Photo: University of Texas Health Science Center at Houston
Opportunities in Allison's wake Since Hurricane Allison struck last June, researchers at the University of Texas Health Science Center, Houston, have been rebuilding and improving their facilities. "We said, 'Let's not just build back what we had, let's aim to do it better,'" says George Stencel, interim vice president for research. He estimates the project's cost in the "several hundred million dollar" range (H. Black, "Allison hits Houston research community," The Scientist, 15:1, July 23, 2001). Destroyed equipment and animals, once housed in the basement, are literally moving up. New imaging equipment, such as MRIs, will be in a "world-class imaging suite" on the ground floor. The suite will be raised by at least three feet to protect against future flooding. Animals will be moved to an upper floor in the eight-story building. Michael Blackburn, assistant professor of chemistry and microbiology, lost an entire colony of transgenic mice. They were susceptible to asthma, and he was studying them to develop a treatment. At first, he thought the new colony would take two years to recover. Instead, it took about six months. "We're essentially back to normal," he says. He credits the resilience of his graduate students and postdocs, and the generosity of his collaborators in other institutions, who sent him animals that he had shared with them. While the colony was being regenerated, "We started doing experiments we probably would not have done," he says. New findings have emerged, which he says might never have happened without Allison.
Photo: Courtesy of Response Biomedical
Anthrax test overlooked? Make way for the world's best anthrax assay. So declares Bill Radvak, president and CEO of Response Biomedical, British Columbia, Canada. He's miffed at a White House recommendation made in July against field use of rapid tests for anthrax detection, which reflects adverse findings in an earlier study by the Centers for Disease Control and Prevention (CDC). Tests of his firm's 15-minute immunoassay by the Maryland State Department of Health, by Seattle-based Intertox, and by the Canadian Department of National Defense all show that it can detect less than 4,000 spores of anthrax, far below the infectious dose of 10,000 spores and much better than any competitor, he says. The device employs a strip of known antibodies that serves as an internal control zone, subject to the same variability as the test antibodies. By performing a ratio of the two sets, the variability is factored out. But high sensitivity also means that high volumes of anthrax will plug up the system. An easy dilution process solves this problem, yet the CDC failed to follow those instructions, Radvak charges. The company has secured $4 million from Canada's government for more tests. Meanwhile, he's courting the White House. "It's been almost a full year since the [anthrax] attacks and the state of the art has not improved. We think we have that improvement," he says.
Photo: Courtesy of Jeff Miller
Miracle mice stay slim without dieting Mice with the SCD-1 gene knocked out gain no weight, a team of researchers from the University of Wisconsin (UW), Madison, and Rockefeller University reports (J.M Ntambi et al., "Loss of stearoyl CoA desaturase-1 function protects mice against adiposity," Proceedings of the National Academy of Sciences, 99:11482-6, Aug. 12, 2002). The finding not only offers an attractive target to help control obesity, but also raises tantalizing basic science questions, says James Ntambi, associate professor of biochemistry at UW-Madison. "We were surprised to see that when this enzyme is knocked out there is a switch in the pathways of lipid metabolism from storage to burning. If you have high levels of this enzyme you prefer storage [of fat]. If you have low levels of this enzyme you burn it," he says. Other enzymes involved in lipid metabolism don't have this effect, he says. "So this makes this enzyme unique," Ntambi comments. Ntambi and his colleagues are trying to decipher the signal instructing the body to burn instead of store the fat. Another member of the team, Alan Attie, professor of biochemistry at UW-Madison, is exploring a possible link between the gene and the mitochondria, in an effort to understand the mechanism. As to the practical implications, Ntambi and his colleagues are looking at compounds to block the gene's promoter.
Image: Anne MacNamara
Diverse answers may be among jumping genes The rearrangement of genes over time on the human genome has allowed evolution to occur. Scientists knew this, but now, the details are emerging. Two groups of researchers, one at Johns Hopkins University, the other at the University of Michigan, have discovered that when genes jump, or retrotranspose, into new locations on the genome, such events not only move genetic information, but they also can result in damage to surrounding DNA (D.E. Symer et al., "Human L1 retrotransposition is associated with genetic instability in vivo," CeIl, 110:327-38, Aug. 9, 2002; G. Gilbert et al., "Genomic deletions created upon LINE-1 retrotransposition," Cell, 110:315-25, Aug. 9, 2002). The act of insertion caused DNA sections to be eliminated about 10% of the time--an unexpected find. Both groups conducted plasmid-based rescue experiments in cultured human tissue cells. Consulting the Human Genome Project, they identified the new location and any alterations after the insertion. The experimental method allowed the groups to capture the effects of large-scale rearrangements associated with the jumping genes that otherwise would be difficult to find because they are often deleterious, says Johns Hopkins' molecular biologist and geneticist Jef Boeke, a lead investigator. Little still is known about how these insertions affect the expression of nearby human genes after placement, but the findings may help explain human diversity. "The question remains open whether similar events occur in human sperm or eggs, and if so, at what frequency," Boeke says.
--Jennifer Fisher Wilson
Image: Erica Johnson
Changing the Ras prescription Ras-associated cancers in mice and humans are triggered by altogether different means, report researchers from Duke University Medical Center, Durham, NC. The findings could have important implications for drug discovery and cancer research. Ras, an oncogene involved in cell-cycle control, is associated with one-third of all human cancers and 90% of pancreatic cancers. In mice, Ras is associated with breast, skin, and lung cancers, but not pancreatic cancer. Only recently, however, have scientists been able to study how Ras transforms normal human cells into cancer cells. Using such human cells, Nesrin Hamad, Joel Elconin, and colleagues at Duke made an unexpected discovery. They found that Ras activated completely different signaling pathways in murine and human cells (N.M. Hamad et al., "Distinct requirements for Ras oncogenesis in human versus mouse cells," Genes and Development, 16:2045-57, Aug. 15, 2002). In mice, Ras transforms cells primarily through the Raf/MEK/ERK pathway. In humans, it triggers the RalGEF pathway, previously thought to play a minor role in Ras transformation. "Here's a pathway that really hadn't been given credit," says lead investigator Christopher Counter. "It was overshadowed by the mouse studies." Bob Weinberg, cancer biologist, Whitehead Institute for Biomedical Research, Cambridge, Mass., says, "This has implications for the interpretation of much work in the area of cancer molecular biology over the past two decades." Consequently, he adds, drug discovery efforts can no longer be based on information drawn exclusively from studying rodent cells and their cancers.
Image: Anne MacNamara
An apple for the postdoc New PhDs could find themselves teaching in public schools instead of universities under a fellowship program proposed by the National Research Council. The program would offer new science and engineering PhDs an opportunity to work with youths, as well as to build links between the school system and colleges and universities. The council recommends launching a two-year, $2 million (US) pilot program limited to 30 people, who each would be paid $30,000 a year. Margaret Cozzens, vice chancellor for academic and student affairs at the University of Colorado at Denver, says the money could come from the National Science Foundation, private foundations, and school districts. The idea draws praise from John Rudolph, assistant professor of education at the University of Wisconsin, Madison. "I would welcome any involvement of research scientists in helping in precollege science education," says Rudolph, who specializes in educating children in the sciences. John See, a public affairs specialist at the American Federation of Teachers, says scientists could provide benefits to the schools. "I see no threat whatever," he says. "Good teachers would welcome this. This would not be a matter of displacing science teachers." Both Rudolph and See are concerned, however, that fellows become steeped in the best teaching techniques before entering the classroom.