NASA's Chemical Transfer Propulsion Program for Pathfinder

Pathfinder is a research and technology project, with specific deliverables, initiated by the National Aeronautics and Space Administration (NASA) which will strengthen the technology base of the United States civil space program in preparation for future space exploration missions. Pathfinder begins in Fiscal Year 1989, and is to advance a collection of critical technologies for these missions and ensure technology readiness for future national decisions regarding exploration of the solar system. The four major thrusts of Pathfinder are: surface exploration, in-space operations, humans-in-space, and space transfer. The space transfer thrust will provide the critical technologies needed for transportation to, and return from, the Moon, Mars, and other planets in the solar system, as well as for reliable and cost-effective Earth-orbit operations. A key element of this thrust is the Chemical Transfer Propulsion program which will provide the propulsion technology for high performance, liquid oxygen/liquid hydrogen expander cycle engines which may be operated and maintained in space. Described here are the program overview including the goals and objectives, management, technical plan, and technology transfer for the Chemical Transfer Propulsion element of Pathfinder

The Pathfinder Chemical Transfer Propulsion Program

Pathfinder is a research and technology initiative by the National Aeronautics and Space Administration (NASA) intended to strengthen the technology base of the United States civil space program in preparation for future space exploration missions. Pathfinder begins in FY-89. One of the four major thrusts is the Chemical Transfer Propulsion program which will provide the propulsion technology for high performance, liquid oxygen/liquid hydrogen expander cycle engines which are expected to be operated and maintained in space. These advanced engines will enhance or enable a variety of future space exploration missions. The goals and objectives, management, technical plan, and technology transfer for the Chemical Transfer Propulsion element of Pathfinder are described

The Pathfinder Chemical Transfer Propulsion program

Pathfinder is a research and technology initiative by the National Aeronautics and Space Administration (NASA) intended to strengthen the technology base of the United States civil space program in preparation for future space exploration missions. Pathfinder begins in FY-89. One of the four major thrusts of Pathfinder is Space Transfer technology. A key element of this thrust is the Chemical Transfer Propulsion program which will provide the propulsion technology for high performance, liquid oxygen/liquid hydrogen expander cycle engines which are expected to be operated and maintained in space. These advanced engines will enhance or enable a variety of future space exploration missions. This paper describes the goals and objectives, management, technical plan, and technology transfer for the Chemical Transfer Propulsion element of Pathfinder

Place-exchange mechanism of Pt (111) oxidation/reduction as observed by synchrotron X-ray scattering

Structural changes in the Pt(111) single crystal surface associated with incipient electrochemical oxidation/reduction were studied by {ital in}{ital situ} synchrotron x-ray reflectivity. It was shown that lifting of Pt atoms of the surface layer occurs, substantiating the long-standing hypothesis of a place-exchange mechanism for solution/metal interface oxidation. It was also shown that, for a charge transfer of {approx_lt}1.7 e{sup -}/Pt atom, the initially flat surface structure could be recovered by electrochemical reduction. In constrast, the surface was irreversibly roughened for amounts of charge transfer exceeding {approx}1.7 e{sup -}/Pt, but the roughening involved only the atoms in the top layer of the original flat surface. A detailed mechanism is proposed for the place-exchange mechanism and the subsequent roughening of the electrode surface

P16-49. Broad types of cytokines secreted by Gag-specific T cells from HIV infected patients on HAART

International audiencen.

Unique Structural Modifications Are Present in the Lipopolysaccharide from Colistin-Resistant Strains of \u3ci\u3eAcinetobacter baumannii\u3c/i\u3e

