POWDER INJECTION MOLDING OF Cu-BASED AMORPHOUS POWDERS AND Fe-BASED METAMORPHIC POWDERS

ABSTRACT Powder injection molding (PIM) process was applied to Cu-based amorphous alloy powders and Fe-based metamorphic alloy powders, and microstructure, hardness, and wear resistance of the PIM products were analyzed. When Cu-based amorphous powders were injection-molded and sintered at 470 o C, sintering was not made since most of amorphous phases were replaced by crystalline phases. When sintered at higher temperatures, volume fraction of pores inside the sintered specimens decreased, but sintering was not properly conducted. When Fe-based metamorphic powders were injection-molded and then sintered at 1200 o C, completely densified products with almost no pores were obtained. They contained 34 vol.% of (Cr,Fe) 2 B borides dispersed in the austenitic matrix without amorphous phases. Since these (Cr,Fe) 2 B borides were hard and thermally stable, hardness, high-temperature hardness, and wear resistance of the PIM products of Fe-based metamorphic powders were twice as high as those of conventional PIM stainless steel products. These findings suggested new applicability of the PIM products of Fe-based metamorphic powders to structures and parts requiring excellent mechanical properties

Selective activation of the c-Jun N-terminal protein kinase pathway during 4-hydroxynonenal-induced apoptosis of PC12 cells

ABSTRACT The by-product of lipid peroxidation, 4-hydroxynonenal (HNE), was shown to cause apoptosis in PC12 cells. In this study, we investigated the molecular mechanism of HNE-induced apoptosis in these cells. Specifically, we determined the effect of HNE on the activities of mitogen-activated protein (MAP) kinases involved in early signal transduction. Within 15 to 30 min after HNE treatment, c-Jun N-terminal protein kinase (JNK) was maximally activated, before it returned to control level at 1 h post-treatment. In contrast, activities of extracellular signalregulated kinase and p38 MAP kinase remained unchanged from their baseline levels. Stress-activated protein kinase kinase (SEK1), an upstream kinase of JNK, was also activated within 5 min after HNE treatment and remained activated for up to 60 min. Marked activation of the JNK pathway through SEK1 and apoptosis signal-regulating kinase 1 (ASK1), an upstream kinase of SEK1, was demonstrated by the transient transfection of cDNA for wild-type SEK1 or ASK1 together with JNK into COS-7 cells. Furthermore, significant reductions in JNK activation and HNE-induced cell death were observed when either of the dominant negative mutant of SEK1 or ASK1 was cotransfected with JNK. Pretreatment of PC12 cells with a survivalpromoting agent, 8-(4-chlorophenylthio)-cAMP, prevented both the HNE-induced JNK activation and apoptosis. Nonaldehyde, a nontoxic aldehyde, neither caused apoptosis nor JNK activation. Pretreatment of PC12 cells with SB203580, a specific inhibitor of p38 MAP kinase, had no effect on HNE-induced apoptosis. All these data suggest that the selective JNK activation by HNE is critical for the apoptosis of PC12 cells and that the HNE-mediated apoptosis is likely to be mediated through the activation of the ASK1-SEK1-JNK pathway without activation of extracellular signal-regulated kinase or p38 MAP kinase. Reactive moieties produced during stressful conditions cause the oxidation of polyunsaturated fatty acids in membrane lipid bilayers. Without sufficient levels of defense mechanisms such as free radical scavengers or antioxidants, increasing levels of lipid hydroperoxides and peroxides can be produced by self-perpetuating chain reactions. Eventually, cytotoxic lipid aldehydes, including 4-hydroxynonenal (HNE), an end product of lipid peroxidation, is produced Extracellular signal-regulated kinase (ERK) plays a major role in cell proliferation and differentiation as well as sur-1 Both authors contributed equally to the present work