Hatching of Echinostoma trivolvis miracidia in response to snail host and non-host chemical cues.

Environmental cues are used by many organisms to time life history transitions and can be important for trematode host location. However, while much is understood about how larval trematodes locate hosts, much less is known about the potential role of host cues in the timing of trematode egg development and hatching. We addressed the potential role of host chemical cues in mediating hatching of Echinostoma trivolvis miracidia by comparing hatching in response to cues from the first intermediate host (the snail Planorbella trivolvis), a non-host snail (the snail Goniobasis proxima), and a non-host invertebrate (earthworm, Lumbricus terrestris). We hypothesized that in the presence of cues from their first intermediate host, E. trivolvis would hatch sooner and would be more synchronized than when host cues were absent. However, we found that hatching was unaffected by our cue treatments. In all treatments, hatching uniformly began at 13 days and was nearly evenly spread over the next 3 weeks.

Dietary modulation of inflammation-induced colorectal cancer through PPARγ.

Mounting evidence suggests that the risk of developing colorectal cancer (CRC) is dramatically increased for patients with chronic inflammatory diseases. For instance, patients with Crohn's Disease (CD) or Ulcerative Colitis (UC) have a 12-20% increased risk for developing CRC. Preventive strategies utilizing nontoxic natural compounds that modulate immune responses could be successful in the suppression of inflammation-driven colorectal cancer in high-risk groups. The increase of peroxisome proliferator-activated receptor-γ (PPAR-γ) expression and its transcriptional activity has been identified as a target for anti-inflammatory efforts, and the suppression of inflammation-driven colon cancer. PPARγ down-modulates inflammation and elicits antiproliferative and proapoptotic actions in epithelial cells. All of which may decrease the risk for inflammation-induced CRC. This review will focus on the use of orally active, naturally occurring chemopreventive approaches against inflammation-induced CRC that target PPARγ and therefore down-modulate inflammation.