A Miniaturized Multiband Antenna Array for Robust Navigation in Aerial Applications.

Satellite navigation is more and more important in a plethora of very different application fields, ranging from bank transactions to shipping, from autonomous driving to aerial applications, such as avionics as well as unmanned aerial vehicles (UAVs). Due to the increasing dependency on satellite navigation, the need for robust systems able to counteract unintentional or intentional interferences is growing. When considering interference-robust designs; however, the complexity increases. Top performance is obtained through the use of multi-antenna receivers capable of performing spatial nulling in the direction of the interference signals. In particular, mobile applications (aeronautics, UAVs, automotive) have a substantial interest in robust navigation, but they also have the strongest constraints on the weight and available places for installation, with the use of bigger and heavier systems posing a substantial problem. In order to overcome this limitation, the present work shows a miniaturized five element (4+1) antenna array, which operates at the L1/E1 band (with array capability), as well as at the L5/E5 band (as a single antenna). The proposed antenna array is able to fit into a 3.5-inch footprint, i.e., is compliant with the most widespread footprints for single antennas. Moreover, it is capable of multiband operation and meets the requirements of dual-frequency multi-constellation (DFMC) systems. Thanks to its extreme miniaturization and its compliance with current airborne single antenna footprints, the presented antenna array is suitable for easy integration in future aerial platforms, while enabling robustness and enhancing interference mitigation techniques using multi-antenna processing.

Developmental stalling and organ-autonomous regulation of morphogenesis.

Timing of organ development during embryogenesis is coordinated such that at birth, organ and fetal size and maturity are appropriately proportioned. The extent to which local developmental timers are integrated with each other and with the signaling interactions that regulate morphogenesis to achieve this end is not understood. Using the absolute requirement for a signaling pathway activity (bone morphogenetic protein, BMP) during a critical stage of tooth development, we show that suboptimal levels of BMP signaling do not lead to abnormal morphogenesis, as suggested by mutants affecting BMP signaling, but to a 24-h stalling of the intrinsic developmental clock of the tooth. During this time, BMP levels accumulate to reach critical levels whereupon tooth development restarts, accelerates to catch up with development of the rest of the embryo and completes normal morphogenesis. This suggests that individual organs can autonomously control their developmental timing to adjust their stage of development to that of other organs. We also find that although BMP signaling is critical for the bud-to-cap transition in all teeth, levels of BMP signaling are regulated differently in multicusped teeth. We identify an interaction between two homeodomain transcription factors, Barx1 and Msx1, which is responsible for setting critical levels of BMP activity in multicusped teeth and provides evidence that correlates the levels of Barx1 transcriptional activity with cuspal complexity. This study highlights the importance of absolute levels of signaling activity for development and illustrates remarkable self-regulation in organogenesis that ensures coordination of developmental processes such that timing is subordinate to developmental structure.

The stomach mesenchymal transcription factor Barx1 specifies gastric epithelial identity through inhibition of transient Wnt signaling.

Inductive interactions between gut endoderm and the underlying mesenchyme pattern the developing digestive tract into regions with specific morphology and functions. The molecular mechanisms behind these interactions are largely unknown. Expression of the conserved homeobox gene Barx1 is restricted to the stomach mesenchyme during gut organogenesis. Using recombinant tissue cultures, we show that Barx1 loss in the mesenchyme prevents stomach epithelial differentiation of overlying endoderm and induces intestine-specific genes instead. Additionally, Barx1 null mouse embryos show visceral homeosis, with intestinal gene expression within a highly disorganized gastric epithelium. Barx1 directs mesenchymal cell expression of two secreted Wnt antagonists, sFRP1 and sFRP2, and these factors are sufficient replacements for Barx1 function. Canonical Wnt signaling is prominent in the prospective gastric endoderm prior to epithelial differentiation, and its inhibition by Barx1-dependent signaling permits development of stomach-specific epithelium. These results define a transcriptional and signaling pathway of inductive cell interactions in vertebrate organogenesis.

Barx1 and evolutionary changes in feeding.

During mouse embryonic development, the Barx1 homeobox gene is expressed in the mesenchymal cells of molar teeth and stomach. During early stages of molar development, Barx1 has an instructive role, directing the as yet undetermined ectomesenchymal cells in the proximal region of the jaws to follow a multicuspid tooth developmental pathway. We review here recent results showing an absence of stomach tissue in Barx1 mutant mice. The data strongly suggest that in the presumptive stomach mesenchyme Barx1 acts to attenuate Wnt signalling allowing digestive tract endoderm to differentiate into a highly specialized stomach epithelium. In the light of these new data, we discuss the possibility that evolutionary changes in the Barx1 gene could have simultaneously altered the dentition and the digestive system, therefore positioning Barx1 as a key gene in the evolution of mammals.