Long term wet corrosion resistance of metals depends on the stability of their corrosion product layer. With immersion corrosion tests, such stability can be predicted. EIS and potentiodynamic polarization were complemented with XPS to investigate the characteristics of Ni corrosion product layer formed after 1 hr. and 72 hr. immersion in 3.5% NaCl solution. Two time constants with decreasing Nyquist semi-circle size and phase angle maxima, based on EIS characterization during the immersion times, indicated the formation of an increasingly porous and less adherent corrosion product layer. The product formation shifted the Ni corrosion potential more negatively and increased cathodic and anodic current densities, during potentiodynamic polarization. XPS characterization suggested that a rapid nucleation of NiO could increase H2O adsorption, subsequently triggering the formation of different forms of Ni(OH)2 in the corrosion product layer. Consequently, the corrosion resistance of the Ni coating decreased after 72 hr. immersion in 3.5% NaCl solution.

A Ni-Al composite was electrodeposited on a Ni substrate, and its corrosion behavior was observed in 2 M NaCl solution, compared with a pure Ni coating. The Al particles increased the porosity of the composite and encouraged charge percolation, both at the corrosion product layer-solution interface and at the substrate-solution interface, based on EIS characterization. This phenomenon greatly decreased the corrosion potential, and increased both cathodic and anodic current densities in the active region, as well as the passive current density in the passive potential range, during polarization of the composite. Although a continuous Al3+ ions supply to the passivation front was suspected, based on the longer passivation potential of the Ni-Al composite, the simultaneous consumption of the Al products by the chloride ions is the reason for serious cracking and localized collapse of the composite corrosion layer, as confirmed by SEM. This conferred lower corrosion resistance on the Ni-Al composite, compared to the pure Ni coating, in the 2 M NaCl solution.

The electrochemical corrosion behaviour of an electrodeposited Ni-28wt.%Al composite coating was characterized after 24 h and 72 h immersion periods in 3.5% NaCl solution, using electrochemical and surface probe techniques. Open circuit potential (OCP) and potentiodynamic polarization revealed that the Al particles modify the electrochemical corrosion behaviour of the Ni coating by shifting its E OCP more negatively and increasing its anodic dissolution current density, after 24 h immersion in 3.5% NaCl solution. Compared with the Ni coating, the composite can exhibit well- reduced anodic current density and slightly increased cathodic current with immersion up to 72 h. XPS characterization showed that a high rate of water adsorption and rapid formation of a continuous Ni(OH)2 initially occurs on the composite surface which, however, readily thickens during prolonged immersion time and promotes the corrosion product enrichment with Al2O3. This greatly decreased the rate of corrosion and susceptibility to pitting for the Ni-28wt.%Al composite after 72 h immersion in 3.5% NaCl solution.

A pharmaceutically active material diclofenac was intercalated into a layered double hydroxide by co-precipitation method, release studies suggest that the result diclofenac acid-pillared hydrotalcites (Dic-LDHs) have significant sustained release effect. The complex materials were characterrized using XRD, FTIR, DSC-TG, EA and ICP. The result show that the interlayer distance of the Dic-LDHs is expanded to 1.83nm and the thermal stability of material increases after the intercalation of diclofenac.

Nasopharyngeal carcinoma (NPC) is notorious for the metastases, which are in close association with Epstein-Barr virus-encoded latent membrane protein 1 (LMP1). Arsenic trioxide (As2O3) has been shown to induce apoptosis and differentiation in NPC xenografts. Then, can it repress the cancer cells' metastasis potential? To elucidate this issue, the present study was performed. LMP1-negative cell line HNE1 and LMP1-positive cell line HNE1-LMP1 were used as in vitro model. Cells (1 x 10(5)/mL) were cultured with or without 3 µM As2O3 for 48 h. Then the survival cells were collected to investigate their potential of colony formation, attachment, invasion, and migration. Both confocal immunofluorescence staining and Western blot were used to detect the changes of LMP1 expression. The changes of MMP-9 were examined by RT-PCR assay and Western blot. The results were as follow: i) the colony formation inhibition rate (75.41 ± 3.9% in HNE1-LMP1 cells vs 37.89 ± 4.9% in HNE1 cells), the rate of attachment (HNE1-LMP1 vs HNE1: 56.40 ± 3.5 vs 65.87 ± 5.9%), the invasion inhibitory rate (HNE1-LMP1 vs HNE1: 56.50 ± 3.7 and 27.91 ± 2.1%), and the migration inhibitory rate (HNE1-LMP1 vs HNE1: 48.70 ± 3.9 vs 29.19 ± 6.27%) were all significantly different between the two cell lines (P < 0.01). ii) LMP1 was down-regulated in As2O3-treated HNE1-LMP1 cells. iii) The reduction of MMP-9 was found in As2O3-treated groups, more evident in HNE1-LMP1 cells. Thus, we conclude that As2O3 can reduce metastasis potential of NPC cells, involving inhibition of MMP-9 expression. LMP1 were also reduced in this process and seemed to enhance anti-metastasis activity of As2O3.