Insights into the dominant factors of porous gold for CO oxidation.

Three different porous Au catalysts that exhibit high catalytic activity for CO oxidation were prepared by the leaching of Al from an intermetallic compound, Al2Au, with 10 wt. %-NaOH, HNO3, or HCl aqueous solutions. The catalysts were investigated using Brunauer-Emmett-Teller measurements, synchrotron X-ray powder diffraction, hard X-ray photoelectron spectroscopy, field emission scanning electron microscopy, and transmission electron microscopy (TEM). Broad diffraction peaks generated during the leaching process correlated with high activity for all the porous Au catalysts. CO oxidation catalyzed by porous Au leached with NaOH and HNO3 is considered to be dominated by different mechanisms at low (< 320 K) and high (> 370 K) temperatures. Activity in the low-temperature region is mainly attributed to the perimeter interface between residual Al species (AlOx) and porous Au, whereas activity in the high-temperature region results from a high density of lattice defects such as twins and dislocations, which were evident from diffraction peak broadening and were observed with high-resolution TEM in the porous Au leached with NaOH. It is proposed that atoms located at lattice defects on the surfaces of porous Au are the active sites for catalytic reactions.

Chemically fixed nurse cells for culturing murine or primate embryonic stem cells.

In current and past practice, murine or primate embryonic stem (ES) cells are usually cultured on live nurse cells for growth that keeps the cells in an undifferentiated state. It is troublesome, however, to prepare nurse cells for each cell culture and it is difficult to completely remove the nurse cells when they are transferred. In this study, mouse and monkey ES cells were therefore grown on chemically fixed mouse embryonic fibroblast (MEF) or human amniotic epithelial (HAE) cells. MEF cells were fixed by incubation in a glutaraldehyde or formaldehyde solution. HAE cells were immortalized by transfection of hTERT and chemically fixed with the same reagents. When mouse ES cells were cultured on these chemically fixed cells, the mouse ES cells grew well and expressed alkaline phosphatase, SSEA-1, and Oct-3/4 as their markers, indicating their undifferentiated state. The monkey ES cells also grew well and expressed alkaline phosphatase, SSEA-4, and Oct-4 as their markers, indicating their undifferentiated state. Freeze-drying HAE or MEF cells did not change their ability to support the undifferentiated growth of ES cells. Additionally, the chemically fixed cells could be utilized repeatedly in the culture of ES cells. These results demonstrate that chemically fixed nurse cells are useful for the maintenance of ES cells in an undifferentiated state in culture.

Human placenta feeder layers support undifferentiated growth of primate embryonic stem cells.

Various undifferentiated embryonic stem (ES) cells can grow on mouse embryonic fibroblast (MEF) feeders. However, the risk of zoonosis from animal feeders to human ES cells generally excludes the clinical use of these human ES cells. We have found that human placenta is a useful source of feeder cells for the undifferentiated growth of primate ES cells. As on MEF feeders, primate ES cells cultured on human amniotic epithelial (HAE) feeder cells and human chorionic plate (HCP) cells had undifferentiated growth. The cultured primate ES cells expressed Oct-4, alkaline phosphatase, and SSEA-4. The primate ES cells on HAE feeder cells produced typical immature teratomas in vivo after injection into severe combined immunodeficient mice. Human placenta is quite novel and important because it would provide a relatively available source of feeders for the growth of human ES cells for therapeutic purposes that are also free of ethical complications.

Chinese medicine induces neurite outgrowth in PC12 mutant cells incapable of differentiation.

During continuous culture of neural PC12 cells, we obtained a drug-hypersensitive PC12 mutant cell that showed high stimulation of neurite outgrowth by various drugs. When several Chinese medicines such as shu-jing-huo-xie-tang and Wu-Ling-San were provided to these PC12 mutant cells, the frequency of nerve growth factor (NGF)-induced neurite outgrowth increased approximately 30-fold compared to NGF alone. Neurite outgrowth induced by NGF in PC12 cells is accompanied by sustained activation of mitogen-activated protein kinase (MAPK); however, these Chinese medicines did not induce MAPK activity. The findings thus indicate that certain Chinese medicines may induce neurite outgrowth by a novel mechanism which is distinct from the NGF-activated pathway in PC12 mutant cells.

Immunosuppressant FK506 induces neurite outgrowth in PC12 mutant cells with impaired NGF-promoted neuritogenesis via a novel MAP kinase signaling pathway.

We obtained a drug-hypersensitive PC12 mutant cell (PC12m3), in which neurite outgrowth was strongly stimulated by various drugs such as FK506, calcimycin and cAMP, under the condition of NGF treatment. The frequency of neurite outgrowth stimulated by FK506 was approximately 40 times greater than by NGF alone. The effects of FK506 on neurite outgrowth in PC12m3 cells were inhibited by rapamycin, an FK506 antagonist, and by calcimycin, a calcium ionophore. PC12m3 cells had a strong NGF-induced MAP kinase activity, the same as PC12 parental cells. However, FK506-induced MAP kinase activity was detected only in PC12m3 cells. The activation of MAP kinase by FK506 in PC12m3 cells was markedly inhibited by rapamicin and calcimycin. FK506-induced MAP kinase activity was also inhibited by MAP kinase inhibitor U0126. These results demonstrate that drug-hypersensitive PC12m3 cells have a novel FK506-induced MAP kinase pathway for neuritogenesis.