DMA precise time and time interval requirements

Defense Mapping Agency timing requirements ranging from milliseconds to tenths of nanoseconds and its use of geodetic astronomy and satellite geodesy programs are discussed in detail

The Generation of Monoclonal Antibodies that Bind Preferentially to Adrenal Chromaffin Cells and the Cells of Embryonic Sympathetic Ganglia

Adrenal chromaffin cells, sympathetic neurons, and small intensely fluorescent (SIF) cells are each derived from the neural crest, produce catecholamines, and share certain morphological features. These cell types are also partially interconvertible in cell culture (Doupe et al., 1985a,b; Anderson and Axel, 1986). Thus, these cells are said to be members of the sympathoadrenal (SA) lineage and could share a common progenitor. To investigate the origins of this lineage further, we used the cyclophosphamide immuno-suppression method (Matthew and Patterson, 1983) to generate five monoclonal antibodies (SA1-5) that bind strongly to chromaffin cells, with little or no labeling of sympathetic neurons or SIF cells in frozen sections from adult rats. Competition experiments indicate that these antibodies bind to at least three distinct epitopes in tissue sections. The SA antibodies also label most of the cells of embryonic sympathetic ganglia and adrenal primordia. Labeling of sympathetic ganglia appears as the cells initially coalesce and express high levels of tyrosine hydroxylase (TH). Not all TH+ cells in the embryo are SA 1-5+, however; carotid body SIF cells, nodose ganglion TH+ cells, and the transiently TH+ cells in the dorsal root ganglia do not display detectable SA 1-5 labeling. Thus, the expression of these markers for the SA 1-5 lineage is selective. SA antigen expression is hormonally controlled; removal of glucocorticoid and addition of NGF to cultured adrenal chromaffin cells result in the loss of SA 1-5 labeling. These results suggest that the presumed precursors for sympathetic neurons and SIF cells initially express chromaffin cell markers

Isolation of the Progenitor Cells of the Sympathoadrenal Lineage from Embryonic Sympathetic Ganglia with the SA Monoclonal Antibodies

Our previous articles in this series described the production of five monoclonal antibodies (SA1-5) that bind to adrenal chromaffin cells and to cells in embryonic sympathetic ganglia and adrenal primordia (Carnahan and Patterson, 1991), and the downregulation of the sympathoadrenal (SA) antigens in vivo as neuronal markers begin to be expressed (Anderson et al., 1991). These results support the hypothesis that sympathetic neurons and adrenal chromaffin cells are derived from a common embryonic progenitor that displays both neuron- and chromaffin cell-specific markers. We have taken advantage of the fact that at least some of the SA antigens are expressed on the cell surface to isolate SA+ cells from embryonic day 14.5 rat superior cervical, sympathetic ganglia by fluorescence-activated cell sorting. This population of cells is significantly enriched in the expression of markers (tyrosine hydroxylase and neurofilament) found in the putative progenitors in situ. Growth in glucocorticoid maintains the expression of the SA antigens in the sorted cells and induces the chromaffin cell marker enzyme phenylethanolamine N-methyl transferase. In contrast, growth of the sorted cells in basic fibroblast growth factor, NGF, and insulin results in the rapid loss of SA 1 expression and the outgrowth of neurites. The ability to manipulate the fate of the SA+ cells in vitro confirms the suggestion from the in vivo observations that the SA+ cells in the ganglia are at least bipotential progenitors, capable of differentiating along the chromaffin or neuronal pathways

Transient terahertz spectroscopy of excitons and unbound carriers in quasi two-dimensional electron-hole gases

We report a comprehensive experimental study and detailed model analysis of the terahertz dielectric response and density kinetics of excitons and unbound electron-hole pairs in GaAs quantum wells. A compact expression is given, in absolute units, for the complex-valued terahertz dielectric function of intra-excitonic transitions between the 1s and higher-energy exciton and continuum levels. It closely describes the terahertz spectra of resonantly generated excitons. Exciton ionization and formation are further explored, where the terahertz response exhibits both intra-excitonic and Drude features. Utilizing a two-component dielectric function, we derive the underlying exciton and unbound pair densities. In the ionized state, excellent agreement is found with the Saha thermodynamic equilibrium, which provides experimental verification of the two-component analysis and density scaling. During exciton formation, in turn, the pair kinetics is quantitatively described by a Saha equilibrium that follows the carrier cooling dynamics. The terahertz-derived kinetics is, moreover, consistent with time-resolved luminescence measured for comparison. Our study establishes a basis for tracking pair densities via transient terahertz spectroscopy of photoexcited quasi-two-dimensional electron-hole gases.Comment: 14 pages, 8 figures, final versio

Pipeline column separation flow regimes

A generalized set of pipeline column separation equations is presented describing all conventional types of low-pressure regions. These include water hammer zones, distributed vaporous cavitation, vapor cavities, and shocks (that eliminate distributed vaporous cavitation zones). Numerical methods for solving these equations are then considered, leading to a review of three numerical models of column separation. These include the discrete vapor cavity model, the discrete gas cavity model, and the generalized interface vaporous cavitation model. The generalized interface vaporous cavitation model enables direct tracking of actual column separation phenomena (e.g., discrete cavities, vaporous cavitation zones), and consequently, better insight into the transient event. Numerical results from the three column separation models are compared with results of measurements for a number of flow regimes initiated by a rapid closure of a downstream valve in a sloping pipeline laboratory apparatus. Finally, conclusions are drawn about the accuracy of the modeling approaches. A new classification of column separation (active or passive) is proposed based on whether the maximum pressure in a pipeline following column separation results in a short-duration pressure pulse that exceeds the magnitude of the Joukowsky pressure rise for rapid valve closure.Anton Bergant and Angus R. Simpso

Antibody Markers Identify a Common Progenitor to Sympathetic Neurons and Chromaffin Cells in vivo and Reveal the Timing of Commitment to Neuronal Differentiation in the Sympathoadrenal Lineage

Using specific antibody markers and double-label immunofluorescence microscopy, we have followed the fate of progenitor cells in the sympathoadrenal (SA) sublineage of the neural crest in developing rat embryos. Such progenitors are first recognizable in the primordial sympathetic ganglia at embryonic day 11.5 (E11.5), when they express tyrosine hydroxylase. At this stage, the progenitors also coexpress neuronal markers such as SCG 10 and neurofilament, together with a series of chromaffin cell markers called SA 1–5 (Carnhan and Patterson, 1991 a). The observation of such doubly labeled cells is consistent with the hypothesis that these cells represent a common progenitor to sympathetic neurons and adrenal chromaffin cells. Subsequent to E 11.5, expression of the chromaffin markers is extinguished in the sympathetic ganglia but retained by cells within the adrenal gland. Concomitant with the loss of the SA 1-5 immunoreactivity in sympathetic ganglia, a later sympathetic neuron-specific marker, B2, appears. In dissociated cell suspensions, some B2+ cells that coexpress SA 1 are seen. This implies a switch in the antigenic phenotype of developing sympathetic neurons, rather than a replacement of one cell population by another. The SA 1--B2 transition does not occur for the majority of cells within the adrenal primordium. In vitro, most B2+ cells fail to differentiate into chromaffin cells in response to glucocorticoid. Instead, they continue to extend neurites and then die. Taken together, these data imply that the SA 1--B2 transition correlates with a loss of competence to respond to an inducer of chromaffin differentiation. Thus, the development of SA derivatives is controlled both by environmental signals and by changes in the ability of differentiating cells to respond to such signals