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This study evaluated the effects of three metal primers and one multi-mode adhesive system on the shear bond strength (SBS) of a flowable composite resin to nickel-chrome metal alloy (Ni-Cr). Ninety plates were cast from Ni-Cr and divided in nine groups (n=10). The surfaces were sandblasted with Al 2 O 3 and primed with three adhesive primers: Alloy Primer (AP), Universal Primer (TP) and RelyX Ceramic Primer (CP), and a multimode adhesive (Scotchbond Universal, SU). The Adper Single Bond Plus (SB) and SU adhesives were also combined with adhesive primers. Control group did not have any surface treatment. The groups were: AP, AP+SB, AP+SU, TP+SB, TP+SU, CP+SB, CP+SU and SU. Composite cylinders were built on alloy surface. After 24 h, half the specimens were subjected to SBS and the other half to thermal cycling before testing. Data were analyzed by two-way ANOVA and Tukey's test (a=0.05). Failure modes were assessed by SEM observation. Higher SBS were obtained with AP and TP combined with adhesives at 24 h and the lowest one for control group. Thermocycling reduced SBS for AP, CP+SU and SU. Combination between TP and SU resulted in the highest SBS after the thermocycling. TP groups showed all types of failures and high incidence of mixed failures. The use of AP and UP metal primers before application of SU and SB adhesive systems increased the SBS of composite to Ni-Cr. These combinations between metal primers and adhesives had the highest SBS after thermocycling.

In this retrospective study we evaluated the pretherapeutic mRNA expression of the hOCT1 (human organic cation transporter 1) gene in patients with chronic-phase (CP) chronic myeloid leukemia (CML) who varied in terms of their response to imatinib (IM). hOCT1 mRNA was quantified by real-time PCR. Patients were classified as expressing either high (n = 44) or low hOCT1 mRNA (n = 44). The complete cytogenetic response rates observed at 6, 12 and 18 months were 47.7, 84.1 and 91%, respectively, in patients with high hOCT1 mRNA and 47.5, 81.8 and 86.3%, respectively, in patients with low hOCT1 transcripts. The major molecular response rates were not significantly different between patients with high and low hOCT1 mRNA after 6 months of therapy (22.7 vs. 9.1%; p = 0.07), but they were significantly different after 12 months (54.5 vs. 31.8%; p = 0.026) and 18 months (77.2 vs. 56.8%; p = 0.034). Complete molecular responses were observed in 5 patients with low and 17 patients with high hOCT1 mRNA (p = 0.003). The 5-year event-free and overall survival analyses revealed no significant differences between the groups. These data imply that knowledge of the pretherapeutic level of hOCT1 could be a useful marker to predict IM therapy outcome in treatment-naïve CP CML patients.