't recognize that there is an invading virus.

One of the reasons Ebola, in particular the strain isolated from Zaire, is so deadly is that the host cells don't have any immune response when the virus enters the cell, said Amarasinghe.

"The question with Ebola has always been 'Why can't host cells mount an immune response against the Ebola virus, like they do against other viruses?'" he said. ]

"The answer is, 'If the cell doesn't know that there's an infection, it cannot build up any response.' So our work really gets at the mechanism Ebola infection and immune evasion."

The collaborative approach taken by Amarasinghe enabled him to team up with virologist Christopher Basler at the Mt. Sinai School of Medicine, New York City, to investigate how the structural findings match up with how these proteins function inside the cell.

"Our initial structure that we solved in 2008 was key to expanding our knowledge, but the structure was just part of the equation, and when we put it together with the functional studies, everything made sense," Amarasinghe said.

The current research describing the protein-RNA complex structure, which was solved by using non-infectious VP35 protein, and associated functional studies is published in the current issue of the journal Nature Structural and Molecular Biology and is available as an advanced online publication.

These findings build on Amarasinghe's research published in the journal Proceedings of the National Academy of Sciences of the United States of America last January.

In his current research, Amarasinghe focused on a specific part of the Zaire Ebola VP35 protein that he thought looked unusual.

As testing results came in, he found that the suspect region of the protein was binding with, or neutralizing, the part of the host cell that triggers the immune system in the cell.

"The interesting thing about the Ebola virus is that it doesn't let cells even get started to defend themselves," he said. "This hides the (viral) RNA from being recognized by the host cell. This is a powerful immune evasion mechanism."

Iowa State University

NEW STUDY SUGGESTS THEORY FOR INSECT COLONIES AS SUPERORGANISMS

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A team of researchers including scientists from the University of Florida has shown insect colonies follow some of the same biological “rules” as individuals, a finding that suggests insect societies operate like a single “superorganism” in terms of their physiology and life cycle.

For more than a century, biologists have marveled at the highly cooperative nature of ants, bees and other social insects that work together to determine the survival and growth of a colony.

The social interactions are much like cells working together in a single body, hence the term “superorganism” — an organism comprised of many organisms, according to James Gillooly, an assistant professor in the department of biology at UF’s College of Liberal Arts and Sciences.

Now, researchers from UF, the University of Oklahoma and the Albert Einstein College of Medicine have taken the same mathematical models that predict lifespan, growth and reproduction in individual organisms and used them to predict these features in whole colonies.

By analyzing data from 168 different social insect species including ants, termites, bees and wasps, the authors found that the lifespan, growth rates and rates of reproduction of whole colonies when considered as superorganisms were nearly indistinguishable from individual organisms.

“This PNAS paper regarding the energetic basis of colonial living in social insects is notable for its originality and also for its importance,” said Edward O. Wilson, a professor of biology at Harvard University and co-author of the book “The Super-Organism,” who was not involved in the research. “The research certainly adds a new perspective to our study of how insect societies are organized and to what degree they are organized.”

The study may also help scientists understand how social systems have arisen through natural selection — the process by which evolution occurs. The evolution of social systems of insects in particular, where sterile workers live only to help the queen reproduce, has long been a mystery, Gillooly said.

“In life, two of the major evolutionary innovations have been how cells came together to function as a single organism, and how individuals joined together to function as a society,” said Gillooly, who is a member of the UF Genetics Institute. “Relatively speaking, we understand a considerable amount about how the size of multicellular organisms affects the life cycle of individuals based on metabolic theory, but now we are showing this same theoretical framework helps predict the life cycle of whole societies of organisms.”

Researchers note that insect societies make up a large fraction of the total biomass on Earth, and say the finding may have implications for human societies.

“Certainly one of the reasons folks have been interested in social insects and the consequences of living in groups is that it tells us about our own species,” said study co-author Michael Kaspari, a presidential professor of zoology, ecology and evolutionary biology at the University of Oklahoma and the Smithsonian Tropical Research Institute. “There is currently a vigorous debate on how sociality evolved. We suggest that any theory of sociality be consistent with the amazing convergence in the way nonsocial and social organisms use energy.”

University of Florida

THE FANTASTIC ARMOR OF A WONDER SNAIL

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Researchers at the National Science Foundation-supported Materials Research Science and Engineering Center at the Massachusetts Institute of Technology are studying the mollusk's physical and mechanical properties. A report, "Protection mechanisms of the iron-plated armor of a deep sea hydrothermal vent gastropod," appears in the Proceedings of the National Academy of Sciences.

The so-called "scaly-foot gastropod," has a unique tri-layered shell that may hold insights for future mechanical design principles. Specifically, it has a highly calcified inner layer, a thick organic middle layer. But, it's the extraordinary outer layer fused with granular iron sulfide that excites researchers.

The Kairei Indian vent field is a series of deep gashes in the planet's surface along a volcanic mountain chain below the Indian Ocean. There, researchers on an expedition discovered the never before seen snail in 1999.

