RESUMO
Ni/Al2O3 catalysts were prepared with Ni(NO3)2·6H2O, NiSO4·6H2O, NiCl2·6H2O, and NiC4H6O4·4H2O as nickel sources by the solution combustion method. The catalysts were characterized by X-ray diffraction, H2 temperature-programmed hydrogenation, TG-DTG, TPH, and transmission electron microscopy methods, and the effect of the nickel source on performance of the Ni/Al2O3 catalyst was investigated via the CO2-CH4 reforming experiment. Results showed that Ni dispersion, Ni size, and the metal-support interaction between active component Ni and the support were influenced significantly by anion in nickel sources, resulting in that the performance of each catalyst was different. Highly dispersed Ni species, small Ni crystallite size, and strong metal-support interaction were presented in the Ni/Al2O3 catalysts with Ni(NO3)2·6H2O and NiSO4·6H2O as nickel sources. Evaluation results showed that the catalyst prepared with Ni(NO3)2·6H2O exhibited higher activity and stability, with CH4 and CO2 conversions of 31.21 and 48.97%. Carbon deposition analysis demonstrated that the catalyst prepared with NiSO4·6H2O contained more graphite carbon.
RESUMO
OBJECTIVE: Natural and synthetic retinoids such as N-(4-hydroxyphenyl)retinamide (4HPR) have been used for prevention and treatment of a variety of cancers; however, relapse usually occurs after treatment is stopped. Furthermore, the retinoid analogues are insoluble in water, making it difficult for systemic administration. The purpose of this study was to develop and evaluate a water-soluble polymeric formulation of 4HPR that can release 4HPR over a period of a few days. METHODS: 4HPR was bound to a synthetic polyamino acid poly(L-glutamic acid) (PG). PG-4HPR was evaluated for its release kinetics and in vitro anti-proliferative and in vivo antitumor activities against ovarian cancer cell lines. RESULTS: The release profile of PG-4HPR in phosphate buffered saline at 37 degrees C followed a first order kinetic, with a rate constant of 8.8x10(-3) h(-1). Approximately 60% of 4HPR was released over a period of 100 h. In vitro, both 4HPR and PG-4HPR inhibited proliferation of three ovarian cancer cells lines (SKOV3, OVCA420, and OVCA433) and an immortalized human ovarian epithelium cell line (IOSE) in a time- and dose-dependent manner. Increasing the exposure time of SKOV3 cells to both agents from 1 to 5 days resulted in an increased apoptotic response. In vivo, PG-4HPR demonstrated significantly enhanced antitumor activities compared to 4HPR in both early treatment and later treatment protocols. Treatments with PG-4HPR suppressed the expression of VEGF and reduced blood flow into the tumor. CONCLUSIONS: PG-4HPR may have potential applications in the prevention and therapy of ovarian cancers.