Employing wavelength diversity to improve SOA gain uniformity

In this paper, we propose a wavelength diversity technique for the semiconductor optical amplifier (SOA) to improve the gain uniformity for ultra-high speed optical routers. In such routers, fast SOA gain recovery is required to ensure the minimum gain standard deviation and thus leading to reduction in the system power penalty. The SOA is modeled using a segmentation technique and the detailed theoretical analysis for the model is presented. A direct temporal analysis of the impact of the signal wavelength on the SOA gain is investigated. The SOA gain profile when injected with a burst of input Gaussian pulses for a single wavelength and the proposed wavelength diversity technique are investigated. The operation principle is simulated and the results show a reduction in the gain standard deviation (at 1 mW input power) of 13.1, 11, 8.1, 6.2 and 4.8 dB for the data rates of 10, 20, 40, 80 and 160 Gb/s, respectively

Optimisation of the key SOA parameters for amplification and switching

Wireless Sensor Networks (WSN) are composed of small, low cost, resource-constrained computing nodes equipped with low power wireless transceivers. Generally, they are embedded in their environment to perform some specific monitoring and/or control function. Unlike wired networks that have dedicated routers for network connectivity and message forwarding, every node in a WSN can act as a router in a multi-hop network. A WSN can offer a cheap, applicationspecific solution in a variety of situations including military and disaster response scenarios, where other approaches are not viable. Due to their unattended nature and deployment in possibly hostile environmental conditions, there are many challenges in ensuring that a WSN is formed effectively and survives long enough to fulfil its function. Securing a WSN against attack is a particular challenge. Traditional encryption mechanisms are resource hungry and are not sufficient alone to provide a complete solution. This project is concerned with secure routing protocols. Formal methods are used to model and analyse the design of existing protocols and to demonstrate some previously unreported weaknesses

Impact of signal wavelength on the semiconductor opticalamplifier gain uniformity for high speed optical routers employing the segmentation model

This paper investigates the impact of a train of input Gaussian pulses wavelength on semiconductor optical amplifier (SOA) gain uniformity for high speed applications. In high speed applications, the linear output gain of the input pulses is necessary in order to minimize the gain standard deviation and power penalties. A segmentation model of the SOA is demonstrated to utilize the complete rate equations. The SOA gain profile when injected with a burst of input signal is presented. A direct temporal analysis of the effect of the burst wavelength on the SOA gain and the output gain standard deviation is investigated. The output gain uniformity dependence on the input burst power and wavelength within the C-band spectrum range is analyzed. Results obtained show the proportionality of the peak-gain conditions for the SOA on the nonlinearity of the output gain achieved by the input pulses

Turing Instability for a Ratio-Dependent Predator-Prey Model with Diffusion

Ratio-dependent predator-prey models have been increasingly favored by field ecologists where predator-prey interactions have to be taken into account the process of predation search. In this paper we study the conditions of the existence and stability properties of the equilibrium solutions in a reaction-diffusion model in which predator mortality is neither a constant nor an unbounded function, but it is increasing with the predator abundance. We show that analytically at a certain critical value a diffusion driven (Turing type) instability occurs, i.e. the stationary solution stays stable with respect to the kinetic system (the system without diffusion). We also show that the stationary solution becomes unstable with respect to the system with diffusion and that Turing bifurcation takes place: a spatially non-homogenous (non-constant) solution (structure or pattern) arises. A numerical scheme that preserve the positivity of the numerical solutions and the boundedness of prey solution will be presented. Numerical examples are also included

The Plasmodium serine-type SERA proteases display distinct expression patterns and non-essential in vivo roles during life cycle progression of the malaria parasite

Parasite proteases play key roles in several fundamental steps of the Plasmodium life cycle, including haemoglobin degradation, host cell invasion and parasite egress. Plasmodium exit from infected host cells appears to be mediated by a class of papain-like cysteine proteases called ‘serine repeat antigens’ (SERAs). A SERA subfamily, represented by Plasmodium falciparum SERA5, contains an atypical active site serine residue instead of a catalytic cysteine. Members of this SERAser subfamily are abundantly expressed in asexual blood stages, rendering them attractive drug and vaccine targets. In this study, we show by antibody localization and in vivo fluorescent tagging with the red fluorescent protein mCherry that the two P. berghei serine-type family members, PbSERA1 and PbSERA2, display differential expression towards the final stages of merozoite formation. Via targeted gene replacement, we generated single and double gene knockouts of the P. berghei SERAser genes. These loss-of-function lines progressed normally through the parasite life cycle, suggesting a specialized, non-vital role for serine-type SERAs in vivo. Parasites lacking PbSERAser showed increased expression of the cysteine-type PbSERA3. Compensatory mechanisms between distinct SERA subfamilies may thus explain the absence of phenotypical defect in SERAser disruptants, and challenge the suitability to develop potent antimalarial drugs based on specific inhibitors of Plasmodium serine-type SERAs

