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In the context of dynamic lightpath service provisioning, this paper evaluates the impact of the colorless, directionless, and contentionless (CDC) features of reconfigurable optical add/drop multiplexers on wavelength division multiplexing optical transport networks (OTNs). Under the assumption of fixed shortest path routing, we first develop analytical models for evaluating the impacts of the CDC features. Next, allowing for adaptive lightpath route selection, we propose three lightpath routing and add/drop port selection strategies. Simulation studies indicate that the proposed analytical models can effectively predict the performance of the OTNs under different add/drop port capabilities. The simulation results also show that, among the three features, the colorless feature seems to play the most important role in improving the lightpath blocking performance. In addition, under the colorless add/drop capability, there exists a saturation phenomenon: when the number of add/drop ports per nodal degree reaches a certain threshold level, performance improvement will be marginal even if the number of add/drop ports is further increased. Finally, comparing the three adaptive lightpath routing and add/drop allocation strategies, the results show that the consideration of the add/drop port state information in lightpath routing and wavelength assignment can significantly improve the lightpath blocking performance.

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Serum- and glucocorticoid-inducible kinase 3 (SGK3) is a downstream mediator of PI3K, which is essential for maintaining the functional integrity of podocytes. However, little is known about the role of SGK3 in podocyte function. Herein, we demonstrated that SGK3 contributes to the maintenance of podocyte integrity. Conditionally immortalized mouse podocyte cells (MPCs) were treated with puromycin aminonucleoside (PAN). PAN treatment inhibited the activity of SGK3 and the expression of podocin. Short hairpin RNA (shRNA)-mediated knockdown of SGK3 also reduced podocin expression in the absence of PAN. Adriamycin (ADR)-treated mice developed proteinuria and had decreased renal glomerular SGK3 expression in comparison to control mice. Consistent with a role for SGK3 in the ADR effect, SGK3 knockout (KO) mice had markedly reduced kidney podocin expression and significantly elevated proteinuria compared with wild-type mice. Electron microscopy revealed that SGK3 KO mice displayed partial effacement of podocyte foot processes. Further, a SGK3 target protein, glycogen synthase kinase-3 (GSK3), was discovered to be dramatically activated in PAN and SGK3 shRNA-treated MPCs and in SGK3 KO mice. Taken together, these data strongly suggest that SGK3 plays a significant role in regulating podocyte function, likely by controlling the expression and activity of GSK3.-Peng, L.-Q., Zhao, H., Liu, S., Yuan, Y.-P., Yuan, C.-Y., Mwamunyi, M.-J., Pearce, D., Yao, L.-J. Lack of serum- and glucocorticoid-inducible kinase 3 leads to podocyte dysfunction.

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