"Hydrothermal vent fluids possess high concentration of sulfides and metals, but this mollusk is unique in that it incorporates materials plentiful to vent field into its shell structure," said MIT project leader Christine Ortiz at MIT's Department of Materials Science and Engineering. "We were interested in looking at the structure and properties of the individual layers and seeing how they behave mechanically," she said noting that the mollusk's organic inner layer is also interesting.

In particular researchers set out to discover what advantages the structure holds for protection against penetrating attacks from predators. Understanding this can give them new ideas for materials that may be used for cars, trucks and military applications.

To test the shell's properties, researchers performed experiments that simulated generic predatory attacks using both computer models and indentation testing. The indentation testing involved hitting the top of shells with the sharp tip of a probe to measure the shell's hardness and stiffness.

A number of potential predators were found in the same region as the scaly-foot gastropod. One predator, the cone snail, uses a harpoon-like tooth to attempt penetration of before injecting it with paralyzing venom. Additionally, sea-faring crabs are known to grab gastropods within their claws and attempt to puncture their shells and/or squeeze them sometimes for days until the mollusks' shells break.

The testing led to a "realization that each layer of the (mollusk's) exoskeleton is responsible for distinct and multifunctional roles in mechanical protection," Ortiz and her colleagues write in the report. The testing reveals that the shell is "advantageous for penetration resistance, energy dissipation, mitigation of fracture and crack arrest, reduction of back deflections, and resistance to bending and tensile loads."

Our study suggests that the scaly-foot gastropod undergoes very different deformation and protection mechanisms compared to other gastropods," said Ortiz. "It is very efficient in protection, more so than the typical mollusk."

(Photo: Zina Deretsky, National Science Foundation, inset after Haimin Yao et al., PNAS, January 2010)

National Science Foundation

WHY HASN'T EARTH WARMED AS MUCH AS EXPECTED?

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Earth has warmed much less than expected during the industrial era based on current best estimates of Earth's "climate sensitivity" -- the amount of global temperature increase expected in response to a given rise in atmospheric concentrations of carbon dioxide.

In a study published online on Jan. 19 in the Journal of Climate, Stephen Schwartz of Brookhaven National Laboratory, Robert Charlson of the University of Washington and colleagues examine the reasons for this discrepancy.

According to current best estimates of climate sensitivity, the amount of carbon dioxide and other heat-trapping gases added to Earth's atmosphere since humanity began burning fossil fuels on a significant scale during the industrial period would be expected to result in a mean global temperature rise of 3.8 degrees Fahrenheit. That is well more than the 1.4 degrees F. increase that has been observed for this time span.

"The data show that either we have 40 years of emissions left before the atmosphere can't absorb any more carbon dioxide, or we're already past the point of no return. In other words, the uncertainty rate is unacceptably high," said Charlson, a UW atmospheric sciences professor who in the 1960s invented a device called the integrating nephelometer to measure atmospheric haze particles, producing data that is still used in climate models today.

The new analysis attributes the reasons for the discrepancy between projected and actual temperature increase to a possible mix of two major factors: Earth's climate may be less sensitive to rising greenhouse gases than currently assumed and/or reflection of sunlight by haze particles in the atmosphere may be offsetting some of the expected warming.

"Because of present uncertainties in climate sensitivity and the enhanced reflectivity of haze particles," said Schwartz, "it is impossible to accurately assign weights to the relative contributions of these two factors. This has major implications for understanding of Earth's climate and how the world will meet its future energy needs."

A third possible reason for the lower-than-expected increase of Earth's temperature over the industrial period is the slow response of temperature to the warming influence of heat-trapping gases.

"This is much like the lag time you experience when heating a pot of water on a stove," said Schwartz. Based on calculations using measurements of the increase in ocean heat content over the past 50 years, however, the present study found the role of so-called thermal lag to be minor.

A key question facing policymakers is how much additional carbon dioxide and other heat-trapping gases can be introduced into the atmosphere, beyond what is already present, without committing the planet to a dangerous level of human interference with the climate system. Many scientists and policymakers consider the threshold for such dangerous interference to be an increase in global temperature of 3.6 degrees F above the preindustrial level, although no single threshold would encompass all effects.

The paper describes three scenarios. If Earth's climate sensitivity is at the low end of current estimates as given by the Intergovernmental Panel on Climate Change, then the total maximum future emissions of heat-trapping gases so as not to exceed the 3.6-degree threshold would correspond to about 35 years of present annual emissions of carbon dioxide from fossil-fuel combustion. A climate sensitivity consistent with the present best estimate would mean that no more heat-trapping gases can be added to the atmosphere without committing the planet to exceeding the threshold. And if the sensitivity is at the high end of current estimates, present atmospheric concentrations of heat-trapping gases are such that the planet is already committed to warming that substantially exceeds the 3.6-degree threshold.

