Comparison of capsule endoscopy and magnetic resonance imaging for the detection of polyps of the small intestine in patients with familial adenomatous polyposis or with Peutz-Jeghers' syndrome.

BACKGROUND AND STUDY AIMS: We have conducted a study to compare the diagnostic yields of magnetic resonance imaging (MRI) and capsule endoscopy for the detection of small-bowel polyps in patients with inherited polyposis syndromes. PATIENTS AND METHODS: MRI was performed in 20 patients, with either Peutz-Jeghers' syndrome (PJS; n = 4) or familial adenomatous polyposis (FAP; n = 16), and capsule endoscopy was done the next day. The number, size, and location of polyps were analyzed. RESULTS: Overall, 448 polyps ranging from about 1 mm to 30 mm in size were detected in eight patients by capsule endoscopy, whereas with MRI only 24 polyps all bigger than 5 mm could be seen in the four PJS patients. CONCLUSIONS: Polyps bigger than 15 mm were detected similarly with capsule endoscopy and MRI, whereas smaller polyps were seen much more often with capsule endoscopy. Polyps smaller than 5 mm were exclusively seen with capsule endoscopy. However, location of the detected polyps and determination of their exact sizes was more accurate by MRI.

UVB activates ERK1/2 and p38 signaling pathways via reactive oxygen species in cultured keratinocytes.

We have previously shown that hydrogen peroxide is an important mediator of ultraviolet B induced phosphorylation of the epidermal growth factor receptor in human keratinocytes. Here we demonstrate that physiologic doses of ultraviolet B and hydrogen peroxide stimulate activation of two related but distinct mitogen-activated protein kinase pathways: extracellular regulated kinase 1 and 2 (ERK1/2), as well as p38, the mammalian homolog of HOG1 in yeast which is a major kinase for a recently identified stress-induced signaling pathway. The time-dependent activation of ERK1/2 and p38 are distinct, and ultraviolet B-induced ERK1/2 activation is downregulated more rapidly than p38. Using dihydrorhodamine or Amplex as specific fluorescent dye probes, we show that ultraviolet B-induced peroxides can be inhibited by ascorbic acid. Ascorbic acid strongly blocks ERK1/2 and p38 activation by ultraviolet B and hydrogen peroxide whereas pyrrolidine dithiocarbamate and butyl hydroxyanisole are less effective. Pyrrolidine dithiocarbamate was unable to inhibit ultraviolet B-induced p38 activation. Cell death was increased after ultraviolet B when ERK1/2 activation was attenuated by the specific inhibitor PD098059. The distinct time courses and extents of activation and inhibition of ERK1/2 and p38 indicate that these pathways are separate and regulated independently in keratinocytes. Specific types of reactive oxygen species induced by ultraviolet B as well as selective activation or inhibition of specific phosphatases may mediate these responses in keratinocytes. These findings demonstrate that reactive oxygen species are important multifunctional mediators of ultraviolet B-induced ERK1/2 and p38 signaling transduction pathways and suggest that ERK1/2 may play an important part in protecting keratinocytes from cell death following oxidative stress.