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      • A Novel, Reactive Green Iron Sulfide (Sulfide Green Rust) Formed on Iron Oxide Nanocrystals

        Jones, Christopher J.,Chattopadhyay, Soma,Gonzalez-Pech, Natalia I.,Avendano, Carolina,Hwang, Nina,Lee, Seung Soo,Cho, Minjung,Ozarowski, Andrew,Prakash, Arjun,Mayo, J. T.,Yavuz, Cafer,Colvin, Vicki. American Chemical Society 2015 Chemistry of materials Vol.27 No.3

        <P>Iron oxide nanocrystals are of great scientific and technological interest. In this work, these materials are the starting point for producing a reactive nanoparticle whose surface resembles that of natural green rusts. Treatment of iron oxide nanoparticles with cysteamine leads to the reduction of iron and the formation of a brilliant green aqueous solution of nanocrystals rich in iron(II). These materials remained crystalline with magnetic and structural features of the original iron oxide. However, new low-angle X-ray diffraction peaks as well as vibrational features characteristic of cysteamine were found in the nanocrystalline product. X-ray absorption spectroscopy (XAS), X-ray photoemission (XPS) and Mössbauer spectroscopies indicated the presence of an iron(II)-rich phase with high sulfur content analogous to the iron–oxygen structures found in natural green rusts. Electron microscopy found that these structural components remained associated with the nonreduced iron oxide cores. These sulfur-rich analogs of natural green rusts are highly reactive and were able to rapidly degrade a model organic dye in water. This observation suggests possible actuation with a cysteamine treatment of inert and magnetic iron oxide particles at the point-of-use for environmental remediation.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/cmatex/2015/cmatex.2015.27.issue-3/cm5028942/production/images/medium/cm-2014-028942_0007.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/cm5028942'>ACS Electronic Supporting Info</A></P>

      • Overexpression of hepatocyte nuclear factor-3α induces apoptosis through the upregulation and accumulation of cytoplasmic p53 in prostate cancer cells

        Lee, Hyun Joo,Chattopadhyay, Soma,Yoon, Wan-Hee,Bahk, Jong Yoon,Kim, Tae-Hyoung,Kang, Hyung Sik,Lee, Keesook Wiley Subscription Services, Inc., A Wiley Company 2010 The Prostate Vol.70 No.4

        <B>BACKGROUND</B><P>Hepatocyte nuclear factor-3α (HNF-3α) has been known to act as a repressor in the pathogenesis of many cancers. Herein, we investigated the effect of HNF-3α overexpression in prostate cancer cells.</P><B>METHODS</B><P>HNF-3α was overexpressed in prostate cancer cells using an adenovirus recombinant expressing wild-type HNF-3α. The apoptosis of prostate cancer cells was determined by TUNEL, FACS, and caspase activity analyses.</P><B>RESULTS</B><P>Adenovirus-mediated overexpression of HNF-3α caused cell death in prostate cancer cells as assessed by changes in cellular and nuclear morphology, TUNEL analysis, and caspase activations. Furthermore, FACS analysis showed an increased sub-G1 phase of cell cycle as well as the G2/M phase with a corresponding decrease in S phases. HNF-3α overexpression caused the upregulation of p53 protein and its accumulation, together with HNF-3α, in the cytoplasm. It also causes Bax protein to localize to the mitochondria-enriched fraction. These findings suggest that multiple apoptotic pathways seem to be involved in the HNF-3α-induced cell death: pathways involving the accumulation of p53 protein in the cytoplasm and subsequent cytochrome c release, and other pathways involving death receptor signaling and caspase-8 activation.</P><B>CONCLUSIONS</B><P>The results of the current study suggest a novel function of HNF-3α as a killer of malignant prostate cancer cells, which reveals HNF-3α as a promising therapeutic molecule for prostate cancers. Prostate 70: 353–361, 2010. © 2009 Wiley-Liss, Inc.</P>

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