Research Notes

Male rhesus monkeys with destroyed amygdala will abandon their normally slow and cautious familiarization process and immediately approach other monkeys with whom they are unfamiliar, according to David Amaral, professor of psychiatry and neuroscience at the University of California, Davis. His study on these animals is slated to appear in an upcoming issue of Behavioral Neuroscience. The study involved six lesioned monkeys, each meeting for many 20-minute sessions with a "stranger" monkey. The

Harvey Black
May 27, 2001
Male rhesus monkeys with destroyed amygdala will abandon their normally slow and cautious familiarization process and immediately approach other monkeys with whom they are unfamiliar, according to David Amaral, professor of psychiatry and neuroscience at the University of California, Davis. His study on these animals is slated to appear in an upcoming issue of Behavioral Neuroscience. The study involved six lesioned monkeys, each meeting for many 20-minute sessions with a "stranger" monkey. The lesioned monkeys, their guards down, groomed and immediately presented themselves for sex to the other monkeys. The lesions, said Amaral, suggest that the amygdala, a brain structure about the size of half a thumb, plays a role in evaluating whether a situation is dangerous. The amygdala, he says, has connections with higher brain regions such as the cerebral cortex, enabling the latter to "attend to a particularly salient stimulus." Unlike intact monkeys, the lesioned animals showed no increase in cortisol levels, a hormone that measures stress level increases. Amaral interprets that finding as another marker in which lesioned monkeys are not evaluating a situation's potential danger. This study is part of a larger project Amaral is conducting to better understand amygdala's role in behavior. Previous lesioning studies, he says, used a cruder technique than his, which involved injecting a neurotoxin that might have damaged other areas of the brain.
--Harvey Black

Cancer Immunosurveillance in Mice Affirmed, Altered

Immunosurveillance, the concept that the immune system protects against constant proliferation of cancerous cells, was introduced more than 30 years ago. After the notion had been challenged and largely abandoned when researchers found no difference in tumor growth between immunodeficient nude mice and wild types, subsequent studies found that nude mice have some functional T cells. Now, researchers at Washington University Medical School in St. Louis might have settled the controversy over whether immune response protects against primary tumor development (V. Shankaran et al., "IFNg and lymphocytes prevent primary tumour development and shape tumour immunogenicity," Nature, 410:1107-11, April 2001). The group's findings affirm this earlier hypothesis of immunosurveillance--but with a slight twist. The Washington University team looked at tumor development in different immunodeficient mouse models. One had a defective recombination-activating gene (RAG2) that is only expressed in lymphocytes. Also tested were gamma interferon (IFNg) insensitive mice that lacked either the IFNg receptor gene, IFNGR1, or STAT1, a transcription factor involved in IFN signaling. Not only did chemically induced tumors grow at a higher, faster rate in these models when compared to wild-type counterparts, but also spontaneous tumors grew in almost all immunodeficient models. Mice with both RAG2 and STAT1 mutations were found to develop tumors at a rate similar to those with one or the other, suggesting that IFNg and lymphocytes work together in the same pathway. And here's the twist: While all tumors transplanted from wild-type mouse to wild-type mouse continued to grow, some tumors from immunodeficient mice were eradicated when injected into wild types. "This is saying that tumors ... undergo some process that makes them more capable of growing in the presence of an immune system," is how Robert D. Schreiber, the study's principal investigator, explains the paradox of tumor formation in an immunosurveillance model. For this reason, the lab suggests the term "immunoediting" as a more applicable descriptor. The next step is determining tumor cell antigens that appear in immunocompetent vs. immunodeficient mice; such identification could lead to better immunotherapy approach.

New Component to Human Body Odor Identified

Here's possibly something new to worry about when turning 40: an additional component to body odor. Researchers at Takasago International Corp. in Hiratsuka, Japan, have identified an unsaturated aldehyde, 2-nonenal that imparts "an unpleasant greasy and grassy odor" (S. Haze et al. "2-nonenal newly found in human body odor tends to increase with aging," The Journal of Investigative Dermatology, 116:520-4, April 2001). The constituents of human body odor read like the table of contents of an organic chemistry textbook--esters and ethers, alcohols and ketones, and various hydrocarbons. Heredity, gender, and habits such as smoking cigarettes and drinking alcohol contribute to individual ambiances. "There is little research about body odor," says senior research scientist Shinichiro Haze. "In Japan, it is said that there is a unique and unpleasant body odor in the middle-aged and the elderly." The investigators analyzed body odor composition in 22 individuals ranging in age from 27 to 75. Each participant wore a clean tee shirt for three consecutive nights, and on the final morning, pieces were cut from the shirts and analyzed by gas chromatography/mass spectrometry. Results were clear: the researchers detected 2-nonenal in none of the individuals under 40, in 9 of 13 middle-aged participants, and in everyone over 60. The telltale biochemical was the only body odor component to change in concentration with age. "Although it is not a sufficient sample, we think that it is a universal phenomenon," Haze says. The researchers deduced and experimentally demonstrated that 2-nonenal forms from the action of peroxidases on certain omega 7 unsaturated fatty acids, particularly palmitoleic and vaccenic acids, which accumulate with age. The reaction is stimulated by squalene, another skin surface lipid. "We think that 2-nonenal occurs by the degradation of the omega 7-unsaturated fatty acids in skin surface lipids, not in sweat, and vaporize from the skin surface," Haze concludes.