Wednesday, December 1, 2010

SLEEP MAKES YOUR MEMORIES STRONGER

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As humans, we spend about a third of our lives asleep. So there must be a point to it, right? Scientists have found that sleep helps consolidate memories, fixing them in the brain so we can retrieve them later. Now, new research is showing that sleep also seems to reorganize memories, picking out the emotional details and reconfiguring the memories to help you produce new and creative ideas, according to the authors of an article in Current Directions in Psychological Science, a journal of the Association for Psychological Science.

“Sleep is making memories stronger,” says Jessica D. Payne of the University of Notre Dame, who cowrote the review with Elizabeth A. Kensinger of Boston College. “It also seems to be doing something which I think is so much more interesting, and that is reorganizing and restructuring memories.”

Payne and Kensinger study what happens to memories during sleep, and they have found that a person tends to hang on to the most emotional part of a memory. For example, if someone is shown a scene with an emotional object, such as a wrecked car, in the foreground, they’re more likely to remember the emotional object than, say, the palm trees in the background—particularly if they’re tested after a night of sleep. They have also measured brain activity during sleep and found that regions of the brain involved with emotion and memory consolidation are active.

“In our fast-paced society, one of the first things to go is our sleep,” Payne says. “I think that’s based on a profound misunderstanding that the sleeping brain isn’t doing anything.” The brain is busy. It’s not just consolidating memories, it’s organizing them and picking out the most salient information. She thinks this is what makes it possible for people to come up with creative, new ideas.

Payne has taken the research to heart. “I give myself an eight-hour sleep opportunity every night. I never used to do that—until I started seeing my data,” she says. People who say they’ll sleep when they’re dead are sacrificing their ability to have good thoughts now, she says. “We can get away with less sleep, but it has a profound effect on our cognitive abilities.”

Association for Psychological Science

A NEW READ ON DNA SEQUENCING

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The twisting, ladder-like form of the DNA molecule – the architectural floor plan of life – contains a universe of information critical to human health. Enormous effort has been invested in deciphering the genetic code, including, most famously, the Human Genome Project. Nevertheless, the process of reading some 3 billion nucleotide "letters" to reveal an individual's full genome remains a costly and complex undertaking.

Now, Stuart Lindsay, biophysicist in ASU’s Biodesign Institute, has demonstrated a technique that may lead to rapid, low-cost reading of whole genomes, through recognition of the basic chemical units – the nucleotide bases that make up the DNA double helix. An affordable technique for DNA sequencing would be a tremendous advance for medicine, allowing routine clinical genomic screening for diagnostic purposes; the design of a new generation of custom-fit pharmaceuticals; and even genomic tinkering to enhance cellular resistance to viral or bacterial infection.

Lindsay is an ASU Regents' Professor and Carson Presidential Chair of Physics and Chemistry, as well as director of the Biodesign Institute's Center for Single Molecule Biophysics. His group's research appears in the current issue of the journal Nature Nanotechnology.

Lindsay's technique for reading the DNA code relies on a fundamental property of matter known as quantum tunneling, which operates at the subatomic scale. According to quantum theory, elementary particles like electrons can do some very strange and counterintuitive things, in defiance of classical laws of physics. Such sub-atomic, quantum entities possess both a particle and a wave-like nature. Part of the consequence of this is that an electron has some probability of moving from one side of a barrier to the other, regardless of the height or width of such a barrier.

Remarkably, an electron can accomplish this feat, even when the potential energy of the barrier exceeds the kinetic energy of the particle. Such behavior is known as quantum tunneling, and the flow of electrons is a tunneling current. Tunneling is confined to small distances – so small that a tunnel junction should be able to read one DNA base (there are four of them in the gentic code, A,T,C and G) at a time without interference from flanking bases. But the same sensitivity to distance means that vibrations of the DNA, or intervening water molecules, ruin the tunneling signal. So the Lindsay group has developed "recognition molecules" that "grab hold" of each base in turn, clutching the base against the electrodes that read out the signal. They call this new method "recognition tunneling."

