The Micro-Shear Bond Strength of Resin Cements to Commercially Pure Titanium Using Universal Adhesives and Alloy Primer.

PURPOSE: To evaluate the micro-shear bond strength (µSBS) of different bonding protocols to commercially pure titanium (CP Ti) using two universal adhesives and Alloy Primer. MATERIALS AND METHODS: A total of 120 cubes of CP Ti were airborne-particle abraded and then divided into 6 groups (n = 20 each) according to bonding protocol: (1) Scotchbond Universal (SU; 3M ESPE), (2) Alloy Primer (AP; Kuraray) + SU; (3) G-Premio Bond (GP; GC); or (4) AP + GP. The specimens from groups 1 to 4 were cemented with RelyX Unicem (3M ESPE), while those from groups 5 and 6 were cemented using Panavia F2.0 cement (PAN; Kuraray) without and with prior AP application, respectively. After 24 hours, half the specimens were subjected to µSBS measurement and the other half to thermocycling (5,000 cycles) before testing. Data were analyzed using Shapiro-Wilk, two-way analysis of variance, Games-Howell, and independent sample t test (α = .05). RESULTS: The µSBS values obtained from the AP + SU group were significantly higher than from the GP (P = .003) and the AP + GP (P = .022) groups. After thermocycling, the µSBS of both groups treated with SU were significantly higher than those other groups (P < .001). The application of AP could not improve adhesion of resin cements to CP Ti. Thermocycling significantly reduced the µSBS values of the PAN group, whereas it noticeably enhanced the adhesion of SU and AP + SU. The predominant failure mode in all groups was adhesive. CONCLUSION: The application of AP, followed by SU, produced the most effective bonding to CP Ti, which was able to endure limited thermal aging.

Carboplatin and epigallocatechin-3-gallate synergistically induce cytotoxic effects in esophageal cancer cells.

BACKGROUND AND PURPOSE: We aimed at evaluating the effects of combinatorial treatments with carboplatin and epigallocatechin-3-gallate (EGCG) on the KYSE-30 esophageal cancer (EC) cell line and elucidate the underlying mechanisms. EXPERIMENTAL APPROACH: EC cells were harvested and exposed to increasing concentrations of carboplatin and EGCG to construct a dose-response plot. Cell inhibitory effects were assessed by the MTT method and apoptosis-related gene expression levels (caspases 8 and 9) and Bcl-2 mRNA were detected using real-time polymerase chain reaction. The lactate levels in the various treated cases were analyzed using the colorimetric assay kit. In addition, total antioxidant capacity was measured. FINDINGS/RESULTS: The results indicated that, following treatments with carboplatin in IC20, IC25, and IC10 concentrations when combined with EGCG in similar concentrations, synergistically decreased cell viability versus single treatments of both agents. Also, in combined treatments at IC20 and IC25 of both agents the gene expression ratio of caspases 8 and 9 upregulated significantly compared to monotherapies (P < 0.05). Bcl-2 gene expression ratios were decreased in double agents treated cells versus monotherapies. Following treatment of KYSE-30 cells with carboplatin and EGCG in double combinations, lactate levels were significantly decreased compared with the untreated cells and single treatments (P < 0.05). Also, in IC25, IC20, and IC10 concentrations of both agents the total antioxidant capacity levels were decreased versus monotherapies and untreated cells. CONCLUSION AND IMPLICATIONS: The presented study determined that treatment with carboplatin and EGCG was capable of promoting cytotoxicity in EC cells and inhibits the cancer progress. Combined treatments with low concentrations of carboplatin and EGCG may promote apoptosis induction and inhibit cell growth. These results confirmed the anticancer effects of carboplatin and EGCG and providing a base for additional use of EGCG to the EC treatment.