An approach to the parametric design of ion thrusters

A methodology that can be used to determine which of several physical constraints can limit ion thruster power and thrust, under various design and operating conditions, is presented. The methodology is exercised to demonstrate typical limitations imposed by grid system span-to-gap ratio, intragrid electric field, discharge chamber power per unit beam area, screen grid lifetime, and accelerator grid lifetime constraints. Limitations on power and thrust for a thruster defined by typical discharge chamber and grid system parameters when it is operated at maximum thrust-to-power are discussed. It is pointed out that other operational objectives such as optimization of payload fraction or mission duration can be substituted for the thrust-to-power objective and that the methodology can be used as a tool for mission analysis

Emission current control system for multiple hollow cathode devices

An emission current control system for balancing the individual emission currents from an array of hollow cathodes has current sensors for determining the current drawn by each cathode from a power supply. Each current sensor has an output signal which has a magnitude proportional to the current. The current sensor output signals are averaged, the average value so obtained being applied to a respective controller for controlling the flow of an ion source material through each cathode. Also applied to each controller are the respective sensor output signals for each cathode and a common reference signal. The flow of source material through each hollow cathode is thereby made proportional to the current drawn by that cathode, the average current drawn by all of the cathodes, and the reference signal. Thus, the emission current of each cathode is controlled such that each is made substantially equal to the emission current of each of the other cathodes. When utilized as a component of a multiple hollow cathode ion propulsion motor, the emission current control system of the invention provides for balancing the thrust of the motor about the thrust axis and also for preventing premature failure of a hollow cathode source due to operation above a maximum rated emission current

Oxygen reduction at the silver/hydroxide-exchange membrane interface

A solid-state cell is used to study the electrocatalysis of oxygen reduction at the silver/hydroxide-exchange membrane interface. The catalyst/membrane interface exhibits improved performance in comparison to a catalyst/aqueous sodium hydroxide interface. Surprisingly, the half-wave potential for oxygen reduction is shown to shift 185 mV higher at the silver/hydroxide-exchange membrane interface than for the silver/aqueous hydroxide solution interface, and the exchange current density is significantly higher at 1.02 × 10−6 A m−2. On a cost per performance basis, silver electrocatalysts in a hydroxide-exchange membrane fuel cell may provide better performance than platinum in a proton-exchange membrane fuel cell. Keywords: Oxygen reduction reaction, Electrocatalyst, Alkaline membrane, Solid-state cell, Silve

Extensive spontaneous plasticity of corticospinal projections after primate spinal cord injury.

Although axonal regeneration after CNS injury is limited, partial injury is frequently accompanied by extensive functional recovery. To investigate mechanisms underlying spontaneous recovery after incomplete spinal cord injury, we administered C7 spinal cord hemisections to adult rhesus monkeys and analyzed behavioral, electrophysiological and anatomical adaptations. We found marked spontaneous plasticity of corticospinal projections, with reconstitution of fully 60% of pre-lesion axon density arising from sprouting of spinal cord midline-crossing axons. This extensive anatomical recovery was associated with improvement in coordinated muscle recruitment, hand function and locomotion. These findings identify what may be the most extensive natural recovery of mammalian axonal projections after nervous system injury observed to date, highlighting an important role for primate models in translational disease research

Availability, outage, and capacity of spatially correlated, Australasian free-space optical networks

Network capacity and reliability for free space optical communication (FSOC) is strongly driven by ground station availability, dominated by local cloud cover causing an outage, and how availability relations between stations produce network diversity. We combine remote sensing data and novel methods to provide a generalised framework for assessing and optimising optical ground station networks. This work is guided by an example network of eight Australian and New Zealand optical communication ground stations which would span approximately $60^\circ$ in longitude and $20^\circ$ in latitude. Utilising time-dependent cloud cover data from five satellites, we present a detailed analysis determining the availability and diversity of the network, finding the Australasian region is well-suited for an optical network with a 69% average site availability and low spatial cloud cover correlations. Employing methods from computational neuroscience, we provide a Monte Carlo method for sampling the joint probability distribution of site availabilities for an arbitrarily sized and point-wise correlated network of ground stations. Furthermore, we develop a general heuristic for site selection under availability and correlation optimisations, and combine this with orbital propagation simulations to compare the data capacity between optimised networks and the example network. We show that the example network may be capable of providing tens of terabits per day to a LEO satellite, and up to 99.97% reliability to GEO satellites. We therefore use the Australasian region to demonstrate novel, generalised tools for assessing and optimising FSOC ground station networks, and additionally, the suitability of the region for hosting such a network.Comment: Accepted in Journal of Optical Communications and Networking. 16 pages, 16 figure

Exome analysis of patients with concurrent pediatric inflammatory bowel disease (PIBD) and autoimmune disease

