3,794 research outputs found

    Radio Imaging of the NGC 1333 IRAS 4B Region

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    The NGC 1333 IRAS 4B region was observed in the 6.9 mm and 1.3 cm continuum with an angular resolution of about 0.4 arcseconds. IRAS 4BI was detected in both bands, and BII was detected in the 6.9 mm continuum only. The 1.3 cm source of BI seems to be a disk-like flattened structure with a size of about 50 AU. IRAS 4BI does not show any sign of multiplicity. Examinations of archival infrared images show that the dominating emission feature in this region is a bright peak in the southern outflow driven by BI, corresponding to the molecular hydrogen emission source HL 9a. Both BI and BII are undetectable in the mid-IR bands. The upper limit on the far-IR flux of IRAS 4BII suggests that it may be a very low luminosity young stellar object.Comment: To appear in the JKA

    Apigenin Induces Apoptosis through a Mitochondria/Caspase-Pathway in Human Breast Cancer MDA-MB-453 Cells

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    In this study, we investigated the mechanistic role of the caspase cascade in extrinsic and intrinsic apoptosis induced by apigenin, which has been targeted as a candidate in the development of noncytotoxic anticancer medicines. Treatment with apigenin (1–100 µM) significantly inhibited the proliferation of MDA-MB-453 human breast cancer cells in a dose- and time-dependent manner with IC50 values of 59.44 and 35.15 µM at 24 and 72 h, respectively. This inhibition resulted in the induction of apoptosis and the release of cytochrome c in cells exposed to apigenin at its 72 h IC50. Subsequently, caspase-9, which acts in mitochondria-mediated apoptosis, was cleaved by apigenin. In addition, apigenin activated caspase-3, which functions downstream of caspase-9. The apigenin-induced activation of caspase-3 was accompanied by the cleavage of capases-6, -7, and -8. These results are supported by evidence showing that the activity patterns of caspases-3, -8, and -9 were similar. The present study supports the hypothesis that apigenin-induced apoptosis involves the activation of both the intrinsic and extrinsic apoptotic pathways
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