Enabling transparent technologies for the development of highly granular flexible optical cross-connects

Flexible optical networking is identified today as the solution that offers smooth system upgradability towards Tb/s capacities and optimized use of network resources. However, in order to fully exploit the potentials of flexible spectrum allocation and networking, the development of a flexible switching node is required capable to adaptively add, drop and switch tributaries with variable bandwidth characteristics from/to ultra-high capacity wavelength channels at the lowest switching granularity. This paper presents the main concept and technology solutions envisioned by the EU funded project FOX-C, which targets the design, development and evaluation of the first functional system prototype of flexible add-drop and switching cross-connects. The key developments enable ultra-fine switching granularity at the optical subcarrier level, providing end-to-end routing of any tributary channel with flexible bandwidth down to 10Gb/s (or even lower) carried over wavelength superchannels, each with an aggregated capacity beyond 1Tb/s. © 2014 IEEE

Spectrally and spatially flexible optical network planning and operations

The advent of spectrally flexible (a.k.a. elastic) optical networking is widely identified as the next generation optical network solution that permits varying bandwidth demands to be dynamically assigned over flexible spectral containers, targeting optimum use of the available network resources. Additionally, the adoption of the space dimension is identified as a promising solution for the capacity expansion of future networks, while novel spatial-spectral switching solutions show that the flexible networking concept can be further expanded over both the spatial and spectral dimensions. This article provides an overview of the latest developments and possible approaches with respect to flexible optical networking and the emerging benefits that spatially flexible networking approaches can offer. The focus is on the network planning and resource optimization functions, the main network operations related to fragmentation and IP/optical layer integration, and the control plane solutions

A multimorphic mutation in IRF4 causes human autosomal dominant combined immunodeficiency

Interferon regulatory factor 4 (IRF4) is a transcription factor (TF) and key regulator of immune cell development and function. We report a recurrent heterozygous mutation in IRF4, p.T95R, causing an autosomal dominant combined immunodeficiency (CID) in seven patients from six unrelated families. The patients exhibited profound susceptibility to opportunistic infections, notably Pneumocystis jirovecii, and presented with agammaglobulinemia. Patients' B cells showed impaired maturation, decreased immunoglobulin isotype switching, and defective plasma cell differentiation, whereas their T cells contained reduced TH(17) and T(FH) populations and exhibited decreased cytokine production. A knock-in mouse model of heterozygous T95R showed a severe defect in antibody production both at the steady state and after immunization with different types of antigens, consistent with the CID observed in these patients. The IRF4(T95R) variant maps to the TF's DNA binding domain, alters its canonical DNA binding specificities, and results in a simultaneous multimorphic combination of loss, gain, and new functions for IRF4. IRF4(T95R) behaved as a gain-of-function hypermorph by binding to DNA with higher affinity than IRF4(WT). Despite this increased affinity for DNA, the transcriptional activity on IRF4 canonical genes was reduced, showcasing a hypomorphic activity of IRF4(T95R). Simultaneously, IRF4(T95R) functions as a neomorph by binding to noncanonical DNA sites to alter the gene expression profile, including the transcription of genes exclusively induced by IRF4(T95R) but not by IRF4(WT). This previously undescribed multimorphic IRF4 pathophysiology disrupts normal lymphocyte biology, causing human disease