Measuring and Correcting Wind-Induced Pointing Errors of the Green Bank Telescope Using an Optical Quadrant Detector

Wind-induced pointing errors are a serious concern for large-aperture high-frequency radio telescopes. In this paper, we describe the implementation of an optical quadrant detector instrument that can detect and provide a correction signal for wind-induced pointing errors on the 100m diameter Green Bank Telescope (GBT). The instrument was calibrated using a combination of astronomical measurements and metrology. We find that the main wind-induced pointing errors on time scales of minutes are caused by the feedarm being blown along the direction of the wind vector. We also find that wind-induced structural excitation is virtually non-existent. We have implemented offline software to apply pointing corrections to the data from imaging instruments such as the MUSTANG 3.3 mm bolometer array, which can recover ~70% of sensitivity lost due to wind-induced pointing errors. We have also performed preliminary tests that show great promise for correcting these pointing errors in real-time using the telescope's subreflector servo system in combination with the quadrant detector signal.Comment: 17 pages, 11 figures; accepted for publication in PAS

Mast cell activation by group A streptococcal polysaccharide in the rat and its role in experimental arthritis.

Acute edematous responses were induced in Sprague-Dawley rats by the intravenous injection of group-specific polysaccharide (PS) isolated from group A streptococci. Thirty minutes after the intravenous injection of PS there was marked degranulation of subcutaneous and periarticular mast cells in all 4 feet, carbon particle labeling of adjacent venules, and an 8-fold increase in Evans blue dye content of the extremities. This acute reaction to PS was completely blocked by pretreatment with compound 48/80, but the polyarticular relapsing arthritis following the systemic injection of an arthropathic dose of streptococcal cell wall fragments containing large, covalently bound peptidoglycan-polysaccharide (PG-PS) was not blocked

Holographic Measurement and Improvement of the Green Bank Telescope Surface

We describe the successful design, implementation, and operation of a 12 GHz holography system installed on the Robert C. Byrd Green Bank Telescope (GBT). We have used a geostationary satellite beacon to construct high-resolution holographic images of the telescope mirror surface irregularities. These images have allowed us to infer and apply improved position offsets for the 2209 actuators which control the active surface of the primary mirror, thereby achieving a dramatic reduction in the total surface error (from 390 microns to ~240 microns, rms). We have also performed manual adjustments of the corner offsets for a few panels. The expected improvement in the radiometric aperture efficiency has been rigorously modeled and confirmed at 43 GHz and 90 GHz. The improvement in the telescope beam pattern has also been measured at 11.7 GHz with greater than 60 dB of dynamic range. Symmetric features in the beam pattern have emerged which are consistent with a repetitive pattern in the aperture due to systematic panel distortions. By computing average images for each tier of panels from the holography images, we confirm that the magnitude and direction of the panel distortions, in response to the combination of gravity and thermal gradients, are in general agreement with finite-element model predictions. The holography system is now fully integrated into the GBT control system, and by enabling the telescope staff to monitor the health of the individual actuators, it continues to be an essential tool to support high-frequency observations.Comment: Accepted for publication in PASP. Contains 28 pages with 2 tables and 9 figures (several at reduced quality). The full resolution version is available at http://wwwlocal.gb.nrao.edu/ptcs/papers/Hunter2011/gbtholo.ps.gz (34MB gzip file unpacks to 134MB postscript

Docosahexaenoic Acid-Derived Neuroprotectin D1 Induces Neuronal Survival via Secretase- and PPARγ-Mediated Mechanisms in Alzheimer's Disease Models

Neuroprotectin D1 (NPD1) is a stereoselective mediator derived from the omega-3 essential fatty acid docosahexaenoic acid (DHA) with potent inflammatory resolving and neuroprotective bioactivity. NPD1 reduces Aβ42 peptide release from aging human brain cells and is severely depleted in Alzheimer's disease (AD) brain. Here we further characterize the mechanism of NPD1's neurogenic actions using 3xTg-AD mouse models and human neuronal-glial (HNG) cells in primary culture, either challenged with Aβ42 oligomeric peptide, or transfected with beta amyloid precursor protein (βAPP)sw (Swedish double mutation APP695sw, K595N-M596L). We also show that NPD1 downregulates Aβ42-triggered expression of the pro-inflammatory enzyme cyclooxygenase-2 (COX-2) and of B-94 (a TNF-α-inducible pro-inflammatory element) and apoptosis in HNG cells. Moreover, NPD1 suppresses Aβ42 peptide shedding by down-regulating β-secretase-1 (BACE1) while activating the α-secretase ADAM10 and up-regulating sAPPα, thus shifting the cleavage of βAPP holoenzyme from an amyloidogenic into the non-amyloidogenic pathway. Use of the thiazolidinedione peroxisome proliferator-activated receptor gamma (PPARγ) agonist rosiglitazone, the irreversible PPARγ antagonist GW9662, and overexpressing PPARγ suggests that the NPD1-mediated down-regulation of BACE1 and Aβ42 peptide release is PPARγ-dependent. In conclusion, NPD1 bioactivity potently down regulates inflammatory signaling, amyloidogenic APP cleavage and apoptosis, underscoring the potential of this lipid mediator to rescue human brain cells in early stages of neurodegenerations

Compartmentalization of total and virus-specific tissue-resident memory CD8+ T Cells in human lymphoid organs

Disruption of T cell memory during severe immune suppression results in reactivation of chronic viral infections, such as Epstein Barr virus (EBV) and Cytomegalovirus (CMV). How different subsets of memory T cells contribute to the protective immunity against these viruses remains poorly defined. In this study we examined the compartmentalization of virus-specific, tissue resident memory CD8+ T cells in human lymphoid organs. This revealed two distinct populations of memory CD8+ T cells, that were CD69+CD103+ and CD69+CD103-, and were retained within the spleen and tonsils in the absence of recent T cell stimulation. These two types of memory cells were distinct not only in their phenotype and transcriptional profile, but also in their anatomical localization within tonsils and spleen. The EBV-specific, but not CMV-specific, CD8+ memory T cells preferentially accumulated in the tonsils and acquired a phenotype that ensured their retention at the epithelial sites where EBV replicates. In vitro studies revealed that the cytokine IL-15 can potentiate the retention of circulating effector memory CD8+ T cells by down-regulating the expression of sphingosine-1-phosphate receptor, required for T cell exit from tissues, and its transcriptional activator, Kruppel-like factor 2 (KLF2). Within the tonsils the expression of IL-15 was detected in regions where CD8+ T cells localized, further supporting a role for this cytokine in T cell retention. Together this study provides evidence for the compartmentalization of distinct types of resident memory T cells that could contribute to the long-term protection against persisting viral infections