The authors emphasize the need to quantify the influences of haze particles to narrow the uncertainty in Earth's climate sensitivity. The task is much more difficult than quantifying the influences of heat-trapping gases, said Charlson, who likens the focus on heat-trapping gases to "looking for the lost key under the lamppost."

Schwartz observes that formulating energy policy with the present uncertainty in climate sensitivity is like navigating a large ship in perilous waters without charts. "We know we have to change the course of this ship, and we know the direction of the change, but we don't know how much we need to change the course or how soon we have to do it."

"These results do not in any way reduce or remove the need for solid action now to move toward a zero-carbon dioxide-emission economy. The results tell us that doing our utmost now might work very well if the most optimistic values of sensitivity are real, but that it is possible that nothing will work no matter how hard we try," Charlson said.

"If we do not reduce uncertainties, we will be in the same boat 10 or 20 years from now as we are today," he said.

University of Washington

SCIENTISTS IDENTIFY MOLECULE THAT INHIBITS STEM CELL DIFFERENTIATION

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Like as not, the recent holidays probably included some reminiscing about family history. There may even have been some remonstrations and recommendations from well-meaning elders to younger kin about their lives’ paths. It turns out stem cells have a similar need for long-term memory to help them know who they are and what they should become. Scientists at the Stanford University School of Medicine have now identified a molecule involved in keeping skin stem cells on the straight and narrow.

“We’re starting to understand the molecular mechanism of cellular memory,” said Paul Khavari, MD, PhD, professor of dermatology. “How a stem cell remembers what it is, and why it might go astray.”

The molecule, called DNMT1, helps the stem cells know whether to self-renew to create more stem cells, or to differentiate into specialized, non-dividing adult skin cells. It’s important because too much self-renewal can lead to cancer, and too little can inhibit wound healing.

Khavari is the senior author of the research, published online Jan. 17 in Nature. He is also a member of Stanford’s Cancer Center and Bio-X and the clinical chief of the dermatology service at the Veterans Affairs Palo Alto Health Care System. Postdoctoral scholar George Sen, PhD, is the lead author of the work.

Much ado is made over pluripotent cells — such as embryonic stem cells and their laboratory doppelgangers, induced pluripotent stem cells — which have the potential to differentiate into any of the body’s different cell types. But adult stem cells, while more limited in their ability to create new types of cells, still have important roles in the body. They’re particularly vital in skin, blood and other tissues that must constantly regenerate new cells.

Skin stem cells, for instance, must know when to self-renew — by dividing to create new daughter stem cells — and when to differentiate into one of the many specialized, but mostly non-dividing cells that migrate upward to form the surface layers of your skin. A misstep in either direction can have dire consequences. Unnecessary differentiation can exhaust the pool of available stem cells and leave the skin unable to maintain itself or heal wounds. Uncontrollable self-renewal of undifferentiated stem cells, however, is the cause of many cancers.

Khavari and Sen found that DNMT1 helps by keeping stem cell differentiation in check. It works by duplicating in newly formed daughter stem cells the parent cell’s patterns of DNA modifications, called methyl groups. These methyl groups turn off genes that are important in differentiation and ensure that the daughter cells remain reliable, steady members of the stem cell society.

This isn’t the first time DNMT1 has been identified as an important regulatory molecule. In fact, it’s so critical to development that certain laboratory mice, engineered so they can’t express the gene, die before birth. This lack of an appropriate animal model has made it difficult to study DNMT1’s function in adult tissues. But Khavari and Sen suspected that it had a role in adult stem cells — in part because it’s been shown to be expressed at high levels in certain human cancers.

“It seems that in these cancers, DNMT1 may be signaling the stem cells to keep dividing and to avoid differentiation,” said Sen.

Khavari and Sen studied human skin cells in a laboratory dish to discover that the expression of the protein is curtailed when the cells begin to differentiate and migrate to the skin’s surface. When they blocked DNMT1 expression in human skin grafted on to laboratory mice, only about one-third of the grafts lasted three weeks or more.

“It’s as if we’re seeing a kind of cellular amnesia in the stem cells without DNMT1 expression,” said Khavari. “Without the proper patterns of methylation, these cells can’t remember they’re supposed to be stem cells, and instead begin differentiating and migrating to the skin’s surface.” In contrast, all of the grafts with unaltered DNMT1 expression remained healthy — most likely because they had an ample pool of stem cells with which to maintain themselves.

Further study showed that the effects of DNMT1 and another protein important in methylation, UHRF1, may be countered in differentiating cells by a family of proteins called GADD45 that removes methyl groups from DNA. This yin and yang activity helps the cells navigate the tricky waters of differentiation and migration.

“Our ability to control the cells’ differentiation state is going to be very important for our future attempts at regenerative medicine,” said Khavari, referring to scientists’ hope of being able to use stem cells to repair injuries or to create entirely new organs. “We have to be able to strike the right balance between methylation and demethylation. There are a lot of other actors to track down.”

(Photo: Stanford U.)

Stanford University School of Medicine

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