By David N. Leff

Editor's note: Science Scan is a roundup of recently published, biotechnology-relevant research.

In some folks, the word "pheromone" evokes a smirk or a snicker. It's thought of as nature's own aphrodisiac. While there's truth in that word picture, a better analogy would be nature's own modem.

Pheromones are specialized hormones secreted by a single individual insect or mammal and broadcast through the atmosphere, to be picked up near or far by other individuals of the same species. So, in a way, a pheromone can also be compared to a biological dot-com e-mail address.

Pushing that comparison, they are like the unsolicited Internet messages that urge its logged-on recipient to take instant action to make a million dollars or turn on to pictures of naked babes. In fact, pheromones trigger a broad spectrum of specific physiological or behavioral responses - including, but not limited to, sexual arousal. A classic example is the synchronization of ovulation and menstruation among the residents of a female school dormitory or women's prison cell block. Pheromones also mediate choice of a mate, onset of puberty, and territorial defense.

Mice receive incoming pheromone traffic on sensory neurons lining a small but strategically placed bone above their nasal cavity, called the vomer. That's the hardware. The software - the molecular mechanism of that reception - is still highly proprietary to Mother Nature. Cracking that code is a field of hot neurobiological research.

One current finding is an article in the September 2000 issue of Nature Genetics, bearing the title: "A putative pheromone receptor gene expressed in human olfactory mucosa." It's known that in rodents those vomeronasal neurons express pheromone receptors. Two large multigene families, V1r and V2r genes, encode the transmembrane proteins.

The paper's co-authors, at The Rockefeller University in New York, used those murine sequences and human receptor fragments to screen a human genomic library, and came up with eight different human sequences. Seven of them were nonfunctional pseudogenes, but the eighth encoded a 313-amino acid polypeptide with strong homology to the mouse receptors. The team named this presumed human gene V1RL1 - standing for V1r-like gene-1. They found that its messenger RNA was expressed in the olfactory mucosa. It seems that the vomeronasal organ occurs during human embryogenesis, but not in adults. The same is true of pigs and rabbits, which receive their pheromonal signals via the main olfactory system, which forwards its messages to the brain.

A separate study by Harvard University scientists, reported in Science dated Sept.1, 2000, carries the title: "Responses of vomeronasal neurons to natural stimuli." Those experimental stimuli consisted of exposing vomeronasal neurons to male and female mouse urine, and measuring the electrical action potentials the neurons evoked. Their paper concluded: "Pheromone-induced behaviors and endocrine changes clearly involve complex sensory recognition that goes beyond mere sex discrimination, requiring identification of the species, familial status, and even individual identity of animals."

Doctrine That Strict Lifetime Adherence To HAART Is Only Way To Stave Off AIDS Ain't Necessarily So

HIV-infected patients prescribed HAART - highly active antiretroviral therapy - are impressed by their physicians with the vital importance of taking their medicine faithfully and nonstop - presumably for life. The presumption is that their ravaged immune defenses can't fight off the replicating virus without HAART.

However, there are three strikes against conscientious patient compliance with that draconian medication: severe side effects, high cost of the treatment, and difficulty adhering to the demanding, multi-pill medication schedule. No wonder large numbers of patients fall by the HAART wayside - quitting off and on, or for good.

However, consider the case of a chronically infected Caucasian man in his 40s. He was diagnosed with HIV in 1987, and had been taking HAART for the past three years. After occasional lapses, he decided to stop the treatment for good. But instead of a vicious upsurge in viral load, his immune system rose to the occasion, and kept his virus levels very low.

This man was one of 10 individuals who signed on to a multicenter clinical test of the hypothesis that dropping HAART from time to time gives the cell-killing T lymphocytes a chance to pull themselves together and fight back. In its September 2000 issue, The Journal of Infectious Diseases reports: "Enhancement of human immunodeficiency virus type-1-specific CD4 and CD8 T-cell responses in chronically infected persons after temporary treatment interruption." Its lead and senior authors are at the Wistar Institute in Philadelphia.

Five of the infected volunteers, who had kept their HIV load down by HAART, were compared with five untreated controls. After swearing off the regimen for an average 55 days, four of the five - who had experienced viral rebound - resumed therapy. By 21 to 33 days later, their new compliance resulted in 98.86 percent suppression of viral load.

Decaffeinating Coffee Plants Genetically, Not Chemically, Takes Initial Biosynthetic Step

It had to come - recombinant decaf. Coffee breaks at meetings, restaurant menus and supermarket shelves, all feature decaffeinated coffee as a rival to the real stuff in the contemporary American culture. At present, the preferred method of decaffeination relies on supercritical fluid extraction with carbon dioxide, an expensive technology. Other, largely phased-out processes employed toxic industrial solvents. To coffee connoisseurs, an added intangible cost of decaf is diminished flavor and aroma.

Caffeine, methyltheobromine, is an alkaloid chemically close to chocolate, and also present in tea leaves. One grain (1/437.5 ounce) of pure caffeine is toxic.

Now a team of biochemists and molecular biologists in Japan and the University of Glasgow in Scotland have isolated a key enzyme that catalyzes the last two steps in the biosynthesis of caffeine, with a view toward creating transgenic, caffeine-free, flavor-retaining coffee (Coffea arabica) and tea (Camellia sinensis). Their progress report in Nature dated Aug. 31, 2000, is titled: "Caffeine synthase gene from tea leaves." Before production of caffeine-deficient coffee plants becomes practical, the paper concludes, "some information is needed about the genes controlling key conversions in the biosynthesis of caffeine."

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