9,629 research outputs found
Method and apparatus for neutralizing potentials induced on spacecraft surfaces
A potential induced on the surface of an orbiting spacecraft is neutralized to the potential of a plasma through which the spacecraft is traveling by directing charged particles into the plasma from the spacecraft surface. The induced potential occurs in response to bombardment of the spacecraft surface by ambient charged particles which may be negative or positive. The charged particles directed into the plasma from the surface have the same polarity as the induced potential to provide the neutralization. The invention can be utilized to maintain different, electrically isolated segments of a spacecraft surface at the same potential to prevent electric discharges between the different parts and thereby protect electric circuits within the spacecraft
Lipopolysaccharide (LPS)-binding protein is carried on lipoproteins and acts as a cofactor in the neutralization of LPS.
Lipoproteins isolated from normal human plasma can bind and neutralize bacterial lipopolysaccharide (LPS) and may represent an important mechanism in host defense against gram-negative septic shock. Recent studies have shown that experimentally elevating the levels of circulating high-density lipoproteins (HDL) provides protection against death in animal models of endotoxic shock. We sought to define the components of HDL that are required for neutralization of LPS. To accomplish this we have studied the functional neutralization of LPS by native and reconstituted HDL using a rapid assay that measures the CD14-dependent activation of leukocyte integrins on human neutrophils. We report here that reconstituted HDL particles (R-HDL), prepared from purified apolipoprotein A-I (apoA-I) combined with phospholipid and free cholesterol, are not sufficient to neutralize the biologic activity of LPS. However, addition of recombinant LPS binding protein (LBP), a protein known to transfer LPS to CD14 and enhance responses of cells to LPS, enabled prompt binding and neutralization of LPS by R-HDL. Thus, LBP appears capable of transferring LPS not only to CD14 but also to lipoprotein particles. In contrast with R-HDL, apoA-I containing lipoproteins (LpA-I) isolated from plasma by selected affinity immunosorption (SAIS) on an anti-apoA-I column, neutralized LPS without addition of exogenous LBP. Several lines of evidence demonstrated that LBP is a constituent of LpA-I in plasma. Passage of plasma over an anti-apoA-I column removed more than 99% of the LBP detectable by ELISA, whereas 31% of the LBP was recovered by elution of the column. Similarly, the ability of plasma to enable activation of neutrophils by LPS (LBP/Septin activity) was depleted and recovered by the same process. Furthermore, an immobilized anti-LBP monoclonal antibody coprecipitated apoA-I. The results described here suggest that in addition to its ability to transfer LPS to CD14, LBP may also transfer LPS to lipoproteins. Since LBP appears to be physically associated with lipoproteins in plasma, it is positioned to play an important role in the neutralization of LPS
Adsorption and Depletion of Polyelectrolytes from Charged Surfaces
Mean-field theory and scaling arguments are presented to model
polyelectrolyte adsorption from semi-dilute solutions onto charged surfaces.
Using numerical solutions of the mean-field equations, we show that adsorption
exists only for highly charged polyelectrolytes in low salt solutions. Simple
scaling laws for the width of the adsorbed layer and the amount of adsorbed
polyelectrolyte are obtained. In other situations the polyelectrolyte chains
will deplete from the surface. For fixed surface potential conditions, the salt
concentration at the adsorption--depletion crossover scales as the product of
the charged fraction of the polyelectrolyte f and the surface potential, while
for a fixed surface charge density, \sigma, it scales as \sigma^{2/3}f^{2/3},
in agreement with single-chain results.Comment: 12 pages, 8 figures, final version to be published in J. Chem. Phys.
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Electric space potential in a cesium thermionic diode
Investigating electric potential in cesium thermionic diode for minimum plasma-loss by electrostatic prob
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Sequence analysis reveals extensive polymorphism and evidence of deletions within the E2 glycoprotein gene of several strains of murine hepatitis virus.
Direct RNA sequence analysis of the E2 gene of wild-type MHV-4 and of neutralization resistant, neuroattenuated variants has identified a polymorphic region with respect to deletions. These variants had large deletions of 142 to 159 amino acids mapping to a localized region in the amino-terminal domain of the peplomer glycoprotein. The nucleotide sequence of the E2 gene for wild-type strain MHV-4 was found to be very similar to that of MHV-JHM but had an insertion of 423 nucleotides resulting in the addition of a stretch of 141 unique amino acids in the amino-terminal domain of E2. We propose that deletions reflect a major source of heterogeneity in the E2 protein of MHV
Blocking entry of hepatitis B and D viruses to hepatocytes as a novel immunotherapy for treating chronic infections
Background. Chronic hepatitis B and D virus (HBV/HDV) infections can cause cancer. Current HBV therapy using nucleoside analogues (NAs) is life-long and reduces but does not eliminate the risk of cancer. A hallmark of chronic hepatitis B is a dysfunctional HBV-specific T-cell response. We therefore designed an immunotherapy driven by naive healthy T cells specific for the HDV antigen (HDAg) to bypass the need for HBV-specific T cells in order to prime PreS1-specific T cells and PreS1 antibodies blocking HBV entry.
Methods. Ten combinations of PreS1 and/or HDAg sequences were evaluated for induction of PreS1 antibodies and HBV- and HDV-specific T cells in vitro and in vivo. Neutralization of HBV by PreS1-specific murine and rabbit antibodies was evaluated in cell culture, and rabbit anti-PreS1 were tested for neutralization of HBV in mice repopulated with human hepatocytes.
Results. The best vaccine candidate induced T cells to PreS1 and HDAg, and PreS1 antibodies blocking HBV entry in vitro. Importantly, adoptive transfer of PreS1 antibodies prevented, or modulated, HBV infection after a subsequent challenge in humanized mice.
Conclusions. We here describe a novel immunotherapy for chronic HBV/HDV that targets viral entry to complement NAs and coming therapies inhibiting viral maturation
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