Tuesday, October 27, 2009
Etiquetas: Computing Sciences
In the quest for smaller, faster computer chips, researchers are increasingly turning to quantum mechanics -- the exotic physics of the small.
The problem: the manufacturing techniques required to make quantum devices have been equally exotic.
That is, until now.
Researchers at Ohio State University have discovered a way to make quantum devices using technology common to the chip-making industry today.
This work might one day enable faster, low-power computer chips. It could also lead to high-resolution cameras for security and public safety, and cameras that provide clear vision through bad weather.
Paul Berger, professor of electrical and computer engineering and professor of physics at Ohio State University, and his colleagues report their findings in an upcoming issue of IEEE Electron Device Letters.
The team fabricated a device called a tunneling diode using the most common chip-making technique, called chemical vapor deposition.
“We wanted to do this using only the tools found in the typical chip-makers toolbox,” Berger said. “Here we have a technique that manufacturers could potentially use to fabricate quantum devices directly on a silicon chip, side-by-side with their regular circuits and switches.”
The quantum device in question is a resonant interband tunneling diode (RITD) -- a device that enables large amounts of current to be regulated through a circuit, but at very low voltages. That means that such devices run on very little power.
RITDs have been difficult to manufacture because they contain dopants -- chemical elements -- that don’t easily fit within a silicon crystal.
Atoms of the RITD dopants antimony or phosphorus, for example, are large compared to atoms of silicon. Because they don’t fit into the natural openings inside a silicon crystal, the dopants tend to collect on the surface of a chip.
“It’s like when you’re playing Tetris and you have a big block raining down, and only a small square to fit it in. The block has to sit on top,” Berger said. “When you’re building up layers of silicon, these dopants don’t readily fit in. Eventually, they clump together on top of the chip.”
In the past, researchers have tried adding the dopants while growing the silicon wafer one crystal layer at a time -- using a slow and expensive process called molecular beam epitaxy, a method which is challenging for high-volume manufacturing. That process also creates too many defects within the silicon.
Berger discovered that RITD dopants could be added during chemical vapor deposition, in which a gas carries the chemical elements to the surface of a wafer many layers at a time. The key was determining the right reactor conditions to deliver the dopants to the silicon, he found.
“One key is hydrogen,” he said. “It binds to the silicon surface and keeps the dopants from clumping. So you don’t have to grow chips at 320 degrees Celsius [approximately 600 degrees Fahrenheit] like you do when using molecular beam epitaxy. You can actually grow them at a higher temperature like 600 degrees Celsius [more than 1100 degrees Fahrenheit] at a lower cost, and with fewer crystal defects.”
Tunneling diodes are so named because they exploit a quantum mechanical effect known as tunneling, which lets electrons pass through thin barriers unhindered.
In theory, interband tunneling diodes could form very dense, very efficient micro-circuits in computer chips. A large amount of data could be stored in a small area on a chip with very little energy required.
Researchers judge the usefulness of tunneling diodes by the abrupt change in the current densities they carry, a characteristic known as “peak-to-valley ratio.” Different ratios are appropriate for different kinds of devices. Logic circuits such as those on a computer chip are best suited by a ratio of about 2.
The RITDs that Berger’s team fabricated had a ratio of 1.85. “We’re close, and I’m sure we can do better,” he said.
He envisions his RITDs being used for ultra-low-power computer chips operating with small voltages and producing less wasted heat.
“Chip makers today are having a great difficulty boosting performance in each generation, so they pack chips with more and more circuitry, and end up generating a lot of heat,” Berger said. “That’s why a laptop computer is often too hot to actually sit atop your lap. Soon, their heat output will rival that of a nuclear reactor per unit volume.”
“That’s why moving to quantum devices will be a game-changer.” RITDs could form high-resolution detectors for imaging devices called focal plane arrays. These arrays operate at wavelengths beyond the human eye and can permit detection of concealed weapons and improvised explosive devices. They can also provide vision through rain, snow, fog, and even mild dust storms, for improved airplane and automobile safety, Berger said. Medical imaging of cancerous tumors is another potential application.
Ohio State University
Now, researchers at the Salk Institute for Biological Studies shed light on the long missing connection: A metabolic master switch, which, when thrown, allows nutrients to directly alter the rhythm of peripheral clocks.
Since the body's circadian rhythm and its metabolism are closely intertwined, the risk for metabolic disease shoots up, when they are out of sync. "Shift workers face a 100 percent increase in the risk for obesity and its consequences, such as high blood pressure, insulin resistance and an increased risk of heart attacks," says Howard Hughes Medical Investigator Ronald M. Evans, Ph.D., a professor in the Salk Institute's Gene Expression Laboratory.
The researchers' findings, which are published in the Oct. 16, 2009, issue of Science, could have far-reaching implications, from providing a better understanding how nutrition and gene expression are linked, to creating new ways to treat obesity, diabetes and other related diseases. "It is estimated that the activity of up to 15 percent of our genes is under the direct control of biological clocks," says Evans. "Our work provides a conceptual way to link nutrition and energy regulation to the genome."
The clocks themselves keep time through the rhythmic waxing and waning of circadian gene expression on a roughly 24-hour schedule that anticipates environmental changes and adapts many of the body's physiological functions to the appropriate time of day. The most obvious one, the sleep-wake rhythm, is tightly linked to the night-day cycle. But so are physical activity and metabolism.
"When we get up in the morning we 'break the fast'," says Evans. While opening the fridge doesn't require a lot of physical activity, the situation for animals in the wild is quite different. "If you are a predatory animal you run to hunt. If you are prey, you run to get away."