Acinetobacter baumannii is a nosocomial opportunistic pathogen that can cause severe infections, including hospital-acquired pneumonia, wound infections, and sepsis. Multidrug-resistant (MDR) strains are prevalent, further complicating patient treatment. Due to the increase in MDR strains, the cationic antimicrobial peptide colistin has been used to treat A. baumannii infections. Colistin-resistant strains of A. baumannii with alterations to the lipid A component of lipopolysaccharide (LPS) have been reported; specifically, the lipid A structure was shown to be hepta-acylated with a phosphoethanolamine (pEtN) modification present on one of the terminal phosphate residues. Using a tandem mass spectrometry platform, we provide definitive evidence that the lipid A isolated from colistin-resistant A. baumannii MAC204 LPS contains a novel structure corresponding to a diphosphoryl hepta-acylated lipid A structure with both pEtN and galactosamine (GalN) modifications. To correlate our structural studies with clinically relevant samples, we characterized colistin-susceptible and -resistant isolates obtained from patients. These results demonstrated that the clinical colistin-resistant isolate had the same pEtN and GalN modifications as those seen in the laboratory-adapted A. baumannii strain MAC204. In summary, this work has shown complete structure characterization including the accurate assignment of acylation, phosphorylation, and glycosylation of lipid A from A. baumannii, which are important for resistance to colistin

Targeting HIV-1 Env gp140 to LOX-1 Elicits Immune Responses in Rhesus Macaques.

Improved antigenicity against HIV-1 envelope (Env) protein is needed to elicit vaccine-induced protective immunity in humans. Here we describe the first tests in non-human primates (NHPs) of Env gp140 protein fused to a humanized anti-LOX-1 recombinant antibody for delivering Env directly to LOX-1-bearing antigen presenting cells, especially dendritic cells (DC). LOX-1, or 1ectin-like oxidized low-density lipoprotein (LDL) receptor-1, is expressed on various antigen presenting cells and endothelial cells, and is involved in promoting humoral immune responses. The anti-LOX-1 Env gp140 fusion protein was tested for priming immune responses and boosting responses in animals primed with replication competent NYVAC-KC Env gp140 vaccinia virus. Anti-LOX-1 Env gp140 vaccination elicited robust cellular and humoral responses when used for either priming or boosting immunity. Co-administration with Poly ICLC, a TLR3 agonist, was superior to GLA, a TLR4 agonist. Both CD4+ and CD8+ Env-specific T cell responses were elicited by anti-LOX-1 Env gp140, but in particular the CD4+ T cells were multifunctional and directed to multiple epitopes. Serum IgG and IgA antibody responses induced by anti-LOX-1 Env gp140 against various gp140 domains were cross-reactive across HIV-1 clades; however, the sera neutralized only HIV-1 bearing sequences most similar to the clade C 96ZM651 Env gp140 carried by the anti-LOX-1 vehicle. These data, as well as the safety of this protein vaccine, justify further exploration of this DC-targeting vaccine approach for protective immunity against HIV-1

Signaling via interleukin-4, receptor alpha chain is required for successful vaccination against schistosomiasis in BALB/c mice

Radiation-attenuated (RA) schistosome larvae are potent stimulators of innate immune responses at the skin site of exposure (pinna) that are likely to be important factors in the development of Th1-mediated protective immunity. In addition to causing an influx of neutrophils, macrophages, and dendritic cells (DCs) into the dermis, RA larvae induced a cascade of chemokine and cytokine secretion following in vitro culture of pinna biopsy samples. While macrophage inflammatory protein 1 and interleukin-1 (IL-1) were produced transiently within the first few days, the Th1-promoting cytokines IL-12 and IL-18 were secreted at high levels until at least day 14. Assay of C3H/HeJ mice confirmed that IL-12 secretion was not due to lipopolysaccharide contaminants binding Toll-like receptor 4. Significantly, IL-12 p40 secretion was sustained in pinnae from vaccinated mice but not in those from nonprotected infected mice. In contrast, IL-10 was produced from both vaccinated and infected mice. This cytokine regulates IL-12-associated dermal inflammation, since in vaccinated IL-10/ mice, pinna thickness was greatly increased concurrent with elevated levels of IL-12 p40. A significant number of IL-12 p40 cells were detected as emigrants from in vitro-cultured pinnae, and most were within a population of rare large granular cells that were Ia, consistent with their being antigen-presenting cells. Labeling of IL-12 cells for CD11c, CD205, CD8, CD11b, and F4/80 indicated that the majority were myeloid DCs, although a proportion were CD11c F4/80, suggesting that macrophages were an additional source of IL-12 in the skin