Fast shape reconstruction of perfectly conducting cracks by using a multi-frequency topological derivative strategy

This paper concerns a fast, one-step iterative technique of imaging extended perfectly conducting cracks with Dirichlet boundary condition. In order to reconstruct the shape of cracks from scattered field data measured at the boundary, we introduce a topological derivative-based electromagnetic imaging function operated at several nonzero frequencies. The properties of the imaging function are carefully analyzed for the configurations of both symmetric and non-symmetric incident field directions. This analysis explains why the application of incident fields with symmetric direction operated at multiple frequencies guarantees a successful reconstruction. Various numerical simulations with noise-corrupted data are conducted to assess the performance, effectiveness, robustness, and limitations of the proposed technique.Comment: 17 pages, 27 figure

Inverse seesaw in supersymmetry

We study a mechanism where tiny neutrino masses arise only from radiative contribution in a supersymmetric model. In each generation, the tree-level light neutrino mass is rotated away by introducing a second SM singlet $s_{L}$ that forms a Dirac mass term with the right-handed neutrino $n_{R}$. Even with non-zero Majorana neutrino mass for the right-handed neutrinos $M_{R} \bar{n^{c}_{R}} n_{R}$, the lightest neutrino remains massless at tree level due to an approximate symmetry as $U(1)_{\nu-s}$. Holomorphic feature of superpotential ensures that the Majorana neutrino masses $M_{R} \bar{n^{c}_{R}} n_{R}$ and $M^{*}_{R} \bar{s^{c}_{L}} s_{L}$ are not generated simultaneously. However, the $U(1)_{\nu-s}$ is not respected by the SM gauge interactions or interaction with Higgs. Consequently, tiny neutrino masses arise from radiative contributions. It is also shown that the right-handed neutrino Majorana mass $M_{R}$ can be at $\cal O$(KeV) to obtain the proper light neutrino mass.Comment: 10 page

State political and economic capacities and the quality of government in Asia

This study analyzes the impacts of state political and economic capacities on the quality of government in 40 Asian countries. Quality of government data for 2002 and 2010 were obtained from four elements of the World Bank Governance Index, and the same or closest year's data for political and economic capacity were collected from other well-known indices. The analysis reveals that economic growth influences four elements in both developed and developing countries, although the effects of economic freedom differ between these two groups of states. While political capacity (i.e. civil empowerment, democracy, and press freedom) is found to have an effect on all four of the governance elements in developed countries, it influences just two elements in developing economies. Thus, the results suggest that the quality of government in Asia is not only improved by economic capacity but might also be enhanced by consolidation of democracy, particularly once a certain degree of economic development is achieved

The politics of government reform in Korea : from tripartite to bipartite politicization

Government reforms in South Korea, beginning in the 1980s, moved toward deconcentration and deregulation in the 1990s and 2000s. However, the contents of the reforms under the “transformational” presidencies following democratization, which aimed to raise the quality of government and respond to increasing social polarization and political discord, did not significantly reduce state power or depoliticize policy making. Instead, state strength was consolidated through tripartite politicization: the rise of ministers as a third force in policy making vis-à-vis the president and legislature. Under the “post-transformational” presidencies of Lee Myung-Bak and Park Geun-Hye, government reforms can be summarized as bipartite politicization between the president and legislature, as ministerial power has been reduced

Structure of the substrate-engaged SecA-SecY protein translocation machine.

The Sec61/SecY channel allows the translocation of many proteins across the eukaryotic endoplasmic reticulum membrane or the prokaryotic plasma membrane. In bacteria, most secretory proteins are transported post-translationally through the SecY channel by the SecA ATPase. How a polypeptide is moved through the SecA-SecY complex is poorly understood, as structural information is lacking. Here, we report an electron cryo-microscopy (cryo-EM) structure of a translocating SecA-SecY complex in a lipid environment. The translocating polypeptide chain can be traced through both SecA and SecY. In the captured transition state of ATP hydrolysis, SecAs two-helix finger is close to the polypeptide, while SecAs clamp interacts with the polypeptide in a sequence-independent manner by inducing a short β-strand. Taking into account previous biochemical and biophysical data, our structure is consistent with a model in which the two-helix finger and clamp cooperate during the ATPase cycle to move a polypeptide through the channel

Pharmacological activation of FOXO3 suppresses triple-negative breast cancer in vitro and in vivo

Triple-negative breast cancer (TNBC) is the most lethal form of breast cancer. Lacking effective therapeutic options hinders treatment of TNBC. Here, we show that bepridil (BPD) and trifluoperazine (TFP), which are FDA-approved drugs for treatment of schizophrenia and angina respectively, inhibit Akt-pS473 phosphorylation and promote FOXO3 nuclear localization and activation in TNBC cells. BPD and TFP inhibit survival and proliferation in TNBC cells and suppress the growth of TNBC tumors, whereas silencing FOXO3 reduces the BPD- and TFP-mediated suppression of survival in TNBC cells. While BPD and TFP decrease the expression of oncogenic c-Myc, KLF5, and dopamine receptor DRD2 in TNBC cells, silencing FOXO3 diminishes BPD- and TFP-mediated repression of the expression of these proteins in TNBC cells. Since c-Myc, KLF5, and DRD2 have been suggested to increase cancer stem cell-like populations in various tumors, reducing these proteins in response to BPD and TFP suggests a novel FOXO3-dependent mechanism underlying BPD- and TFP-induced apoptosis in TNBC cells