But how pacemakers in peripheral tissues such as the liver and muscle knew that it was time to scurry and replenish their energy stores was still an open question. When postdoctoral researcher and first author Katja Lamia, Ph.D., started probing the relationship between metabolism and circadian cycles, she discovered a highly conserved phosporylation site in CRY1, short for cryptochrome 1. Cryptochromes originally evolved as a blue light photoreceptor in plants and, although no longer sensitive to light, are now an integral part of the clock in vertebrates.
The phosphorylation site is specific for AMPK, which acts like a gas gauge by sensing how much energy a cell has. When a cell has plenty of energy, AMPK remains inactive and the cell carries out its normal processes. Her experiments revealed that if a cell runs on empty, AMPK is turned on and attaches a phosphate molecule to CRY1, which initiates the destruction of CRY1. As a result the circadian rhythm speeds up and the clock is reset.
"The insertion of an AMPK phosphorylation site transformed a light sensor into an energy sensor, which now allows nutrients to provide metabolic input to circadian clocks," explain Lamia. "Insertion of a novel sensor into an existing signaling pathway is a very elegant solution to a rather complicated problem."
Genetic inactivation of AMPK in mice blocks these effects, stabilizing CRY1 and severely disrupting peripheral clocks. In contrast, treating mice with AICAR, a synthetic drug that directly activates AMPK, reset the clock in cultured cells as well as in animals, confirming that cryptochromes act as energy sensors that allow to circadian clocks.
While some scientists have argued that cancer is such a complex genetic disease that you'd have to sequence a person's complete genome in order to predict his or her cancer risk, a University of California, Berkeley, cell biologist suggests that the risk may be more simply determined by inexpensively culturing a few skin cells.
Harry Rubin, professor emeritus of molecular and cell biology at UC Berkeley, acknowledges that cancer cells have mutations in hundreds of genes, making it hard to determine which are the key triggers and making prognosis and treatment equally difficult. Even normal tissue differs from person to person because of a myriad of less disruptive mutations and because of different environmental exposures, both of which affect future cancer risk.
But in the September issue of the journal Cancer Epidemiology, Biomarkers and Prevention, Rubin argues that, while it may be hard to dissect the role of each of these mutations, their collective effect should be observable in tissue before any cancers develop.
Specifically, increases in how densely the cells grow, which Rubin argues are a prelude to cancer, may be detectable even before the cancer appears, warning of risks that could be lessened by behavioral changes.
"Over a 50-year career, I've worked with cells transforming (into cancer) in culture and seen the first step in a dynamic way, seen cells continuing to multiply when they should have stopped," Rubin said. "This is the first step in cancer, though not yet cancer, and you can measure these changes quantitatively."
The problem, of course, is that it is impractical to test all the body's tissues to determine whether they have abnormal cell growth. But Rubin has found evidence from other studies that, in some cases, skin fibroblasts show these early changes even before cancer appears in other tissues, such as the colon.
"The abnormal growth behavior of skin fibroblasts in cancer-prone individuals has suggested that, at least in some cases, cancer can be considered a systemic disease and that this difference in the behavior of skin fibroblast cells from such individuals may be a practical basis for prevention, diagnosis and management of the disease," he concluded in his paper.
"It's a great idea, scientifically; the question is, 'Is it there clinically?'" said Douglas Brash, professor of therapeutic radiology, genetics and dermatology at Yale School of Medicine. "This is interesting enough that someone should look to see whether it is clinically reliable."
Dr. Stuart H. Yuspa, co-chief of the Laboratory of Cancer Biology and Genetics at the National Cancer Institute, agreed. "Harry's ideas are always amazing, and I admired the paper," he said. "His idea has scientific support, and if it turned out to be correct, it could be extremely valuable for people, assuming they would want to know their risk."
Rubin bases his argument on various studies over the past 50+ years that show that cancers grow from a larger "field" of abnormally multiplying cells that otherwise look normal. These "field" cells are generally ignored by surgeons when they remove solid cancers - in fact, the large size of the field would make its total removal impossible - but pathologists have shown that the cells are capable of again giving rise to cancers.
"These cells have early mutations that could lead to cancer," Rubin said. "Even though they look normal, they multiply in places where they shouldn't and eventually accumulate enough mutations to form a carcinoma. They are the first stage in cancer, but not cancer."
The inappropriate growth - called cancerization - is a sign that the normal processes that stop growth when cells contact one another have been disrupted, though not fully, because otherwise the cells would invade the underlying connective tissue and become cancerous.
Rubin showed in experiments 15 years ago that if you take cells that grow normally in cell culture and encourage mutations, then select for behavioral abnormalities involving growth, you can get proliferation of cells that behave like cancerization field cells.
Similarly, while normal skin fibroblast cells grow to a certain density and stop, fibroblasts from cancer-susceptible individuals grow to an unusually high density in a Petri dish. That difference between fibroblasts from normal and cancer-susceptible individuals can be amplified to improve identification of those at risk of cancer, Rubin said.
Rubin suspects that the growth change in skin fibroblasts heralds a general change in all the body's epithelial tissue, that is, the tissues that line all the body organs. The most prevalent cancers - including colon, breast, lung, skin, head and neck - arise from epithelial tissue. In certain cancer-prone families, for example, the same mutated gene is found in all tissues, and the fibroblasts grow to high densities in culture, just like epithelial cells in a precancerous field do in the body.
"If this works out after studying a large number of cases, then the people who are found to have a high probability of developing cancer would be more likely to pay attention to their diet, exercise, weight, smoking and behaviors that are known to contribute to an increased risk of cancer," he said. "Basic studies of a cell culture model for field cancerization should reveal the conditions that drive or delay the process and could be applied in prevention of cancer."