The study, conducted by researchers at Marshfield Clinic Research Foundation, Marshfield, Wis., is published in the latest issue of the Wisconsin Medical Journal (Volume 106, No. 2).

The regions studied were in the West (Los Angeles, Denver, Portland), Midwest (Milwaukee, Detroit, Kansas City), South (Washington D.C., Dallas, Jacksonville) and the Northeast (New York, Philadelphia, Boston).

"The average total caloric content of dessert recipes was significantly associated with the percent obese in the metropolitan cities," reports the study, regarding recipes that were published the last week of August 2000. The researchers studied 64 entr'e and 38 dessert recipes published in major newspapers serving cities with populations of 400,000 or more. The study found no association between the entr'e recipes and obesity.

"While these data cannot be interpreted as causal, they are intriguing and suggest that newspapers may play a greater role in promoting or preventing obesity than previously recognized," said Catherine McCarty, Ph.D, MPH, Lead Scientist and Interim Director, Center for Human Genetics, Marshfield Clinic.

The report notes that the news media play an important role in providing nutrition information, but with respect to recipes, "this information is seldom studied." The authors add that the study results underscore "the importance of publishing recipes to help readers achieve and maintain a healthy weight."

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While RfaH's control over gene expression is limited, it seems that its structure lets it control key sequences of the genome during transcription, the process of transferring genetic information inside a cell and one of the first steps of gene expression.

"Making RfaH work only at specific sites is, in a sense, a genius way to prevent it from interfering with NusG," Artsimovitch said. "It seems that the only genes that RfaH can't regulate are those controlled by NusG."

Bacteria can survive without RfaH, but not without NusG. Yet without RfaH, bacteria lose the ability to infect. In previous laboratory experiments, the researchers found that pathogens lacking RfaH grow at much slower rates.

"Cells usually don't die when RfaH use changes," Svetlov said. "Rather, bacteria seem to manipulate the protein, to play around with it. Too much RfaH will kill a cell, while too little would prevent it from infecting any living being.

"We think that RfaH is responsible for more than making a microbe infectious," he continued. "Actually seeing what happens at the molecular level will help us figure out what else this protein regulates."

Svetlov and Artsimovitch conducted the study with Georgy Belogurov, a postdoctoral research associate in microbiology at Ohio State, and with researchers from the University of Alabama at Birmingham, the Howard Hughes Medical Institute and the University of Texas Southwestern Medical Center in Dallas.

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