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Bats to the rescue. The subjects of mythology and folklore, bats have traditionally been maligned as blood-sucking harbingers of evil. In fact, bats perform a vital economic function throughout the world, feeding on insects that if left uncontrolled would devastate crops and threaten food production and local economies. A novel multidisciplinary study is quantifying the economic impact of bats, specifically the enormous colonies of Mexican free-tailed bats that migrate each spring to south central Texas.

Led by CAS Geography Associate Professor Cutler Cleveland, director of the Center for Energy and Environmental Studies, CAS Biology Professor Thomas Kunz, and colleagues at the center, the National Science Foundation-funded effort also includes entomologists, agricultural scientists, and biologists who specialize in modeling animal populations from institutions throughout the United States and in Mexico.

To get an accurate picture of the scope of the bats' impact, Cleveland and Kunz use a novel thermal infrared video camera correlated with Doppler radar to count and track the bats, who eat up to half their body weight in insects every night. On one evening they counted more than 1.5 million bats emerging from a single cave and tracked them as they disbursed over a distance of more than 10 kilometers.

In calculating the economic value, Cleveland notes, it is necessary to consider some factors that are fairly evident, such as the value of the crops undamaged by the insects eaten by the bats and of the chemicals that do not need to be used. But there are other, less evident, savings, such as preventing insects from becoming resistant to pesticides and avoiding losses of fish and wildlife from pesticide runoff. The bats also have an ecotourism impact. Visitors gather every evening at the mouth of the cave to witness the colony of bats as they emerge on their nightly search for food. At another site, right in the middle of Austin, Tex., a colony of bats roosts under a bridge, again drawing hundreds of tourists each night, who spend money that supports the local economy. The state of Texas even designs new bridges with roosting habitats built into the design.

Strategic warfare in the battle against cancer. Despite decades of research, chemotherapy for cancer is still very much an inexact science. Two major issues -- delivery of therapeutic agents directly to cancer cells with minimal impact on the rest of the body and preventing recurrence of the cancer in a more resistant form after treatment -- are being addressed by CAS Biology Professor David Waxman and associates. Last year Waxman and colleagues at Massachusetts General Hospital and the Dana-Farber Cancer Institute licensed a new gene therapy approach for generating an active chemotherapeutic drug directly at the site of the tumor target. The therapy is based on P450, a naturally occurring liver enzyme necessary to activate the commonly used chemotherapeutic agent cyclophosphamide. Studies have shown that this approach has the potential to eradicate tumors using lower concentrations of cyclophosphamide, drastically reducing damage to healthy cells. The licensee, London-based Oxford BioMedica, is now testing the therapy's efficacy in breast and ovarian cancer.

The second issue, preventing a resistant recurrence, is being addressed by Pamela Schwartz (GRS'02), one of Waxman's Ph.D. students. She recently presented her work at BU's Science Day, winning the Community Technology Fund Award for research with high potential for producing a commercial product.

Schwartz's work builds on the knowledge that patients who have high levels of the protein Bcl-2 have a poorer prognosis for recurrence of cancer. The presence of Bcl-2 in cancer cells causes them to arrest -- that is, to remain in a dormant phase of the cell cycle -- rather than die when they are exposed to a chemotherapeutic agent. In this case, the cancer may go into remission, but since the cells can reactivate at any point, the cancer can recur. Schwartz's research revealed the critical role that Bcl-2 plays in regulating cyclophosphamide-induced cell death. With this knowledge she is now investigating ways to counteract the effects of Bcl-2. One approach seeks to prolong the life of cells in which P450 has successfully activated cyclophosphamide so that these producer cells continue to generate enough toxin to kill off even Bcl-2-rich cells.

"Research Briefs" is written by Joan Schwartz in the Office of the Provost. To read more about BU research, visit


15 May 2003
Boston University
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