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Chip Wizardry: Transistors That Build Themselves


Building computer chips packed with millions of transistors is a costly affair, with new plants running upward of $1 billion. That's one reason scientists at Lucent Technologies' Bell Labs (LU) are intent on inducing at least some of the elements on a chip to assemble themselves.

In the Oct. 18 issue of Nature, a Bell Labs team headed by Hendrik Schon describes an important step in this direction. The team has created a transistor in which one of the key features is an ultrathin layer of organic molecules, called thiols. These deposit themselves with perfect precision on a gold-coated silicon substrate. No fancy photolithography is required, says John Rogers, Bell Labs' director of nanotechnology research, referring to today's standard circuit-printing technology. "The whole thing just happens in a beaker at a chemistry bench," he says, and the device performs well as both an amplifier and an on-off switch.

Like all transistors, this one channels a current between two electrodes. In conventional transistors, these elements must be carefully designed and processed, with special attention to shrinking the distance between the electrodes. At Bell Labs, that's not necessary. Instead, the distance is defined by the size of the minuscule thiol molecules--just one nanometer in length, or about the size of five carbon atoms in a row.

Hendrik Schon says it could be 10 years before his new chemistry is adopted in commercial chipmaking. But other applications could come faster. The process may be ideal for manufacturing high-tech fabrics for wearable computers, and flexible computer displays that can be folded or rolled. Taking Remicade, a popular drug for the treatment of rheumatoid arthritis and Crohn's disease, nearly quadruples the risk of developing tuberculosis, say researchers for the Food & Drug Administration. Their study, published in the Oct. 11 issue of The New England Journal of Medicine, found that from August, 1998, when the drug was approved, to May, 2000, 70 people treated with Remicade developed TB, and four of those patients died as a result. The annual incidence of TB cases in arthritis sufferers is normally 6.2 cases per 100,000, while for patients taking Remicade the rate was 24.4 per 100,000, the researchers said.

Some 170,000 people worldwide have received Remicade, made by Johnson & Johnson's (JNJ) Centocor unit, to control the pain associated with both arthritis and Crohn's, an intestinal disease. Centocor reported the high incidence of TB cases to the FDA this summer and, in August, changed Remicade's label to recommend that doctors test patients for TB infection before prescribing the drug. The company says its surveys show that 90% of doctors are now doing so.

Remicade is an antibody that suppresses tumor necrosis factor (TNF), a protein that plays a key role in inflammation. But TNF may also protect people who have been infected with the TB bacterium, says Dr. Joseph Keane of Boston University School of Medicine, the study's lead author. The World Health Organization estimates that one in three people worldwide harbors the bacterium, but only 10% ever develop the disease. Remicade may trigger these latent infections, Keane says. When terrorists struck on September 11, cell phones let desperate people exchange precious last words. But as callers crowded the airwaves, cell towers were swamped and connections were lost. A system called iCAR, for integrated cellular ad hoc relay, might help in such situations. It's a miniature base station, which might be no bigger than a headphone stereo, devised by University of Buffalo computer scientist Chunming Qiao and his colleagues. In emergencies, cellular service providers could slap iCAR devices on walls around the city. They would automatically pick up calls overflowing from congested cell towers and relay them to the nearest unburdened towers. Qiao's iCAR research was funded by the National Science Foundation and Finland's Nokia (NOK). So far, the phone giant has no plans to build the devices. The latest effort to come up with a male contraceptive focuses not on blocking or killing the sperm but on temporarily slowing it down. Researchers at the Howard Hughes Medical Institute and Harvard Medical School have discovered a protein found only in the tail of the sperm that plays a key role in powering it up to burst through to the center of the egg, where fertilization occurs.

The scientists believe that a drug aimed at temporarily blocking this protein could be taken by men or women, before or even right after sex, with no lasting effect on fertility. The research is described in the Oct. 11 issue of Nature.

After discovering the protein, which they call CatSper, the scientists removed the gene that produces it from a strain of mice. The sperm of the altered mice were less vigorous than normal, and the mice were completely infertile. However, the researchers discovered that if they removed the outer coating of an egg, the weakened sperm could fertilize it normally. Howard Hughes researcher David Clapham says the protein may give the sperm's tail a turbocharge at the last minute to penetrate the egg.


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