Laser Tracker Calibration - Testing the Angle Measurement System -

Physics experiments at the SLAC National Accelerator Laboratory (SLAC) usually require high accuracy positioning, e. g. 100 {micro}m over a distance of 150 m or 25 {micro}m in a 10 x 10 x 3 meter volume. Laser tracker measurement systems have become one of the most important tools for achieving these accuracies when mapping components. The accuracy of these measurements is related to the manufacturing tolerances of various individual components, the resolutions of measurement systems, the overall precision of the assembly, and how well imperfections can be modeled. As with theodolites and total stations, one can remove the effects of most assembly and calibration errors by measuring targets in both direct and reverse positions and computing the mean to obtain the result. However, this approach does not compensate for errors originating from the encoder system. In order to improve and gain a better understanding of laser tracker angle measurement tolerances we extended our laboratory's capabilities with the addition of a horizontal angle calibration test stand. This setup is based on the use of a high precision rotary table providing an angular accuracy of better than 0.2 arcsec. Presently, our setup permits only tests of the horizontal angle measurement system. A test stand for vertical angle calibration is under construction. Distance measurements (LECOCQ & FUSS, 2000) are compared to an interferometer bench for distances of up to 32 m. Together both tests provide a better understanding of the instrument and how it should be operated. The observations also provide a reasonable estimate of covariance information of the measurements according to their actual performance for network adjustments

The SLAC Vertical Comparator for the Calibration of Digital Levels

Digital levels replaced spirit levels in most fields of precise height measurements because of the automation of the height readings. Three manufacturers offer digital levels with a single reading resolution of 10 {micro}m, and for all of them systematic effects are known. In Europe several facilities for system calibration of digital levels using vertical comparators were established within the last decade. However, there still was no system calibration facility in North America. In order to guarantee the accuracy required for the alignment of experiments at the Stanford Linear Accelerator Center (SLAC) a calibration facility for the system calibration of digital levels was built. In this paper the setup of the SLAC vertical comparator is described in detail and its standard uncertainty is derived. In order to perform traditional rod calibration of conventional line-scaled rods, a CCD camera was integrated into the SLAC comparator. The CCD camera setup is also briefly described. To demonstrate the capabilities of the comparator, results of system and rod calibration are shown

Stellar Iron Abundances at the Galactic Center

We present measurements of [Fe/H] for six M supergiant stars and three giant stars within 0.5 pc of the Galactic Center (GC) and one M supergiant star within 30 pc of the GC. The results are based on high-resolution (lambda / Delta lambda =40,000) K-band spectra, taken with CSHELL at the NASA Infrared Telescope Facility.We determine the iron abundance by detailed abundance analysis,performed with the spectral synthesis program MOOG.The mean [Fe/H] of the GC stars is determined to be near solar,[Fe/H] = +0.12 $\pm$ 0.22. Our analysis is a differential analysis, as we have observed and applied the same analysis technique to eleven cool, luminous stars in the solar neighborhood with similar temperatures and luminosities as the GC stars. The mean [Fe/H] of the solar neighborhood comparison stars, [Fe/H] = +0.03 $\pm$ 0.16, is similar to that of the GC stars. The width of the GC [Fe/H] distribution is found to be narrower than the width of the [Fe/H] distribution of Baade's Window in the bulge but consistent with the width of the [Fe/H] distribution of giant and supergiant stars in the solar neighborhood.Comment: 41 pages, 9 figures, ApJ, in pres

Predicting functional gains in a stroke trial.

A number of therapies in development for patients with central nervous system injury aim to reduce disability by improving function of surviving brain elements rather than by salvaging tissue. The current study tested the hypothesis that, after adjusting for a number of clinical assessments, a measure of brain function at baseline would improve prediction of behavioral gains after treatment.Twenty-four patients with chronic stroke underwent baseline clinical and functional MRI assessments, received 6 weeks of rehabilitation therapy with or without investigational motor cortex stimulation, and then had repeat assessments. Thirteen baseline clinical/radiological measures were evaluated for ability to predict subsequent trial-related gains.Across all patients, bivariate analyses found that greater trial-related functional gains were predicted by (1) smaller infarct volume, (2) greater baseline clinical status, and (3) lower degree of activation in stroke-affected motor cortex on baseline functional MRI. When these 3 variables were further assessed using multivariate linear regression modeling, only lower motor cortex activation and greater clinical status at baseline remained significant predictors. Note that lower baseline motor cortex activation was also associated with larger increases in motor cortex activation after treatment.Lower motor cortex activity at baseline predicted greater behavioral gains after therapy, even after controlling for a number of clinical assessments. The boosts in cortical activity that paralleled behavioral gains suggest that in some patients, low baseline cortical activity represents underuse of surviving cortical resources. A measure of brain function might be important for optimal clinical decision-making in the context of a restorative intervention

The Nlrp3 inflammasome regulates acute graft-versus-host disease

The success of allogeneic hematopoietic cell transplantation is limited by acute graft-versus-host disease (GvHD), a severe complication accompanied by high mortality rates. Yet, the molecular mechanisms initiating this disease remain poorly defined. In this study, we show that, after conditioning therapy, intestinal commensal bacteria and the damage-associated molecular pattern uric acid contribute to Nlrp3 inflammasome-mediated IL-1β production and that gastrointestinal decontamination and uric acid depletion reduced GvHD severity. Early blockade of IL-1β or genetic deficiency of the IL-1 receptor in dendritic cells (DCs) and T cells improved survival. The Nlrp3 inflammasome components Nlrp3 and Asc, which are required for pro-IL-1β cleavage, were critical for the full manifestation of GvHD. In transplanted mice, IL-1β originated from multiple intestinal cell compartments and exerted its effects on DCs and T cells, the latter being preferentially skewed toward Th17. Compatible with these mouse data, increased levels of active caspase-1 and IL-1β were found in circulating leukocytes and intestinal GvHD lesions of patients. Thus, the identification of a crucial role for the Nlrp3 inflammasome sheds new light on the pathogenesis of GvHD and opens a potential new avenue for the targeted therapy of this severe complication

Protein kinase c-β-dependent activation of NF-κB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia B cells in vivo

Tumor cell survival critically depends on heterotypic communication with benign cells in the microenvironrnent. Here, we describe a survival signaling pathway activated in stromal cells by contact to B cells from patients with chronic lymphocytic leukemia (CLL). The expression of protein kinase C (PKC)-beta II and the subsequent activation of NF-kappa B in bone marrow stromal cells are prerequisites to support the survival of malignant B cells. PKC-beta knockout mice are insusceptible to CLL transplantations, underscoring the in vivo significance of the PKC-beta II-NF-kappa B signaling pathway in the tumor microenvironment. Upregulated stromal PKG-beta II in biopsies from patients with CLL, acute lymphoblastic leukemia, and mantle cell lymphoma suggests that this pathway may commonly be activated in a variety of hematological malignancies