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Development of a 60 Hz Power Standard Using SNS Programmable Josephson Voltage Standards
Burroughs, C.J.,Benz, S.P.,Dresselhaus, P.D.,Waltrip, B.C.,Nelson, T.L.,Yonuk Chong,Williams, J.M.,Henderson, D.,Patel, P.,Palafox, L.,Behr, R. Institute of Electrical and Electronics Engineers 2007 IEEE transactions on instrumentation and measureme Vol.56 No.2
<P>We are implementing a new standard for 60 Hz power measurements based on precision sinusoidal reference voltages from two independent programmable Josephson voltage standards (PJVS): one for voltage and one for current. The National Institute of Standards and Technology PJVS systems use series arrays of Josephson junctions to produce accurate quantum-based DC voltages. Using stepwise-approximation synthesis, the PJVS systems produce sinewaves with precisely calculable RMS voltage and spectral content. We present measurements and calculations that elucidate the sources of error in the RMS voltage that are intrinsic to the digital-synthesis technique and that are due to the finite rise times and transients that occur when switching between the discrete voltages. Our goal is to reduce all error sources and uncertainty contributions from the PJVS synthesized waveforms to a few parts in 10 <SUP>7</SUP> so that the overall uncertainty in the AC-power standard is a few parts in 10<SUP>6</SUP></P>
Baek, Ji Yeon,Morris, Shelli M.,Campbell, Jean,Fausto, Nelson,Yeh, Matthew M.,Grady, William M. Wiley Subscription Services, Inc., A Wiley Company 2010 International journal of cancer: Journal internati Vol.127 No.5
<P>Hepatocellular carcinoma (HCC) results from the cumulative effects of deregulated tumor suppressor genes and oncogenes. The tumor suppressor and oncogenes commonly affected include growth factors, receptors and their downstream signaling pathway components. The overexpression of transforming growth factor alpha (TGF-α) and the inhibition of TGF-β signaling are especially common in human liver cancer. Thus, we assessed whether TGF-α overexpression and TGF-β signaling inactivation cooperate in hepatocarcinogenesis using an in vivo mouse model, MT1/TGFa;AlbCre/Tgfbr2<SUP>flx/flx</SUP> mice (“TGFa;Tgfbr2<SUP>hepko</SUP>”), which overexpresses TGF-α and lacks a TGF-β receptor in the liver. TGF-β signaling inactivation did not alter the frequency or number of cancers in mice with overexpression of TGF-α. However, the tumors in the TGFa;Tgfbr2<SUP>hepko</SUP> mice displayed increased proliferation and increased cdk2, cyclin E and cyclin A expression as well as decreased Cdkn1a/p21 expression compared to normal liver and compared to the cancers arising in the TGF-α overexpressing mice with intact TGF-β receptors. Increased phosphorylated ERK1/2 expression was also present in the tumors from the TGFa;Tgfbr2<SUP>hepko</SUP> mice and correlated with downregulated Raf kinase inhibitor protein expression, which is a common molecular event in human HCC. Thus, TGF-β signaling inactivation appears to cooperate with TGF-α in vivo to promote the formation of liver cancer that recapitulates molecular features of human HCC.</P>
Kang, Hyunook,Bang, Injin,Jin, Kyeong Sik,Lee, Boyun,Lee, Junho,Shao, Xiangqiang,Heier, Jonathon A.,Kwiatkowski, Adam V.,Nelson, W. James,Hardin, Jeff,Weis, William I.,Choi, Hee-Jung American Society for Biochemistry and Molecular Bi 2017 The Journal of biological chemistry Vol.292 No.17
<P>Intercellular epithelial junctions formed by classical cadherins, beta-catenin, and the actin-binding protein alpha-catenin link the actin cytoskeletons of adjacent cells into a structural continuum. These assemblies transmit forces through the tissue and respond to intracellular and extracellular signals. However, the mechanisms of junctional assembly and regulation are poorly understood. Studies of cadherin-catenin assembly in a number of metazoans have revealed both similarities and unexpected differences in the biochemical properties of the cadherin center dot catenin complex that likely reflect the developmental and environmental requirements of different tissues and organisms. Here, we report the structural and biochemical characterization of HMP-1, the Caenorhabditis elegans alpha-catenin homolog, and compare it with mammalian alpha-catenin. HMP-1 shares overall similarity in structure and actin-binding properties, but displayed differences in conformational flexibility and allosteric regulation from mammalian alpha-catenin. HMP-1 bound filamentous actin with an affinity in the single micromolar range, even when complexed with the beta-catenin homolog HMP-2 or when present in a complex of HMP-2 and the cadherin homolog HMR-1, indicating that HMP-1 binding to F-actin is not allosterically regulated by the HMP-2.HMR-1 complex. The middle (i.e. M) domain of HMP-1 appeared to be less conformationally flexible than mammalian alpha-catenin, which may underlie the dampened effect of HMP-2 binding on HMP-1 actin-binding activity compared with that of the mammalian homolog. In conclusion, our data indicate that HMP-1 constitutively binds beta-catenin and F-actin, and although the overall structure and function of HMP-1 and related alpha-catenins are similar, the vertebrate proteins appear to be under more complex conformational regulation.</P>