The current paper in Nature Nanotechnology shows that single bases inside a DNA chain can indeed be read with tunneling, without interference from neighboring bases. Each base generates a distinct electronic signal, current spikes of a particular size and frequency that serve to identify each base. Surprisingly, the technique even recognizes a small chemical change that nature sometimes uses to fine-tune the expression of genes, the so-called "epigenetic" code. While an individual's genetic code is the same in every cell, the epigenetic code is tissue and cell specific and unlike the genome itself, the epigenome can respond to environmental changes during an individual's life.

To read longer lengths of DNA, Lindsay's group is working to couple the tunneling readout to a nanopore – a tiny hole through which DNA is dragged, one base at a time, by an electric field. The paper in Nature Nanotechnology has something to say about this problem too.

"It has always been believed that the problem with passing DNA through a nanopore is that it flies through so quickly that there is no time to read the sequence," Lindsay said. Surprisingly, the tunneling signals reported in the paper last for a long time – nearly a second per base read. To test this result, Lindsay teamed with a colleague, Robert Ros, to measure how hard one has to pull to break the complex of a DNA base plus the recognition molecules. They did this with an atomic force microscope.

"These measurements confirmed the long lifetime of the complex, and also showed that the reading time could be speeded up at will by the application of a small additional pulling force," Ros said.

"Thus the stage is set for combining tunneling reads with a device that passes DNA through a nanopore," Lindsay said.

Sequencing through recognition tunneling, if proven successful for whole genome reading, could represent a substantial savings in cost and hopefully, in time as well. Existing methods of DNA sequencing typically rely on cutting the full molecule into thousands of component bits, snipping apart the ladder of complementary bases and reading these fragments. Later, the pieces must be meticulously re-assembled, with the aid of massive computing power.

"Direct readout of the epigenetic code holds the key to understanding why cells in different tissues are different, despite having the same genome," Lindsay added, a reference to the new ability to read epigenetic modifications with tunneling.

Lindsay stresses much work remains to be done before the application of sequencing by recognition can become a clinical reality.

"Right now, we can only read two or three bases as the tunneling probe drifts over them, and some bases are more accurately identified than others," he said. However, the group expects this to improve as future generations of recognition molecules are synthesized.

"The basic physics is now demonstrated" Lindsay said, adding "perhaps it will soon be possible to incorporate these principles into mass produced computer chips."

The day of the "genome on a lap-top" might be coming sooner than previously thought possible.

(Photo: ASU)

Arizona State University

MYTH OF A GERM-FREE WORLD: A CLOSER LOOK AT ANTIMICROBIAL PRODUCTS

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Killing microorganisms has become a national obsession. A pair of antimicrobial compounds known as triclosan and triclocarban are lately the weapons of choice in our war of attrition against the microbial world. Both chemicals are found in an array of personal care products like antimicrobial soaps, and triclosan also is formulated into everyday items ranging from plastics and toys to articles of clothing.

But are these antimicrobial chemicals, as commonly used by people across the nation, really safe for human health and the environment? More pointedly, do they even work? According to associate professor Rolf Halden, of the Biodesign Institute at Arizona State University, the answer to these questions is an emphatic “No.”

A biologist and engineer, Halden is interested in chemicals produced in high volume for consumer use. “I follow the pathways of these substances and try to figure out what they do to the environment, what they do to us and how we can better manage them.”

The antimicrobial triclosan was patented in 1964, and began its use in clinical settings, where it was found to be a potent bacterial killer, useful before surgical procedures. Since then, industry’s drive to convince consumers of the need for antimicrobials has been aggressive and highly effective. Antimicrobials made their first appearance in commercial hand soaps in the 1980s and by 2001, 76 percent of liquid hand soaps contained the chemical.

Antimicrobials have become a billion dollar a year industry and these chemicals now pervade the environment and our bodies. Levels of triclosan in humans have increased by an average of 50 percent since 2004, according to newly updated data from the Centers for Disease Control and Prevention (CDC).Triclosan and triclocarban are present in 60 percent of all rivers and streams nationwide and analysis of lake sediments have shown a steady increase in triclosan since the 1960s. Antimicrobial chemicals appear in household dust where they may act as allergens, and alarmingly, 97 percent of all U.S. women show detectable levels of triclosan in their breast milk. Such unnecessary exposures carry risks which, at present, are ill-defined.

