Notebook

Another Vote To Nix The Pox Four Scientists Get Met-It Pay Help For Insomniacs? Cleaning Up The Cleanup Mullis On HIV: Where's The Beef? Hope For The Heavy Date: February 19, 1996 CONDEMNED: One of the two remaining smallpox stores Like a death-row inmate running out of chances to appeal, the last two remaining stores of smallpox virus have again been condemned to destruction. Late last month the governing board of the World Heath Organization (WHO) in Geneva recommended that the smallpox stocks-one padlocked and chained in Russia and another held in a high-security area at the Centers for Disease Control and Prevention in Atlanta-be eradicated by June 30, 1999 (L.K. Altman, New York Times, Jan. 25, 1996, page A1). The final decision to get rid of the virus may be made at WHO's next annual meeting in May. The destiny of the virus has been in limbo for the last 15 years. WHO declared the deadly disease eradicated in 1980. In 1986, a WHO panel of experts unanimously agreed to do away with viral stores, but it took until 1990 to decide to set Dec. 30, 1993, as the date of destruction. These delays occurred primarily because of objections from leading virologists worldwide (K.Y. Kreeger, The Scientist, Nov. 14, 1994, page 1), who thought the virus still had useful biomedical secrets to yield. Then in January 1995, the virus won a stay of execution until June of last year because of "behind-the-scenes" efforts of unnamed British and American scientists (L.K. Altman, New York Times, Jan. 19, 1995, page A15). That date came and went with no move to destroy the virus. In the most recent decision, WHO expert committees concluded that the risk of future smallpox epidemics from inadvertent or intentional escape far outweighed any scientific knowledge gained in keeping it. To play the saga out further, WHO representatives from France and Australia proposed a compromise-delaying the microbe's death by autoclave and incineration by 3 1/2 years. "I do hope some work will be done to exploit this reprieve," remarks Wolfgang Joklik, the James B. Duke Professor of Microbiology at Duke University and a long-standing and vociferous proponent of saving the virus. Date: February 19, 1996 FAB FOUR: The 1996 MetLife awardees are, clockwise from left, are Thomas Bird, Gerar Schellenberg, Ellen Wijsman and Rudolg Tanzi The Metropolitan Life Foundation has presented a total of $500,000 to four scientists in honor of their contributions to understanding the molecular genetics of Alzheimer's disease. Rudolph Tanzi, director of the genetics and aging unit at the Massachusetts General Hospital in Boston and an associate professor of neurology at Harvard Medical School; and the University of Washington team of Thomas D. Bird, Gerard D. Schellenberg, and Ellen M. Wijsman shared the foundation's Award for Medical Research in Alzheimer's Disease. Bird is chief of neurology at the Seattle Veterans Affairs Medical Center and a professor of neurology and medical genetics at Washington. Schellenberg is associate director for research at the center's geriatric research education clinical center and a research professor in Washington's School of Medicine. Wijsman is a research associate professor in Washington's School of Medicine and biostatistics department. They were honored last month at a Washington, D.C., ceremony that also celebrated the 10th anniversary of MetLife's awards program. The investigators each received personal awards of $25,000 and research awards of $100,000. They were specifically recognized for the significance and collaborative nature of their work. The four are credited with genetic AD discoveries-both separately and collaboratively-involving three chromosomes. Their latest achievement came last year. Tanzi collaborated with Schellenberg, Bird, and Wijisman to pinpoint a third familial AD gene to chromosome 1 (E. Levy-Lahad, W. Wasco et al., Science, 269:973-7, 1995). The New York-based Metropolitan Life Insurance Co. established the foundation in 1976. Date: February 19, 1996 A cluster of brain cells that helps turn on and off sleep may eventually lead to improved treatments for insomnia. Scientists from Harvard Medical School recently reported uncovering a so-called master switch in the brain that controls sleep. According to a report in the New York Times (S. Blakeslee, Jan. 12, 1996, page A18), when the switch is turned on, all brain cells involved in arousal and awareness are turned off. The brain wakes up when the switch is turned off. Clifford Saper, chairman of neurology at Beth Israel Hospital and James Jackson Putnam Professor of neurology and neuroscience at Harvard Medical School, who led the research, notes that the group of cells "is in the perfect position to be a master switch to turn off the arousal systems of the brain and allow sleep to occur." The work (J.E. Sherin et al., Science, 271:216-9, 1996), was performed in rats, though the researchers think the findings will apply to humans because of similarities in brain circuitry among mammals. In the experiments, the scientists found that during sleep most nerve cells of the brain are shut down by a signal sent by cells in the hypothalamus. The researchers used chemical tracers to track the activity of rat brain cells during sleep. They found that a nerve cell group called the ventrolateral preoptic area, or VLPO, was the only cell group that was active, and acting as a sleep switch. "The next step is to identify nerve inputs to the VLPO to see what turns these cells on," says Saper. "If we can find the neurotransmitters and receptors involved, we may be able to design drugs that induce natural sleep." Date: February 19, 1996 Two new National