A closure mechanism for screech coupling in rectangular twin jets

Twin-jet configuration allows two different scenarios to close the screech feedback. For each jet, there is one loop involving disturbances which originate in that jet and arrive at its own receptivity point in-phase (self-excitation). The other loop is associated with free-stream acoustic waves that radiate from the other jet, reinforcing the self-excited screech (cross-excitation). In this work, the role of the free-stream acoustic mode and the guided jet mode as a closure mechanism for twin rectangular jet screech is explored by identifying eligible points of return for each path, where upstream waves propagating from such a point arrive at the receptivity location with an appropriate phase relation. Screech tones generated by these jets are found to be intermittent with an out-of-phase coupling as a dominant coupling mode. Instantaneous phase difference between the twin jets computed by the Hilbert transform suggests that a competition between out-of-phase and in-phase coupling is responsible for the intermittency. To model wave components of the screech feedback while ensuring perfect phase-locking, an ensemble average of leading spectral proper orthogonal decomposition modes is obtained from several segments of large-eddy simulations data that correspond to periods of invariant phase difference between the two jets. Each mode is then extracted by retaining relevant wavenumber components produced via a streamwise Fourier transform. Spatial cross-correlation analysis of the resulting modes shows that most of the identified points of return for the cross-excitation are synchronised with the guided jet mode self-excitation, supporting that it is preferred in closing rectangular twin-jet screech coupling

Transdifferentiation-inducing HCCR-1 oncogene

<p>Abstract</p> <p>Background</p> <p>Cell transdifferentiation is characterized by loss of some phenotypes along with acquisition of new phenotypes in differentiated cells. The differentiated state of a given cell is not irreversible. It depends on the up- and downregulation exerted by specific molecules.</p> <p>Results</p> <p>We report here that <it>HCCR-1</it>, previously shown to play an oncogenic role in human cancers, induces epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) in human and mouse, respectively. The stem cell factor receptor CD117/c-Kit was induced in this transdifferentiated (EMT) sarcoma tissues. This MET occurring in <it>HCCR-1 </it>transfected cells is reminiscent of the transdifferentiation process during nephrogenesis. Indeed, expression of <it>HCCR-1 </it>was observed during the embryonic development of the kidney. This suggests that <it>HCCR-1 </it>might be involved in the transdifferentiation process of cancer stem cell.</p> <p>Conclusions</p> <p>Therefore, we propose that <it>HCCR-1 </it>may be a regulatory factor that stimulates morphogenesis of epithelia or mesenchyme during neoplastic transformation.</p