156 research outputs found

    Elementary excitation families and their frequency ordering in cylindrically symmetric Bose-Einstein condensates

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    We present a systematic classification of the elementary excitations of Bose-Einstein condensates in cylindrical traps in terms of their shapes. The classification generalizes the concept of families of excitations first identified by Hutchinson and Zaremba (1998) Phys. Rev. A 57 1280 by introducing a second classification number that allows all possible modes to be assigned to a family. We relate the energy ordering of the modes to their family classification, and provide a simple model which explains the relationship.Comment: 15 pages, 8 figures; abstract complemented, section 4.2 shortened, references corrected; to be published in J. Phys.

    Characterization of the NEXT Hollow Cathode Inserts After Long-Duration Testing

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    Hollow dispenser cathode inserts are a critical element of electric propulsion systems, and should therefore be well understood during long term operation to ensure reliable system performance. This work destructively investigated cathode inserts from the NEXT long-duration test which demonstrated 51,184 hours of high-voltage operation, 918 kg of propellant throughput, and 35.5 MN-s of total impulse. The characterization methods used include scanning electron microscopy with energy dispersive spectroscopy and X-ray diffraction. Microscopy analysis has been performed on fractured surfaces, emission surfaces, and metallographically polished cross-sections of post-test inserts and unused inserts. Impregnate distribution, etch region thickness, impregnate chemical content, emission surface topography, and emission surface phase identification are the primary factors investigated

    Diversity of tfdC genes: distribution and polymorphism among 2,4-dichlorophenoxyacetic acid degrading soil bacteria

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    The aim of the present work was to study the occurrence, distribution and diversity of 1,2-dichlorocatechol dioxygenase genes among 2,4-dichlorophenoxyacetic acid degrading bacteria. Phylogenetic relationships between the 31 strains or isolates were evaluated by amplified ribosomal DNA restriction analysis of the 16S rDNA gene. All the strains could be assigned to the beta or gamma subdivisions of the Proteobacteria. tfdC genes were detected by PCR amplification using degenerated primers. Two specific probes were produced from Ralstonia eutropha strain JMP134 and from a soil isolate strain PLAE6 which was grouped with Variovorax paradoxus. Sequence analysis of the probes revealed that they were homologous to the tfdC genes of JMP134 located on plasmid pJP4 and to the tfdC gene of Pseudomonas putida strain PaW85 located on plasmid pEST4011, The localization and the copy number of tfdC genes were determined by hybridization of plasmid profiles and genomic DNA restriction fragment length polymorphism profiles with the two probes. Most of the strains were found to bear tfdC genes on plasmids ranging from 78 to 532 kb; two strains without any plasmids were also found to hybridize with the probes, revealing a chromosomal localization of catabolic genes. Sequence analysis of the PCR products from different strains confirmed that four different classes of chlorocatechol 1,2-dioxygenase genes were present in the strains and isolates studied

    A computational study of grid erosion through ion impact

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/77047/1/AIAA-2000-3664-398.pd

    Minocycline Inhibition of Monocyte Activation Correlates with Neuronal Protection in SIV NeuroAIDS

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    Background: Minocycline is a tetracycline antibiotic that has been proposed as a potential conjunctive therapy for HIV-1 associated cognitive disorders. Precise mechanism(s) of minocycline’s functions are not well defined. Methods: Fourteen rhesus macaques were SIV infected and neuronal metabolites measured by proton magnetic resonance spectroscopy (1H MRS). Seven received minocycline (4 mg/kg) daily starting at day 28 post-infection (pi). Monocyte expansion and activation were assessed by flow cytometry, cell traffic to lymph nodes, CD16 regulation, viral replication, and cytokine production were studied. Results: Minocycline treatment decreased plasma virus and pro-inflammatory CD14+CD16+ and CD14loCD16+ monocytes, and reduced their expression of CD11b, CD163, CD64, CCR2 and HLA-DR. There was reduced recruitment of monocyte/ macrophages and productively infected cells in axillary lymph nodes. There was an inverse correlation between brain NAA/ Cr (neuronal injury) and circulating CD14+CD16+ and CD14loCD16+ monocytes. Minocycline treatment in vitro reduced SIV replication CD16 expression on activated CD14+CD16+ monocytes, and IL-6 production by monocytes following LPS stimulation. Conclusion: Neuroprotective effects of minocycline are due in part to reduction of activated monocytes, monocyte traffic. Mechanisms for these effects include CD16 regulation, reduced viral replication, and inhibited immune activation. Citation: Campbell JH, Burdo TH, Autissier P, Bombardier JP, Westmoreland SV, et al. (2011) Minocycline Inhibition of Monocyte Activation Correlate

