Summary of Recent AdvancesMast cells play as the major effector cells in immediate hypersensitivity through activation via the high-affinity IgE receptor, FcεRI, although many other functions have recently been discovered for this cell type. Given the broad array of proinflammatory mediators secreted from FcεRI-activated mast cells, as well as sensitization to allergens, IgE elevation, and increased mast cells in a majority of atopic dermatitis patients, mast cells are believed to be involved in the pathogenesis of atopic dermatitis. Numerous animal models have been used to study this epidemic disease. Here we review the recent progress to synthesize our current understanding of this disease and potential mechanisms for a mast cell's role in the disease.

Endoscopic bilateral drainage using SEMS for malignant hilar biliary obstruction is more effective than unilateral drainage in terms of cumulative stent patency, especially in cases of cholangiocarcinoma.

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The IDUS findings were useful for distinction of IgG4-SC from cholangiocarcinoma. Transpapillary biopsy was not useful for direct diagnosis of IgG4-SC even after IgG4 immunostaining, but it did allow distinction of IgG4-SC from cholangiocarcinoma in some cases. IDUS and transpapillary biopsy after endoscopic retrograde cholangiopancreatography can provide further information for precise diagnosis of IgG4-SC.

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Although a major effect of p21, a cyclin-dependent kinase inhibitor, is considered to be exerted during G 1 phase of the cell cycle, p21 gene knock-out studies suggested its involvement in G 2 /M checkpoint as well. Here we demonstrate evidence that p21 is required for the cell cycle arrest at G 2 upon DNA damage. We found that expression of wild-type p21 (p21 WT ), not mutant p21 (p21 PCNA؊ ) lacking the interaction with proliferating cell nuclear antigen (PCNA), caused G 2 cell cycle arrest in p53-deficient DLD1 colon cancer cell line after the DNA damage by treatment with cis-diamminedichloroplatinum (II). We also found that p21 WT was associated with Cdc2/cyclin B1 together with PCNA. Furthermore, coimmunoprecipitation experiments revealed that PCNA interacted with Cdc25C at the G 2 /M transition, and this interaction was abolished when p21WT was expressed presumably due to the competition between p21 WT and Cdc25C in the binding to PCNA. These findings suggest that p21 plays a regulatory role in the maintenance of cell cycle arrest at G 2 by blocking the interaction of Cdc25C with PCNA.

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IgE