Wednesday, February 16, 2011

Building block for smaller, smarter electronics?

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Using a concept called DNA origami, Arizona State University researchers are trying to pave the way to produce the next generations of electronics products.

They’re pursuing advances in nanotechnology that have the potential to enable creation of smaller components for consumer and industrial electronics such as iPods, iPads and similar devices.

Manufacturers want to make the devices smaller and “smarter.” The problem is that this requires making the internal electrical parts of such devices at an even smaller nanometer scale, while also increasing the ability of the components to perform an array of computing, communication and multimedia functions.

Making these components smaller would become vastly more expensive using the current method of manufacturing microelectronic components such as the central processing units (CPUs) of all computers.

ASU’s Hongbin Yu and Hao Yan are teaming up to develop the basis of a new manufacturing method that would keep costs down.

Yu is an assistant professor in the School of Electrical, Computer, and Energy Engineering, one of ASU’s Ira A. Fulton Schools of Engineering. Yan is a professor in the Department of Chemistry and Biochemistry in ASU’s College of Liberal Arts and Sciences.

Details of their progress have recently been reported in Nano Letters, a leading nanoscience and technology journal published by the American Chemical Society. The news has also been featured on Chemistry World, a science and technology news website of the Royal Society of Chemistry, the leading European organization for advancing chemical sciences.

Yu explains that he and Yan are exploring “how to use top-down lithography combined with modified bottom-up self-assembling nanostructures to guide the placement of nanostructures on silicon wafer surface.”

Top-down lithography is a process by which electrical circuit elements on a silicon wafer are constructed by cutting and etching, in a way similar to how sculptures are made. This is how today’s computer chips are manufactured.

Bottom-up self-assembly is a process in which molecules and/or nanoscale materials are self-assembled into desired structures using chemical bonds or various similar interactions.

Yu and Yan have discovered a way to use DNA to effectively combine top-down lithography with chemical bonding involving bottom-up self-assembly.

This involves a “DNA origami” design technique similar to the traditional Japanese art or technique of folding paper into decorative or representational forms. It allows DNA strands to be folded into something resembling a pegboard on which different molecules can be attached.

Enabling various molecules to attach to the DNA produces smaller nanostructure configurations – thus opening the way to construction of smaller electronic device components.

In the past it has proven difficult to combine top-down lithography with bottom-up self-assembly because the DNA nanostructures required to make it happen would bind indiscriminately to the silicon platform (called a substrate) – the material on which an electronic circuit is fabricated.

“There have been few successful demonstrations of how to put these bottom-up assembled nanostructures on the surface of the substrate where you want them to be,” Yu explains, “because you cannot just run these devices, you need to know where to connect what.”

To solve the problem, Yu’s research team prefabricated a gold “nano-island” at specific locations on a silicon substrate, then applied the DNA origami that has specific chemical ends that will bond only to the gold island and not the silicon wafer. This allows the DNA nanotubes to attach only to the islands.

The work demonstrates that it’s possible that a DNA double helix can be used to build one-dimensional and two-dimensional structures to enable the manufacture of smaller electronic memory devices – at a cost that would be far less than current manufacturing methods.

More progress is needed, Yu says.

“With this demonstration we were able to build patterns on surface that consist of only one-dimensional DNA nanotubes, but our research shows it is possible to produce two-dimensional and even more sophisticated structures that are essential building blocks for nanoscale electronic circuits,” Yu says. “So this is just the beginning of many fascinating possibilities to be realized.”

(Photo: Arizona SU)

Arizona State University

Ancient body clock discovered that helps to keep all living things on time

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The mechanism that controls the internal 24-hour clock of all forms of life from human cells to algae has been identified by BBSRC-funded scientists.

Not only does the research provide important insight into health-related problems linked to individuals with disrupted clocks - such as pilots and shift workers - it also indicates that the 24-hour circadian clock found in human cells is the same as that found in algae and dates back millions of years to early life on Earth.