BACKGROUND: Pediatric Inflammatory Bowel Disease (PIBD) is a chronic condition seen in genetically predisposed individuals. Genome-wide association studies have implicated >160 genomic loci in IBD with many genes coding for proteins in key immune pathways. This study looks at autoimmune disease burden in patients diagnosed with PIBD and interrogates exome data of a subset of patients. METHODS: Patients were recruited from the Southampton Genetics of PIBD cohort. Clinical diagnosis of autoimmune disease in these individuals was ascertained from medical records. For a subset of patients with PIBD and concurrent asthma, exome data was interrogated to ascertain the burden of pathogenic variants within genes implicated in asthma. Association testing was conducted between cases and population controls using the SKAT-O test. RESULTS: Forty-nine (28.3%) PIBD children (18.49% CD, 8.6% UC, and 21.15% IBDU patients) had a concurrent clinical diagnosis of at least one other autoimmune disorder; asthma was the most prevalent, affecting 16.2% of the PIBD cohort. Rare and common variant association testing revealed 6 significant genes (P < 0.05) before Bonferroni adjustment. Three of these genes were previously implicated in both asthma and IBD (ZPBP2 IL1R1, and IL18R1) and 3 in asthma only (PYHIN1, IL2RB, and GSTP1). CONCLUSIONS: One-third of our cohort had a concurrent autoimmune condition. We observed higher incidence of asthma compared with the overall pediatric prevalence. Despite a small sample size, SKAT-O evaluated a significant burden of rare and common mutations in 6 genes. Variant burden suggests that a systemic immune dysregulation rather than organ-specific could underpin immune dysfunction for a subset of patients

Machine Intelligence Identifies Soluble TNFa as a Therapeutic Target for Spinal Cord Injury

Traumatic spinal cord injury (SCI) produces a complex syndrome that is expressed across multiple endpoints ranging from molecular and cellular changes to functional behavioral deficits. Effective therapeutic strategies for CNS injury are therefore likely to manifest multi-factorial effects across a broad range of biological and functional outcome measures. Thus, multivariate analytic approaches are needed to capture the linkage between biological and neurobehavioral outcomes. Injury-induced neuroinflammation (NI) presents a particularly challenging therapeutic target, since NI is involved in both degeneration and repair. Here, we used big-data integration and large-scale analytics to examine a large dataset of preclinical efficacy tests combining five different blinded, fully counter-balanced treatment trials for different acute anti-inflammatory treatments for cervical spinal cord injury in rats. Multi-dimensional discovery, using topological data analysis (TDA) and principal components analysis (PCA) revealed that only one showed consistent multidimensional syndromic benefit: intrathecal application of recombinant soluble TNFα receptor 1 (sTNFR1), which showed an inverse-U dose response efficacy. Using the optimal acute dose, we showed that clinically-relevant 90 min delayed treatment profoundly affected multiple biological indices of NI in the first 48 h after injury, including reduction in pro-inflammatory cytokines and gene expression of a coherent complex of acute inflammatory mediators and receptors. Further, a 90 min delayed bolus dose of sTNFR1 reduced the expression of NI markers in the chronic perilesional spinal cord, and consistently improved neurological function over 6 weeks post SCI. These results provide validation of a novel strategy for precision preclinical drug discovery that is likely to improve translation in the difficult landscape of CNS trauma, and confirm the importance of TNFα signaling as a therapeutic target

GPX-Macrophage Expression Atlas: A database for expression profiles of macrophages challenged with a variety of pro-inflammatory, anti-inflammatory, benign and pathogen insults

BACKGROUND: Macrophages play an integral role in the host immune system, bridging innate and adaptive immunity. As such, they are finely attuned to extracellular and intracellular stimuli and respond by rapidly initiating multiple signalling cascades with diverse effector functions. The macrophage cell is therefore an experimentally and clinically amenable biological system for the mapping of biological pathways. The goal of the macrophage expression atlas is to systematically investigate the pathway biology and interaction network of macrophages challenged with a variety of insults, in particular via infection and activation with key inflammatory mediators. As an important first step towards this we present a single searchable database resource containing high-throughput macrophage gene expression studies. DESCRIPTION: The GPX Macrophage Expression Atlas (GPX-MEA) is an online resource for gene expression based studies of a range of macrophage cell types following treatment with pathogens and immune modulators. GPX-MEA follows the MIAME standard and includes an objective quality score with each experiment. It places special emphasis on rigorously capturing the experimental design and enables the searching of expression data from different microarray experiments. Studies may be queried on the basis of experimental parameters, sample information and quality assessment score. The ability to compare the expression values of individual genes across multiple experiments is provided. In addition, the database offers access to experimental annotation and analysis files and includes experiments and raw data previously unavailable to the research community. CONCLUSION: GPX-MEA is the first example of a quality scored gene expression database focussed on a macrophage cellular system that allows efficient identification of transcriptional patterns. The resource will provide novel insights into the phenotypic response of macrophages to a variety of benign, inflammatory, and pathogen insults. GPX-MEA is available through the GPX website at