Halden and his team conducted a series of experiments aimed at tracking the environmental course of the active ingredients in personal care products. The disturbing results of their research indicate that triclosan and triclocarban first aggregate in wastewater sludge and are transferred to soils and natural water environments, where they were observed to persist for months or years.

The chemistry behind these compounds, which contain benzene ring structures that have been chlorinated, make them notoriously difficult to break down. Further, they are averse to water or hydrophobic, tending to stick to particles, which decreases their availability for breakdown processes and facilitates long-range transport in water and air. A recent study demonstrated the accumulation of triclosan in dolphins from contaminated coastal waters.

Earlier, the EPA had been provided with industry-funded studies of wastewater treatment plant effluent, seemingly indicating elimination of triclosan and triclocarban during the treatment process. But Halden speculated that these chemicals might in fact persist in the solid byproduct left over after treatment – the sewage sludge. The group’s suspicions were confirmed through an initial testing of a large wastewater treatment plant serving 1.3 million people, located in the Mid Atlantic region of the U.S.

In the first study of its kind, conducted by the team in 2006, it was determined that three quarters of the mass of triclocarban entering the wastewater treatment facility was simply moved from the water into the sludge. Similar tests confirmed the accumulation of triclosan in sludge with 50 percent efficiency.

“We make 13 billion pounds of dry sludge per year,” Halden notes. “That is equal to a railroad train filled with sludge stretching 750 miles from Phoenix to San Francisco.” One half of this sludge winds up on agricultural fields. The potential for these chemicals to migrate into food or leach into groundwater, has not received adequate consideration. It is likely that antimicrobials are capable of moving up the food chain, through a process known as biomagnification.

Both triclosan and triclocarban have been linked to endocrine disruption, with potential adverse impacts on sexual and neurological development. Further, the accumulation of these antimicrobials in the environment is exerting selective pressure on microorganisms exposed to them, thereby increasing the likelihood that a super-bug, resistant to the very antimicrobials developed to kill them, will emerge – with potentially dire consequences for human health.

On the positive side, Halden’s team identified specific microorganisms adapted to not only tolerate but also break down pervasive antimicrobials. The research is part of a wider effort aimed at alerting the public and regulatory agencies, including the EPA and FDA, of the dangers of these chemicals as well as developing effective remediation strategies.

As Halden explains, “these microbes have the dual advantage of being resistant to destruction by antimicrobials and being able to break down these chemicals. You could put them to use for example by adding them to high-strength industrial wastewater before it gets combined with the domestic sewage.”

In the group’s recent studies, appearing in Water Research and The Journal of Hazardous Materials, levels of triclosan and triclocarban were measured, to determine the degree to which these chemicals, along with other antimicrobials, become concentrated in sludge, and what happens to them thereafter. Triclosan and triclocarban account for two-thirds of the mass of all the antimicrobials in sludge, Halden found, based on a survey of 72 chemicals entering the wastewater treatment stream. Further, massive bioaccumulation of antimicrobial chemicals has been observed in various species. Earthworms exposed to triclosan, for example, showed accumulation of the chemical by a factor of 2700 percent.

Halden notes the impact these persistent chemicals can have on other life forms in the environment that are not their intended target. The thresholds for killing microbes are much higher than those for other, more fragile life forms, like algae, crustaceans and fish.

“This explains why residual concentrations of antimicrobials found in aquatic environments are still sufficiently harmful to wipe out the small and sensitive crustaceans, which are critical to the aquatic life cycle and food web,” Halden says.

For certain, chemicals like triclosan and triclocarban have their place in public health, particularly in clinical settings, among people who are trained in their proper use. However, in 2005, the FDA put together an expert panel to review all the available information on these chemicals. Halden was among the voting members of this committee, which concluded that regular use of antimicrobial products by the general public was no more effective than traditional methods of proper hygiene – simply washing thoroughly with regular soap and water.

Society, Halden insists, is participating in a grand experiment in which we are all guinea pigs. While effective regulation of these chemicals is badly needed, Halden says that the inertia of regulatory agencies is a formidable obstacle. In the meantime, the best hope is for consumers to avoid triclosan and triclocarban containing products.