Malarial proteases and host cell egress: an ‘emerging’ cascade

Malaria is a scourge of large swathes of the globe, stressing the need for a continuing effort to better understand the biology of its aetiological agent. Like all pathogens of the phylum Apicomplexa, the malaria parasite spends part of its life inside a host cell or cyst. It eventually needs to escape (egress) from this protective environment to progress through its life cycle. Egress of Plasmodium blood-stage merozoites, liver-stage merozoites and mosquito midgut sporozoites relies on protease activity, so the enzymes involved have potential as antimalarial drug targets. This review examines the role of parasite proteases in egress, in the light of current knowledge of the mechanics of the process. Proteases implicated in egress include the cytoskeleton-degrading malarial proteases falcipain-2 and plasmepsin II, plus a family of putative papain-like proteases called SERA. Recent revelations have shown that activation of the SERA proteases may be triggered by regulated secretion of a subtilisin-like serine protease called SUB1. These findings are discussed in the context of the potential for development of new chemotherapeutics targeting this stage in the parasite's life cycle

General Relativistic Magnetohydrodynamic Simulations of Magnetically Choked Accretion Flows around Black Holes

Black hole (BH) accretion flows and jets are qualitatively affected by the presence of ordered magnetic fields. We study fully three-dimensional global general relativistic magnetohydrodynamic (MHD) simulations of radially extended and thick (height $H$ to cylindrical radius $R$ ratio of $|H/R|\sim 0.2--1$) accretion flows around BHs with various dimensionless spins ($a/M$, with BH mass $M$) and with initially toroidally-dominated ($\phi$-directed) and poloidally-dominated ($R-z$ directed) magnetic fields. Firstly, for toroidal field models and BHs with high enough $|a/M|$, coherent large-scale (i.e. $\gg H$) dipolar poloidal magnetic flux patches emerge, thread the BH, and generate transient relativistic jets. Secondly, for poloidal field models, poloidal magnetic flux readily accretes through the disk from large radii and builds-up to a natural saturation point near the BH. For sufficiently high $|a/M|$ or low $|H/R|$ the polar magnetic field compresses the inflow into a geometrically thin highly non-axisymmetric "magnetically choked accretion flow" (MCAF) within which the standard linear magneto-rotational instability is suppressed. The condition of a highly-magnetized state over most of the horizon is optimal for the Blandford-Znajek mechanism that generates persistent relativistic jets with $\gtrsim 100$% efficiency for $|a/M|\gtrsim 0.9$. A magnetic Rayleigh-Taylor and Kelvin-Helmholtz unstable magnetospheric interface forms between the compressed inflow and bulging jet magnetosphere, which drives a new jet-disk quasi-periodic oscillation (JD-QPO) mechanism. The high-frequency QPO has spherical harmonic $|m|=1$ mode period of $\tau\sim 70GM/c^3$ for $a/M\sim 0.9$ with coherence quality factors $Q\gtrsim 10$. [abridged]Comment: 32 pages + acks/appendix/references, 22 figures, 10 tables. MNRAS in press. High-Res Version: http://www.slac.stanford.edu/~jmckinne/mcaf.pdf . Fiducial Movie: http://youtu.be/V2WoJOkIin

Subcellular discharge of a serine protease mediates release of invasive malaria parasites from host erythrocytes.

The most virulent form of malaria is caused by waves of replication of blood stages of the protozoan pathogen Plasmodium falciparum. The parasite divides within an intraerythrocytic parasitophorous vacuole until rupture of the vacuole and host-cell membranes releases merozoites that invade fresh erythrocytes to repeat the cycle. Despite the importance of merozoite egress for disease progression, none of the molecular factors involved are known. We report that, just prior to egress, an essential serine protease called PfSUB1 is discharged from previously unrecognized parasite organelles (termed exonemes) into the parasitophorous vacuole space. There, PfSUB1 mediates the proteolytic maturation of at least two essential members of another enzyme family called SERA. Pharmacological blockade of PfSUB1 inhibits egress and ablates the invasive capacity of released merozoites. Our findings reveal the presence in the malarial parasitophorous vacuole of a regulated, PfSUB1-mediated proteolytic processing event required for release of viable parasites from the host erythrocyte

Inhibitory Potential of Prodomain of Plasmodium falciparum Protease Serine Repeat Antigen 5 for Asexual Blood Stages of Parasite

Plasmodium falciparum serine repeat antigen 5 (SERA5) is a target for both drug and vaccine intervention against malaria. SERA5 is secreted in the parasitophorous vacuole where it is proteolytically processed before schizont rupture. Among the processed products is a 50.8-kDa central domain of the protease, which possesses chymotrypsin-like activity and consists of a 28.9-kDa catalytic domain with a 21.9-kDa N-terminal prodomain, which remain attached together. Because SERA5 has been implicated in merozoite egress from host erythrocytes, the effect of the prodomain and a heptapeptide derived from its C-terminus spanning from D560 to F566 (DNSDNMF) on parasite growth was studied. When E. coli-expressed prodomain was incubated with parasite culture, a significant delay in transition from schizont to ring stages was observed up to nanomolar concentrations. The peptide, DNSDNMF also showed similar effects but at nearly 1000-fold higher concentrations. The peptide was also found to interact with the catalytic domain. These data demonstrate the crucial role of SERA5 prodomain for the egress process. Given the inhibitory potential of the prodomain for the parasite, we suggest that peptidomimetic inhibitors based on SERA5 prodomain sequences can be developed as future therapeutics against malaria