Research Council (NRC) reports on environmental cleanup by the Department of Energy (DOE) simultaneously commend DOE for its recent efforts and chide the agency for inefficiency and slowness. The job of cleansing 120 sites is estimated by DOE to cost between $200 billion and $350 billion and take 75 years. Improving the Environment: An Evaluation of the DOE's Environmental Management Program says that DOE and its contractors have little incentive for proceeding quickly with the cleanup. The report's authors blame the federal budget process, stating that the budget procedure discourages rapid cleanup because money allocated decreases as contractors succeed in reducing the size and seriousness of environmental pollution. The document calls for improved incentives to speed cleanup efforts, among other suggestions. Another related report, Barriers to Science: Technical Management of the Department of Energy Environmental Remediation Program, produced by a committee affiliated with NRC's Board on Radioactive Waste Management, addresses DOE's management of buried hazardous wastes. This report also criticizes DOE for inefficiencies and "narrow interpretations of regulations." According to an NRC statement, "DOE faces large penalties for any criticism, whether deserved or not, and receives little reward for substantive accomplishments, resulting in incentive structures which are distorted." Both reports are available from the National Academy of Sciences, 2101 Constitution Ave., N.W., Washington, D.C. 20418. For Improving the Environment, call the National Academy Press, (202) 334-3313. For Barriers to Science, call the Board on Radioactive Waste Management, (202) 334-3066. PERPLEXED: Nobelist Kary Mullis wants proof that HIV causes AIDS. Kary Mullis wants to see the evidence that the human immunodeficiency virus, or HIV, is the culprit behind AIDS. "How do we know that HIV causes AIDS?" he asked a standing-room-only audience of students and scientists at Thomas Jefferson University in Philadelphia on February 6. "I asked people and I read the literature and decided eventually that there was not a paper or series of papers or a review that said these were the reasons we should think HIV is the probable cause of AIDS." Mullis, who shared the 1993 Nobel Prize in chemistry for inventing the polymerase chain reaction, the now-indispensable tool of geneticists worldwide, was at the university to visit a colleague, Eric Kmiec, an associate professor of pharmacology. Mullis's lecture was titled, "HIV Does Not Cause AIDS." He offered little hard evidence to support this notion, but rather contended that there is a lack of conclusive proof in the scientific literature to pin the blame for AIDS exclusively on HIV. "I started asking, who should we credit, who should we thank for demonstrating that HIV causes AIDS?," he told the audience. "There is not a scientific paper to demonstrate that HIV causes AIDS. All of the arguments that HIV causes AIDS, as far as I can tell, are vacuous. How does everyone here know that it does so?" he asked. "Where are the papers or paper that I can read and say, 'I trust this experiment or I don't trust this experiment but I can repeat it,' and I can come to a conclusion without raising my voice or having to shout someone down or someone telling me I'm saying something dangerous?" According to Mullis, "we're dealing with very serious issues, and no one seems to be worrying whether or not if we as the medical establishment are poisoning about 100,000 people a year [with AZT and other anti-HIV drugs] under a hypothesis that we have no evidence to prove." Audience members' questions following the talk indicated that they were skeptical of, but intrigued by, Mullis's presentation. Date: February 19, 1996 Dieters rejoice. While no one's invented an anti-weight-gain pill yet, and researchers are hardly claiming they completely understand the body's weight-control mechanisms, a pair of recent scientific discoveries gives hope to those fighting the battle of the bulge. A team led by Stephen R. Bloom at Hammersmith Hospital in London reported finding a protein-dubbed GLP-1, or glucagon-like peptide-1-that tells the brain immediately when enough food is enough. When the protein was injected into the brains of hungry rats, they suddenly lost their appetites. The scientists think humans also have the protein, since it has been found in many other vertebrate species. The work was published on January 4 in Nature (M.D. Turton et al., 379:69-72, 1996). The report came just a week after two teams of investigators announced that they had uncovered another key piece of the weight-control puzzle. They located a molecular gateway, or receptor, that receives a message from the protein leptin, which keeps body weight at a set level. The leptin receptor relays the protein's signal to fat-burning and appetite-control centers in the brain. Louis A. Tartaglia and coworkers at Millennium Pharmaceuticals in Cambridge, Mass., and researchers at Hoffmann-La Roche Inc. in Nutley, N.J., reported the discovery on December 29 in Cell (L.A. Tartaglia et al., 83:1263-71, 1995). "Undoubtedly, the work has therapeutic potential, though not immediately," comments obesity expert Albert Stunkard, a professor of psychiatry at the University of Pennsylvania. This pair of findings comes six months after a team led by Jeffrey Friedman of Rockefeller University announced the discovery of leptin (J.L. Halass et al., Science, 269:543-7, 1995). Together the findings may eventually help scientists better understand how and when people feel full and lead to effective treatments for obesity.

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