Edge Vs Kane
Mellissa Sprock
And finally, Jacobs hit his stride as Kane, the long-running persona with whom he has won most of the awards on his impressive Wrestling Observer rsum. Of course, that list of accolades looks like this:
On the wrestling end of the feud, things started off to a nice stupid start, as their world title match at Survivor Series ended in a double pin, with Edge neglecting to take his own shoulders off the mat after spearing Kane. Details, details.
Even WWE had to acknowledge how silly this entire feud was, especially given that it was over the World title and made a complete fool of a character who two months prior had not only utterly dominated The Undertaker, but ostensibly murdered him.
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We propose two experiments to probe the Majorana fermion edge states that occur at a junction between a superconductor and a magnet deposited on the surface of a topological insulator. Combining two Majorana fermions into a single Dirac fermion on a magnetic domain wall allows the neutral Majorana fermions to be probed with charge transport. We will discuss a novel interferometer for Majorana fermions, which probes their Z2 phase. This setup also allows the transmission of neutral Majorana fermions through a point contact to be measured. We introduce a point contact formed by a superconducting junction and show that its transmission can be controlled by the phase difference across the junction. We discuss the feasibility of these experiments using the recently discovered topological insulator Bi2Se3.
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To explain the disappearance of medial edge epithelial (MEE) cells during palatal fusion, programmed cell death, epithelial-mesenchymal transformation, and migration of these cells to the oral and nasal epithelia have been proposed. However, MEE cell death has not always been accepted as a mechanism involved in midline epithelial seam disappearance. Similarly, labeling of MEE cells with vital lipophilic markers has not led to a clear conclusion as to whether MEE cells migrate, transform into mesenchyme, or both. To clarify these controversies, we first utilized TUNEL techniques to detect apoptosis in mouse palates at the fusion stage and concomitantly analyzed the presence of macrophages by immunochemistry and confocal microscopy. Second, we in vitro infected the MEE with the replication-defective helper-free retroviral vector CXL, which carries the Escherichia coli lacZ gene, and analyzed beta-galactosidase activity in cells after fusion to follow their fate. Our results demonstrate that MEE cells die and transform into mesenchyme during palatal fusion and that dead cells are phagocytosed by macrophages. In addition, we have investigated the effects of the absence of transforming growth factor beta(3) (TGF-beta(3)) during palatal fusion. Using environmental scanning electron microscopy and TUNEL labeling we compared the MEE of the clefted TGF-beta(3) null and wild-type mice. We show that MEE cell death in TGF-beta(3) null palates is greatly reduced at the time of fusion, revealing that TGF-beta(3) has an important role as an inducer of apoptosis during palatal fusion. Likewise, the bulging cells observed on the MEE surface of wild-type mice prior to palatal shelf contact are very rare in the TGF-beta(3) null mutants. We hypothesize that these protruding cells are critical for palatal adhesion, being morphological evidence of increased cell motility/migration.
We investigate the dependence of band dispersion of the quantum spin Hall effect (QSHE) edge states in the Kane-Mele model on crystallographic orientation of the edges. Band structures of the one-dimensional honeycomb lattice ribbons show the presence of the QSHE edge states at all orientations of the edges given sufficiently strong spin-orbit interactions. We find that the Fermi velocities of the QSHE edge-state bands increase monotonically when the edge orientation changes from zigzag (chirality angle theta = 0 degrees) to armchair (theta = 30 degrees). We propose a simple analytical model to explain the numerical results. (C) 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
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