Two new studies out today in the journal Nature from the Universities of Cambridge and Edinburgh give insight into the circadian clock which controls patterns of daily and seasonal activity, from sleep cycles to butterfly migrations to flower opening.

One study, from the University of Cambridge's Institute of Metabolic Science, has for the first time identified 24-hour rhythms in red blood cells. This is significant because circadian rhythms have always been assumed to be linked to DNA and gene activity, but - unlike most of the other cells in the body - red blood cells do not have DNA.

Akhilesh Reddy, from the University of Cambridge and lead author of the study, said: "We know that clocks exist in all our cells; they're hard-wired into the cell. Imagine what we'd be like without a clock to guide us through our days. The cell would be in the same position if it didn't have a clock to coordinate its daily activities.

"The implications of this for health are manifold. We already know that disrupted clocks - for example, caused by shift-work and jet-lag - are associated with metabolic disorders such as diabetes, mental health problems and even cancer. By furthering our knowledge of how the 24-hour clock in cells works, we hope that the links to these disorders - and others - will be made clearer. This will, in the longer term, lead to new therapies that we couldn't even have thought about a couple of years ago."

For the study, the scientists, funded by the Wellcome Trust, incubated purified red blood cells from healthy volunteers in the dark and at body temperature, and sampled them at regular intervals for several days. They then examined the levels of biochemical markers - proteins called peroxiredoxins - that are produced in high levels in blood and found that they underwent a 24-hour cycle. Peroxiredoxins are found in virtually all known organisms.

A further study, by scientists working together at the Universities of Edinburgh and Cambridge, and the Observatoire Oceanologique in Banyuls, France, found a similar 24-hour cycle in marine algae, indicating that internal body clocks have always been important, even for ancient forms of life.

The researchers in this study found the rhythms by sampling the peroxiredoxins in algae at regular intervals over several days. When the algae were kept in darkness, their DNA was no longer active, but the algae kept their circadian clocks ticking without active genes. Scientists had thought that the circadian clock was driven by gene activity, but both the algae and the red blood cells kept time without it.

Andrew Millar of the University of Edinburgh's School of Biological Sciences, who led the study, said: "This groundbreaking research shows that body clocks are ancient mechanisms that have stayed with us through a billion years of evolution. They must be far more important and sophisticated than we previously realised. More work is needed to determine how and why these clocks developed in people - and most likely all other living things on earth - and what role they play in controlling our bodies."

Biotechnology and Biological Sciences Research Council

Disruptions in calcium flow linked to heart failure

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Excessive release of calcium inside cardiac muscle can cause sudden cardiac death in heart failure patients. New research has revealed how this could happen, opening up new possibilities for combating heart disease.

Calcium plays a vital role in regulating cardiac muscle contraction. With each heartbeat, calcium is released from intracellular stores known as the sarcoplasmic reticulum (SR), through specialised channels called ryanodine receptors (RyR2). The normal trigger for this response is calcium itself, in a process known as calcium-induced calcium-release.

Experts in physiology and pharmacology from the University of Bristol conducted a series of tests which showed that a protein called protein kinase C (PKC) can cause excessive openings of these RyR2 channels, causing too much calcium to be released into the cardiac muscle.

Reporting their findings in the Journal of Membrane Biology, the researchers describe how this excess of calcium could lead to a disturbance in the normal rhythm of the heart, referred to as arrhythmias.

Dr Rebecca Sitsapesan, Reader in Pharmacology from Bristol University, explained: “Our findings reveal a novel mechanism for opening calcium channels inside heart cells. We show that a protein called PKC can disrupt the normal behaviour of the calcium channels, causing excessive openings at the wrong time. This new information will help us to design treatments that can prevent this occurring and help in the fight against heart disease.

“Our experiments measure the opening and closing of single calcium channels. We have been able to show that PKC changes the way in which the calcium channels open and this may be one of the reasons why too much calcium is released in heart cells at the wrong time and why patients with heart failure are at risk of sudden cardiac death.”

(Photo: Bristol U.)

University of Bristol

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