“The culture of fear leads people to make impulsive decisions and buy a lot of antimicrobial products that are not really needed,” Halden says. “It's a profitable market to be in, but not one that is ultimately sustainable or a good idea.”

(Photo: ASU)

Arizona State University

MASTERMIND STEROID FOUND IN PLANTS

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Scientists have known for some time how important plant steroids called brassinosteroids are for regulating plant growth and development. But until now, they did not know how extensive their reach is. Now researchers, including Yu Sun and Zhi-Yong Wang at Carnegie’s Department of Plant Biology, have identified about a thousand brassinosteroid target genes, which reveal molecular links between the steroid and numerous cellular functions and other hormonal and light-activated chain reactions.

The study, published in the November 16, 2010, issue of Developmental Cell, provides the first comprehensive action map for a plant hormone. The research will help accelerate basic plant science and crop research.

Steroids are important hormones in animals and plants. Unlike animals, plants do not have glands to produce hormones. As a result, each cell has the ability to generate hormones. Animal cells typically respond to steroids using receptor molecules within the cell nucleus. The receptors in plants, called receptor-like kinases, are anchored to the outside surface of the cell membranes. Research has shown that brassinosteroids are involved in acclimation to environmental stresses, promote cell elongation, and enhance resistance to pathogens, thus increasing plant growth and crop yield. But it has been unclear how one steroid hormone controls so many different processes. The breadth of its role has also been incomplete because its target genes have not been identified until now.

“We performed a genome-wide analysis of genes that are direct targets of brassinosteroid in the model plant Arabidopsis, a relative of mustard.” explained coauthor Yu Sun. “We identified DNA sequences in the genome where a transcription factor resides—that is a protein that begins the process of turning a gene on or off. In this case, a protein called BZR1 is the major transcription factor responsible for bassinosteroid-regulated gene expression. It acts at the end of a chain reaction triggered by a steroid binding to the receptor called Brassinosteroid Insensitive 1 (BRI1) at the cell membrane. We were very surprised by the large number of genes involved. Arabidopsis has about 32,000 genes in total and this hormone appears to be masterminding a lot of different physiological responses.”

Scientists have observed a wide range of effects of brassinosteroid on plant growth and plant responses to the environment. They have also worked out the molecular chain that pass the signal from cell surface receptor to BZR1 in the nucleus. How this signaling chain controls various growth and physiological behavior and what cellular machinery it controls was unclear. The scientists found that brassinosteroid target genes turn on a wide range of proteins, including cell-wall enzymes, such as cellulose, a large number of genes concerned with transporting materials throughout plant body and organizing the scaffolding that gives cells their shape, among other developmental processes. Although brasssinosteroid has been known to have a close relationship with several other hormones and light signals, the mechanisms involved with the steroid’s interactions with them are not known. The researchers found that BZR1 protein directly controls the activity of many genes involved in plant responses to other hormones and light. The brassinosteroid action map provided in this study shows for the first time that multiple hormonal and light signals are integrated into an extensive network to control plant growth and development.

(Photo: Carnegie I.)

Carnegie Institution

HOW DO NEURAL STEM CELLS DECIDE WHAT TO BE -- AND WHEN?

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Researchers at Duke-NUS Graduate Medical School in Singapore have uncovered a novel feedback mechanism that controls the delicate balance of brain stem cells.

Zif, a newly discovered protein, controls whether brain stem cells renew themselves as stem cells or differentiate into a dedicated type of neuron (nerve cell).

In preclinical studies, the researchers showed that Zif is important for inhibiting overgrowth of neural stem cells in fruit flies (genus Drosophila) by ensuring that a proliferation factor (known as aPKC) maintains appropriate levels in neural stem cells.

“There is a Zif-related protein in humans, and its function remains to be analyzed,” said senior and corresponding author Hongyan Wang, PhD. “Our finding has paved the way for future study of this human protein in the context of diseases, including glioblastomas, the most severe form of brain tumors.”

She said it may be “possible to manipulate Zif function into a form of therapy against diseases, including cancer.”

The study was published in the Nov. 16 issue of Developmental Cell journal.

