First Experimental Demonstration of Full-Duplex Optical Communications on a Single Laser Beam

We present the results of the first experimental demonstration a novel communications architecture that will be deployed on a Space Shuttle mission in 2003. This architecture can provide a very lightweight, low power consumption, low data rate communications link between the earth and LEO satellites. A unique characteristic of this system is that it provides full-duplex communications on a single beam is presented. The results of first experiments demonstrating this full duplex communications architecture are presented

Lightweight Optical Wavelength Communications without a Laser in Space

We will present a model for an earth-to-low-earthorbit optical communications system. The system modeled herein is designed to offer a very lightweight, low power consumption, low data rate communications link from LEO satellites. A novel architecture for a free-space optical communications link is presented and analyzed. For the first time, a method that offers full-duplex communications on a single beam is presented. In addition, a novel data format for free-space optical communications is presented. In this system, both the laser and the downlink receiver are located on the ground. The optical elements located on the spacecraft are a simple uplink receiver and a retromodulator. In fact, the laser transmitter for the system is a semiconductor device. We will present a simple feasibility model for the LOWCAL experiment that provides an estimate of the performance capability and identifies major system tradeoffs. Assuming a laser transmitter power of - 7-dB and a communications data rate of 10-kbps, we expect link margins of 17 dB for the downlink. For the uplink, an SC-FSK format is proposed that is invisible to the downlink and provides a link margin of 20 dB

The genetic architecture of the human cerebral cortex

INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function