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The purpose of this study was to evaluate the effects of acid-etched titanium on the biological responses of osteoblast-like MC3T3-E1 cells. Four types of treatments (polishing, sandblasting, concentrated H2SO4 etching, and concentrated H2SO4 etching with vacuum firing) were carried out on the surfaces of commercially pure titanium (cpTi) disks. MC3T3-E1 cells were then cultured on the treated cpTi surfaces. Through surface roughness measurement and SEM analysis, it was found that the acid-etched surfaces showed higher roughness values than the sandblasted ones. Scanning electron microscope analysis showed that the cells on the disks treated with acid-etching and acid-etching with vacuum firing spread as well as the sandblasted ones. There were no significant differences in cell proliferation and collagen production on cpTi among the four different surface treatments. Based on the results of this study, it was concluded that etching with concentrated sulfuric acid was a simple and effective way to roughen the surface of titanium without compromising its biocompatibility.

The results indicated that H(2)S inhibits cell proliferation and induces cell cycle arrest via the expression of p21(Cip1) in Ca9-22 cells.

T22, an analog of polyphemusin II (18 amino acid residues), was found to block T-tropic human immunodeficiency virus type 1 (HIV-1) entry into target cells as a CXCR4 inhibitor. We synthesized T134, a small analog (14 amino acid residues) of T22 with reduced positive charges. T134 exhibited highly potent activity and significantly less cytotoxicity in comparison to that of T22. T134 prevents the anti-CXCR4 monoclonal antibody from binding to peripheral blood mononuclear cells but has no effect on the binding of anti-CCR5 monoclonal antibodies. Since T134 inhibits the binding of stromal cell-derived factor-1 (SDF-1) to MT-4 cells, it seems that T134 prevents HIV-1 entry by binding to CXCR4. The bicyclam AMD3100 has also been shown to block HIV-1 entry via CXCR4 but not via CCR5. Both T134 and AMD3100 are CXCR4 antagonists and low-molecular-weight compounds but have different structures. Our results indicate that T134 is active against wild-type T-tropic HIV-1 strains and against AMD3100-resistant strains.