The findings suggest that a lack of Zif protein expression correlates with neural stem cell overpopulation in Drosophila.

The mechanism is circular: Zif is a transcription factor that inhibits the manufacture of aPKC. But Zif can also be tagged with a phosphate by aPKC, which excludes Zif from the cell nucleus, and leads to Zif inactivation, which in turn means an overgrowth of stem cells.

“Next, we would like to investigate the mechanisms of neural stem cells’ self-renewal in mammals, and we are looking for the right collaborators,” Wang said. “We will also continue to use Drosophila as a powerful model system to uncover critical players in neural stem cell self-renewal so that we can understand the network involved in this regulation.”

Other authors on the paper included four co-lead authors, Kai Chen Chang and Gisela Garcia Alvarez of the Neuroscience and Behavioral Disorder Program at Duke-NUS Graduate Medical School; Gregory Somers of the Department of Genetics, La Trobe Institute for Molecular Science (LIMS), La Trobe University, in Australia; and Rita Sousa-Nunes of the National Institute for Medical Research, Mill Hill, in London. Fabrizio Rossi is from the Cell Division Group, IRB-Barcelona, PCB, in Barcelona, Swee Beng Soon is also with Duke-NUS Neuroscience and Behavioral Disorder Program, and Cayetano Gonzalez is with both the Cell Division Group, IRB-Barcelona, and the Institucio Catalana de Recerca de Estudis Avançats in Barcelona. William Chia and Kai Chen Chang are both with the Temasek Life Science Laboratory in Singapore.

Duke University Health System

CRACKS IN YOUR CONCRETE? YOU NEED BACILLAFILLA

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A bacteria that can knit together cracks in concrete structures by producing a special ‘glue’ has been developed by a team of students at Newcastle University.

The genetically-modified microbe has been programmed to swim down fine cracks in the concrete. Once at the bottom it produces a mixture of calcium carbonate and a bacterial glue which combine with the filamentous bacterial cells to ‘knit’ the building back together.

Ultimately hardening to the same strength as the surrounding concrete, the ‘BacillaFilla’ – as it has been aptly named – has been developed to prolong the life of structures which are environmentally costly to build.

Designed as part of a major international science competition in the US, the students have scooped Gold for their research.

Joint project instructor Dr Jennifer Hallinan explains: “Around five per cent of all man-made carbon dioxide emissions are from the production of concrete, making it a significant contributor to global warming.

“Finding a way of prolonging the lifespan of existing structures means we could reduce this environmental impact and work towards a more sustainable solution.

“This could be particularly useful in earthquake zones where hundreds of buildings have to be flattened because there is currently no easy way of repairing the cracks and making them structurally sound.”

As part of the research, the students have not only considered the advantages of their engineered bacteria, but also the potential risks to the environment.

The BacillaFilla spores only start germinating when they make contact with concrete – triggered by the very specific pH of the material – and they have an in-built self-destruct gene which means they would be unable to survive in the environment.

Once the cells have germinated, they swarm down the fine cracks in the concrete and are able to sense when they reach the bottom because of the clumping of the bacteria.

This clumping activates concrete repair, with the cells differentiating into three types: cells which produce calcium carbonate crystals, cells which become filamentous acting as reinforcing fibres and cells which produce a Levans glue which acts as a binding agent and fills the gap.

The nine students, whose backgrounds range from computer science, civil engineering and bioinformatics to microbiology and biochemistry, took part in the International Genetically Engineered Machines contest (iGEM), is run out of the Massachusetts Institute of Technology (MIT) in Cambridge, Boston.

The aim is to get together a team of students from a variety of backgrounds to design and genetically engineer a bacterium to do something novel and useful.

Over 130 teams took part in this year’s event and it is now the third time Newcastle University has won Gold. The team instructors were Professor Neil Wipat and Dr Jennifer Hallinan, and the advisors were Dr Wendy Smith, Dr Matthew Pocock, Dr Colin Davies, Dr Jem Stach and Professor Colin Harwood.

Professor Neil Wipat added: “The students have done extremely well – this is a great achievement. Their work will now be used as a basis for research which is being carried out here at the University.”

(Photo: Newcastle University)

Newcastle University

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