Orbitofacial cleft number 5: radiographic, anatomical, and histologic study of a 24-week-old fetus.

BACKGROUND: Orbitofacial clefts are caused by a congenital absence of midfacial tissues between the eye and the upper lip just medial to the corner of the mouth. As a whole, facial clefts occur with an incidence of 1.43 to 4.85 per 100,000 births. The exact incidence of these unusual orbital facial clefts is unknown. Only a few clinical cases and their treatment have been reported in the world literature, and no anatomical or histologic study has been presented. METHODS: The authors present a detailed anatomical and histologic study in a 24-week-old fetus with a right-side no. 5 orbitofacial cleft (according to Tessier's classification). RESULTS: During the anatomical dissection, it was observed that in the trigeminal Gasser ganglion on the right side there was no infraorbital branch of this nerve. Both the foramen rotundum and the infraorbital groove, where the nerve exits, were hypotrophic. CONCLUSION: After embryologic analysis of their observation, the authors propose that the orbitofacial no. 5 cleft should be considered as a tissular disruption of the face secondary to damage of the terminal branches of the maxillary nerve.

Trypsin is produced by and activates protease-activated receptor-2 in human cancer colon cells: evidence for new autocrine loop.

In this work, we showed that human colon cancer cell lines produce trypsin which can activate a receptor for trypsin, the protease-activated receptor-2 (PAR-2), in these cells. RT-PCR experiments showed that trypsinogen transcripts were present in four colon cancer cell lines: T84, Caco-2, HT-29 and C1.19A. By Western blot analysis we found a 25 kDa immunoreactive band identified as trypsinogen I in cell lysates and in the corresponding culture media. Concentrations of trypsin in cell media were found in nanomolar range, thus compatible with activation of protease-activated receptor 2 (PAR-2). This was further demonstrated in a colon cancer cell line (H-29) Ca2+i assay since increases in Ca2+i were observed in response to media from T84, Caco-2 or C1.19A cells that were similar to that observed with 2-5 nM trypsin and were abolished by trypsin inhibitor. Altogether, these data show that colon cancer cell lines produce and secrete trypsin at concentrations compatible with activation of PAR-2. They support possible autocrine/paracrine regulation of PAR-2 activity by trypsin in colon cancer cells.