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Microstructure evolution in Alloy 617 B after a long-term creep and thermal aging at 700°C
Speicher, Magdalena,Kauffmann, Florian,Shim, Jae-Hyeok,Chandran, Mahesh Elsevier 2018 Materials science & engineering. properties, micro Vol.711 No.-
<P><B>Abstract</B></P> <P>Changes in the microstructure of heat-resistant materials may influence their long-term behaviour. For this reason, materials chosen for high temperature-based applications, e.g. advanced ultra-supercritical (A-USC) steam power plants, must exhibit long-term microstructure stability. Therefore, changes in the microstructure of frequently used materials must be determined and correlated with their creep behaviour to assure a reliable operation of components. In this work, a long-term study investigated the microstructure of a creep rupture specimen made of a nickel-based alloy 617 B. The creep tests were carried out at 700°C for up to 45,148h. By using optical microscopy (OM), scanning electron microscopy (SEM) and transmission electron microscopy (TEM) the virgin, thermal-loaded and creep states were characterized. The precipitate location, number and size have been determined. The experiment results were compared, discussed and correlated to the creep and failure behaviour. Furthermore, the long-term precipitation kinetics of Alloy 617 B was simulated, which considered its thermal history, using the MatCalc software. The simulated precipitates fraction and size were compared with the experimental data obtained in this study. The comparison between the experimental and simulation results demonstrated comparable gamma prime (γ') phases. The simulation results of the carbides identified at the grain boundaries were satisfactory. However, the size of the intragranular fine carbides M<SUB>23</SUB>C<SUB>6</SUB> was not reproduced correctly.</P>
The HUPO Plasma Proteome Project: A report from the Munich congress
Omenn, Gilbert S.,Paik, Young-Ki,Speicher, David WILEY-VCH Verlag 2006 Proteomics Vol.6 No.1
<P>The Human Proteome Organization has several major collaborative research initiatives, including the Plasma Proteome Project. A major feature of the HUPO World Congress in Munich in August 2005 was the release of the special issue of PROTEOMICS with 28 articles from the pilot phase of the Plasma Proteome Project. An open Workshop and a presentation in the closing plenary session of the congress focused on next phases for the Plasma Proteome Project.</P>
MFF Regulation of Mitochondrial Cell Death Is a Therapeutic Target in Cancer
Seo, Jae Ho,Chae, Young Chan,Kossenkov, Andrew V.,Lee, Yu Geon,Tang, Hsin-Yao,Agarwal, Ekta,Gabrilovich, Dmitry I.,Languino, Lucia R.,Speicher, David W.,Shastrula, Prashanth K.,Storaci, Alessandra Mar American Association for Cancer Research 2019 Cancer Research Vol.79 No.24
<P>These findings describe mitochondrial fission regulation using a peptidomimetic agent that disturbs the MFF-VDAC complex and displays anticancer activity in multiple tumor models.</P><P><B></B></P><P>The regulators of mitochondrial cell death in cancer have remained elusive, hampering the development of new therapies. Here, we showed that protein isoforms of mitochondrial fission factor (MFF1 and MFF2), a molecule that controls mitochondrial size and shape, that is, mitochondrial dynamics, were overexpressed in patients with non–small cell lung cancer and formed homo- and heterodimeric complexes with the voltage-dependent anion channel-1 (VDAC1), a key regulator of mitochondrial outer membrane permeability. MFF inserted into the interior hole of the VDAC1 ring using Arg225, Arg236, and Gln241 as key contact sites. A cell-permeable MFF Ser223-Leu243 <SMALL>D</SMALL>-enantiomeric peptidomimetic disrupted the MFF–VDAC1 complex, acutely depolarized mitochondria, and triggered cell death in heterogeneous tumor types, including drug-resistant melanoma, but had no effect on normal cells. In preclinical models, treatment with the MFF peptidomimetic was well-tolerated and demonstrated anticancer activity in patient-derived xenografts, primary breast and lung adenocarcinoma 3D organoids, and glioblastoma neurospheres. These data identify the MFF–VDAC1 complex as a novel regulator of mitochondrial cell death and an actionable therapeutic target in cancer.</P><P><B>Significance:</B></P><P>These findings describe mitochondrial fission regulation using a peptidomimetic agent that disturbs the MFF–VDAC complex and displays anticancer activity in multiple tumor models.</P><P><I>See related commentary by Rao, p. 6074</I></P>