THIS STORY HAS BEEN FORMATTED FOR EASY PRINTING
Discoveries

Uncovering the link between lungs and reflux disease

Email|Print|Single Page| Text size +
July 28, 2008

ASTHMA
We often think of the different processes of our body as separate - digestion, respiration, and circulation - but there are constant clues that the systems of our body are intimately coordinated. The most painful reminder of this interdependence is in illness. Gastroesophageal reflux disease, or GERD, for example, is probably one of the most common ailments affecting Americans. While its true incidence is not known, up to 40 percent of the nation may suffer from its symptoms, including heartburn and regurgitation. Frequently, people with GERD go on to develop asthma-like symptoms, a disease process involving an entirely different organ system. Up until now, the guess has been that people with GERD send stomach acid up into the lungs, leading them to cough and wheeze. Now, a study from Duke University confirms this idea in the laboratory for the first time. Principal investigator Dr. Shu Lin, an assistant professor of surgery and immunology at Duke University, inserted stomach acid into the lungs of mice. The researchers found that those mice went on to develop changes in the immune system of the lungs similar to those seen in human patients with asthma. "There's a lot of people affected by both asthma and GERD," says Lin, "and now we have a model that lets us work on the connection between both in the laboratory."

BOTTOM LINE: This study for the first time provides physiological proof that gastroesophageal reflux disease is linked to asthma. CAUTIONS: The studies were done in mice, not humans. WHAT'S NEXT: The authors plan to figure out precisely how stomach acid might lead to changes in the immune system of the lungs.

WHERE TO FIND IT: The European Journal of Clinical Investigation, July 17.

SUSHRUT JANGI

AGING

Scientist offers new theory of how creatures grow old
Biologists have long thought that aging was the result of accumulated damage from radiation, disease, stress, and other contributing factors throughout an organism's life, much like rust accumulation in a car.The effects of such damage would be difficult or impossible to counteract. Now, a study performed with worms suggests that aging may be the result of altered gene regulation - similar to having a car's brakes adjusted too strongly, while the gas pedal is too weak. If this alternative theory is true, aging may be more easily reversed. Stuart Kim, a professor of developmental biology and genetics at Stanford University, and colleagues studied aging in C. elegans, a type of worm with about 20,000 genes - similar in number to humans - but with a typical life span of less than two weeks. Instead of finding accumulated damage in older worms, Kim and his colleagues found evidence that the worms might have an "intrinsic clock" governing the gene regulators responsible for the worms' development. Over time, the regulators become imbalanced and lead to aging. "This is a normal developmental pathway intended to make a normal young healthy worm," Kim explains. "It makes healthy skin and a well-functioning intestine, but after a certain amount of time, the gene regulatory molecules become unbalanced." When the researchers "rebalanced" the system, the worms lived longer. "Although old age is caused by many things going wrong, if they're all caused by a small set of regulatory genes, you can rebalance that," he explains. "It's not so impossible."

BOTTOM LINE: If a new theory about aging is correct, it might be possible to reverse genetic imbalances that develop over time, slowing or halting aging.

CAUTIONS: Kim stresses that although humans have a similar regulatory model called GATA-3, there is no evidence that it has anything to do with longevity, and it's unknown whether human aging is regulated by a similar developmental pathway.

WHAT'S NEXT: Kim and his colleagues are using their results from worm studies to study aging in mice and humans.

WHERE TO FIND IT: Cell, July 24.

MICHELLE SIPICS

  • Email
  • Email
  • Print
  • Print
  • Single page
  • Single page
  • Reprints
  • Reprints
  • Share
  • Share
  • Comment
  • Comment
 
  • Share on DiggShare on Digg
  • Tag with Del.icio.us Save this article
  • powered by Del.icio.us
Your Name Your e-mail address (for return address purposes) E-mail address of recipients (separate multiple addresses with commas) Name and both e-mail fields are required.
Message (optional)
Disclaimer: Boston.com does not share this information or keep it permanently, as it is for the sole purpose of sending this one time e-mail.