Bibliothek

Notizen: Tracer dispersion has been simulated in three-dimensional models of regular and random sphere packings for a range of Peclet numbers. A random-walk particle-tracking (PT) method was used to simulate tracer movement within pore-scale flow fields computed with the lattice-Boltzmann (LB) method. The simulation results illustrate the time evolution of dispersion, and they corroborate a number of theoretical and empirical results for the scaling of asymptotic longitudinal and transverse dispersion with Peclet number. Comparisons with nuclear magnetic resonance (NMR) spectroscopy experiments show agreement on transient, as well as asymptotic, dispersion rates. These results support both NMR findings that longitudinal dispersion rates are significantly lower than reported in earlier experimental literature, as well as the fact that asymptotic rates are observed in relatively short times by techniques that employ a uniform initial distribution of tracers, like NMR. © 2000 American Institute of Physics.

Notizen: The velocity profile of O2(b 1Σg+,v=0) produced by photolysis of O3 in the Huggins band region at 351.4 nm has been measured using a delayed pulsed field extraction time-of-flight technique confirming that this fragment is formed by single-photon absorption. The velocity profile of O(3P0) produced by photolysis at 322.64 nm has also been obtained. O(3P0) fragments are shown to be produced in coincidence with O2(X 3Σg−), O2(a 1Δg), and O2(b 1Σg+). The relative contribution of each of these channels to the total O(3P0) signal is reported and it is shown that spin-forbidden channels dominate the dissociation process at this wavelength. Two quite different primary crossings of the initially excited state are suggested to account for the change in the relative contribution of these three channels when photolysis is changed from resonance with a vibronic band of ozone to an off-resonance wavelength. The determination of the anisotropy parameter, β(v), for these dissociation processes suggests that the transition dipole responsible for all of the Huggins band absorption has B2 symmetry. © 1999 American Institute of Physics.

Notizen: When the Lattice Boltzmann Method (LBM) is used for simulating continuum fluid flow, the discrete mass distribution must satisfy imposed constraints for density and momentum along the boundaries of the lattice. These constraints uniquely determine the three-dimensional (3-D) mass distribution for boundary nodes only when the number of external (inward-pointing) lattice links does not exceed four. We propose supplementary rules for computing the boundary distribution where the number of external links does exceed four, which is the case for all except simple rectangular lattices. Results obtained with 3-D body-centered-cubic lattices are presented for Poiseuille flow, porous-plate Couette flow, pipe flow, and rectangular duct flow. The accuracy of the two-dimensional (2-D) Poiseuille and Couette flows persists even when the mean free path between collisions is large, but that of the 3-D duct flow deteriorates markedly when the mean free path exceeds the lattice spacing. Accuracy in general decreases with Knudsen number and Mach number, and the product of these two quantities is a useful index for the applicability of LBM to 3-D low-Reynolds-number flow. © 1996 American Institute of Physics.

Notizen: The nickel-containing enzymes hydrogenase and urease require accessory proteins in order to incorporate properly the nickel atom(s) into the active sites. The Helicobacter pylori genome contains the full complement of both urease and hydrogenase accessory proteins. Two of these, the hydrogenase accessory proteins HypA (encoded by hypA) and HypB (encoded by hypB), are required for the full activity of both the hydrogenase and the urease enzymes in H. pylori. Under normal growth conditions, hydrogenase activity is abolished in strains in which either hypA (HypA:kan) or hypB (HypB:kan) have been interrupted by a kanamycin resistance cassette. Urease activity in these strains is 40 (HypA:kan)- and 200 (HypB:kan)-fold lower than for the wild-type (wt) strain 43504. Nickel supplementation in the growth media restored urease activity to almost wt levels. Hydrogenase activity was restored to a lesser extent, as has been observed for hyp mutants in other (H2-oxidizing) bacteria. Expression levels of UreB (the urease large subunit) were not affected by inactivation of either hypA or hypB, as determined by immunoblotting. Urease activity was not affected by lesions in the genes for either the hydrogenase accessory proteins HypD or HypF or the hydrogenase large subunit structural gene, indicating that the urease deficiency was not caused by lack of hydrogenase activity. When crude extracts of wt, HypA:kan and HypB:kan were separated by anion exchange chromatography, the urease-containing fractions of the mutant strains contained about four (HypA:kan)- and five (HypB:kan)-fold less nickel than did the urease from wt, indicating that the lack of urease activity in these strains results from a nickel deficiency in the urease enzyme.

Notizen: The HypB protein from Bradyrhizobium japonicum is a metal-binding GTPase required for hydrogenase expression. In-frame mutagenesis of hypB resulted in strains that were partially or completely deficient in hydrogenase expression, depending on the degree of disruption of the gene. Complete deletion of the gene yielded a strain (JHΔEg) which lacked hydrogenase activity under all conditions tested, including the situation as bacteroids from soybean nodules. Mutant strain JHΔ23H lacking only the N-terminal histidine-rich region (38 amino acids deleted, 23 of which are His residues) expressed partial hydrogenase activity. The activity of strain JHΔ23H was low in comparison to the wild type in 10–50 nM nickel levels, but could be cured to nearly wild-type levels by including 50 μM nickel during the derepression incubation. Studies on strains harbouring the hup promoter–lacZ fusion plasmid showed that the complete deletion of hypB nearly abolished hup promoter activity, whereas the histidine deletion mutant had 60% of the wild-type promoter activity in 50 μM NiCl2. Further evidence that HypB is required for hup promoter-binding activity was obtained from gel-shift assays. HypB could not be detected by immunoblotting when the cells were cultured heterotrophically, but when there was a switch to microaerobic conditions (1% partial pressure O2, 10% partial pressure H2) HypB was detected, and its expression preceded hydrogenase synthesis by 3–6 h. 63Ni accumulation by whole cells showed that both of the mutant strains accumulate less nickel than the wild-type strain at all time points tested during the derepression incubation. Wild-type cultures that received nickel during the HypB expression-specific period and were then washed and derepressed for hydrogenase without nickel had activities comparable to those cells that were derepressed for hydrogenase with nickel for the entire time period. In contrast to the wild type, strain JHΔ23H cultures supplied with nickel only during the HypB expression period achieved hydrogenase activities that were 30% of those cultures supplied with nickel for the entire hydrogenase derepression period. These results indicate that the loss of the metal-binding area of HypB causes a decrease in the ability of the cells to sequester and store nickel for later use in one or more hydrogenase expression steps.