    Increased Monocyte Turnover from Bone Marrow Correlates with Severity of SIV Encephalitis and CD163 Levels in Plasma

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    Cells of the myeloid lineage are significant targets for human immunodeficiency virus (HIV) in humans and simian immunodeficiency virus (SIV) in monkeys. Monocytes play critical roles in innate and adaptive immunity during inflammation. We hypothesize that specific subsets of monocytes expand with AIDS and drive central nervous system (CNS) disease. Additionally, there may be expansion of cells from the bone marrow through blood with subsequent macrophage accumulation in tissues driving pathogenesis. To identify monocytes that recently emigrated from bone marrow, we used 5-bromo-2β€²-deoxyuridine (BrdU) labeling in a longitudinal study of SIV-infected CD8+ T lymphocyte depleted macaques. Monocyte expansion and kinetics in blood was assessed and newly migrated monocyte/macrophages were identified within the CNS. Five animals developed rapid AIDS with differing severity of SIVE. The percentages of BrdU+ monocytes in these animals increased dramatically, early after infection, peaking at necropsy where the percentage of BrdU+ monocytes correlated with the severity of SIVE. Early analysis revealed changes in the percentages of BrdU+ monocytes between slow and rapid progressors as early as 8 days and consistently by 27 days post infection. Soluble CD163 (sCD163) in plasma correlated with the percentage of BrdU+ monocytes in blood, demonstrating a relationship between monocyte activation and expansion with disease. BrdU+ monocytes/macrophages were found within perivascular spaces and SIVE lesions. The majority (80–90%) of the BrdU+ cells were Mac387+ that were not productively infected. There was a minor population of CD68+BrdU+ cells (<10%), very few of which were infected (<1% of total BrdU+ cells). Our results suggest that an increased rate of monocyte recruitment from bone marrow into the blood correlates with rapid progression to AIDS, and the magnitude of BrdU+ monocytes correlates with the severity of SIVE

    Overview of the Development of the Solar Electric Propulsion Technology Demonstration Mission 12.5-kW Hall Thruster

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    NASA is developing mission concepts for a solar electric propulsion technology demonstration mission. A number of mission concepts are being evaluated including ambitious missions to near Earth objects. The demonstration of a high-power solar electric propulsion capability is one of the objectives of the candidate missions under consideration. In support of NASA's exploration goals, a number of projects are developing extensible technologies to support NASA's near and long term mission needs. Specifically, the Space Technology Mission Directorate Solar Electric Propulsion Technology Demonstration Mission project is funding the development of a 12.5-kilowatt magnetically shielded Hall thruster system to support future NASA missions. This paper presents the design attributes of the thruster that was collaboratively developed by the NASA Glenn Research Center and the Jet Propulsion Laboratory. The paper provides an overview of the magnetic, plasma, thermal, and structural modeling activities that were carried out in support of the thruster design. The paper also summarizes the results of the functional tests that have been carried out to date. The planned thruster performance, plasma diagnostics (internal and in the plume), thermal, wear, and mechanical tests are outlined

    Ku Regulates the Non-Homologous End Joining Pathway Choice of DNA Double-Strand Break Repair in Human Somatic Cells

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    The repair of DNA double-strand breaks (DSBs) is critical for the maintenance of genomic integrity and viability for all organisms. Mammals have evolved at least two genetically discrete ways to mediate DNA DSB repair: homologous recombination (HR) and non-homologous end joining (NHEJ). In mammalian cells, most DSBs are preferentially repaired by NHEJ. Recent work has demonstrated that NHEJ consists of at least two sub-pathwaysβ€”the main Ku heterodimer-dependent or β€œclassic” NHEJ (C-NHEJ) pathway and an β€œalternative” NHEJ (A-NHEJ) pathway, which usually generates microhomology-mediated signatures at repair junctions. In our study, recombinant adeno-associated virus knockout vectors were utilized to construct a series of isogenic human somatic cell lines deficient in the core C-NHEJ factors (Ku, DNA-PKcs, XLF, and LIGIV), and the resulting cell lines were characterized for their ability to carry out DNA DSB repair. The absence of DNA-PKcs, XLF, or LIGIV resulted in cell lines that were profoundly impaired in DNA DSB repair activity. Unexpectedly, Ku86-null cells showed wild-type levels of DNA DSB repair activity that was dominated by microhomology joining events indicative of A-NHEJ. Importantly, A-NHEJ DNA DSB repair activity could also be efficiently de-repressed in LIGIV-null and DNA-PKcs-null cells by subsequently reducing the level of Ku70. These studies demonstrate that in human cells C-NHEJ is the major DNA DSB repair pathway and they show that Ku is the critical C-NHEJ factor that regulates DNA NHEJ DSB pathway choice
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