In vitro degradation of resin–dentin bonds with one-bottle self-etching adhesives

The purpose of this study was to evaluate the durability of one-bottle self-etching adhesive during long-term water-storage testing. Resin–dentin bonded specimens were prepared using four commercially available one-bottle self-etching adhesives. The specimens were sectioned perpendicular to the adhesive interface to produce beam-shaped specimens that were stored in water for 24 h (control group) and 100, 200, and 300 d (experimental groups). After each storage period, the beams were subjected to a microtensile bond test. After the bond test, fractured surfaces were examined using a scanning electron microscope. In addition, interfacial observations of the silver tracer were performed using the secondary and back-scatter modes of the scanning electron microscope. The bond strength of all tested adhesives decreased significantly after 100 or more days in water. The interfacial observations showed an oxygen-inhibition zone as electron lucent in the adhesive–composite border in control specimens, displaying silver impregnation with breakage after aging. The deterioration of the oxygen-inhibition zone in the adhesive–resin composite junction resulted in a decrease in bond strength after 100 d in water for one-bottle self-etching adhesives.     

Chromosomal and microsatellite instability in sporadic gastric cancer

BACKGROUND: Gastric cancer can progress through two pathways of genomic instability: chromosomal (CIN) and microsatellite instability (MSI). It is hypothesized that these two pathways are not always independent and that some tumors show overlap between these two mechanisms. METHODS: A total of 98 sporadic gastric cancers were classified based on their MSI status, using microsatellite assay with BAT26. Evidence for CIN was investigated by identifying loss of heterozygosity (LOH) events on chromosome arms, 5q, 10p, 17p, 17q, and 18q, which are regions harboring tumor suppressor genes that are significant in gastric cancer development. RESULTS: Twelve tumors (12%) showed high-frequency MSI (MSI-H). Overall, 43 of the tumors (44%) had at least one LOH event, with most frequent chromosomal losses observed on 10p and 18q (30%, respectively), followed by 5q (21%), 17p (14%), and 17q (12%). Interestingly, overlap was observed between CIN and MSI pathways. Of 43 cancers with LOH events, four (9%) were also MSI-H. It was also found that 48% of cancers without MSI-H had no LOH events identified, comprising a subgroup of tumors that were not representative of either of these two pathways of genomic instability. CONCLUSION: These results suggest that molecular mechanisms of genomic instability are not necessarily independent and may not be fully defined by either the MSI or CIN pathways in sporadic gastric cancers.