LAKE TAHOE'S FOOD WEB ALTERED: UC Davis researchers at Lake Tahoe have published the first evidence that climate change alters the makeup of tiny plant communities called algae, which are the very foundation of the web of life in freshwater lakes.

Other scientists had predicted that climate change would reduce the overall amount, or biovolume, of an important algae group called diatoms. However, the UC Davis researchers found that the warming of the lake changed not the overall biovolume but rather the relative populations of various diatom species.

"There are greater numbers of small-sized diatom species in recent years than there were 20 years ago," said postdoctoral researcher Monika Winder, lead author for the study published online Sept. 24 by the Proceedings of the Royal Society B.

Co-author Geoffrey Schladow, director of UC Davis' Tahoe Environmental Research Center, tied the find to the lake's reduced mixing, the result of changing climate conditions such as warmer air temperatures. "With less mixing, it is difficult for larger algae to stay suspended at the surface of the lake, where there is light to facilitate their growth," he said. "This allowed the smaller diatoms, which sink more slowly, to proliferate."

Diatoms form the base of the food chain in large bodies of freshwater and saltwater around the world.

"It is inconceivable that you could alter the base of the food web and not have other things start changing," Winder said.

She said "we don't know yet" what the changes will be. Some zooplankton species may decline, which would lead to declines in fish numbers. Clarity could suffer as well -- because smaller algae stay at the surface longer, scattering light and making the water appear greener.

Learn more about this study.

-- Sylvia Wright

DEFINING AN INFLAMMATION PROCESS: By defining a cellular process that promotes inflammation, UC Davis researchers set the starting point for developing drugs for diseases such as sepsis, rheumatoid arthritis, cardiovascular disease and some cancers.

The scientists discovered that a protein called sPLA2-IIA binds to two integrins labeled alpha-V-beta-3 and alpha-4-beta-1, causing them to multiply rapidly and boost an immune system response already gone awry due to disease.

Dermatology professor Yoshikazu Takada, lead author of the study published Sept. 19 in The Journal of Biological Chemistry, said researchers had known for a while that sPLA2-IIA is elevated with inflammation.

"Our outcome shows with much more precision how the protein actually works to advance inflammation. The potential impact of the finding on our ability to block inflammation and stop the disease process in its tracks is enormous."

Read more about this discovery.

-- Karen Finney, UC Davis Health System