In patients receiving hemodialysis, a conjugate vaccine can confer partial immunity against S. aureus bacteremia for approximately 40 weeks, after which protection wanes as antibody levels decrease.

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Numerical modeling of gas hydrates can provide an integrated understanding of the various process mechanisms controlling methane (CH4) production from hydrates and carbon dioxide (CO2) sequestration as a gas hydrate in geologic reservoirs. This work describes a new unified kinetic model which, when coupled with a compositional thermal reservoir simulator, can simulate the dynamics of CH4 and CO2 hydrate formation and decomposition in a geological formation. The kinetic model contains two mass transfer equations: one equation converts gas and water into hydrate and the other equation decomposes hydrate into gas and water. The model structure and parameters were investigated in comparison with a previously published model. The proposed kinetic model was evaluated in two case studies. Case 1 considers a single well within a natural hydrate reservoir for studying the kinetics of CH4 and CO2 hydrate decomposition and formation. A close agreement was achieved between the present numerical simulations and results reported by Hong and Pooladi-Darvish (2003, “A Numerical Study on Gas Production From Formations Containing Gas Hydrates,” Petroleum Society’s Canadian International Petroleum Conference, Calgary, AB, Jun. 10–12, Paper No. 2003-060). Case 2 considers multiple wells within a natural hydrate reservoir for studying the unified kinetic model to demonstrate the feasibility of CO2 sequestration in a natural hydrate reservoir with potential enhancement of CH4 recovery. The model will be applied in future field-scale simulations to predict the dynamics of gas hydrate formation and decomposition processes in actual geological reservoirs.

The effect of acute and chronic administration of three different prostaglandin (PG) synthesis inhibitors–aspirin, indomethacin and naproxen–on the basal and CO2‐stimulated cerebral blood flow (CBF) was studied in healthy subjects, using the N2O wash‐in technique for assessment of CBF. The regional O2 extraction over the brain, the regional production of free fatty acids (FFA)–including the PG precursor arachidonic acid (AA)–and the regional production of two prostacyclin (PGI2) metabolites, were also measured. The efficacy of cyclo‐oxygenase inhibition by these drugs was monitored through AA‐induced platelet aggregation in blood samples taken before and after drug administration. In the basal state there was no detectable release of AA, other FFA or PGI2 metabolites over the brain. Acute administration of aspirin (45 mg/kg) failed to affect CBF, as did chronic administration of this drug (15 mg/kg × 3 daily). Indomethacin (1.5 mg/kg) significantly (p<0.05)reduced CBF after acute administration, but after one week's treatment (0.8 mg/kg × 3 daily) this effect had disappeared. Acute administration of naproxen (4 mg/kg) did not affect O2 extraction over the brain, thus indicating that CBF was unchanged. After chronic administration, naproxen (4 mg/kg × 2 daily) also failed to change CBF. During inhalation of CO2, no release of AA, other FFA or PGI2 metabolites occurred in untreated subjects. In subjects given indomethacin there was a small but significant release of AA during inhalation of CO2. Both acute and chronic administration of aspirin failed to affect the CO2‐induced elevation of CBF, whereas both forms of indomethacin administration significantly reduced this rise. Chronic administration of naproxen did not affect the CO2‐induced increase in CBF. We conclude that in healthy subjects: 1) local PGI2 production does not appear to be involved in the regulation of cerebral blood flow: 2) indomethacin reduces basal and CO2‐stimulated CBF, an effect not shared by the other structurally unrelated cyclo‐oxygenase inhibitors: 3) the mechanism(s) of indomethacin‐induced reduction of CBF does not appear to be related to inhibition of PG‐synthesis and remains to be determined.

No abstract

Background and Purpose-Alterations of neuroangiogenic response play important roles in the development of aging-related neurodisorders and affect gene-based therapies. We tested brain response to vascular endothelial growth factor (VEGF) in aged mice. Methods-Adeno-associated viral vector (AAV)-VEGF, an adeno-associated viral vector expressing VEGF, was injected into the brain of 3-, 12-, and 24-month-old mice. AAV-LacZ-injected mice were used as controls (nϭ6). Before euthanasia at 6 weeks after vector injection, the mice were intraperitoneally injected with 5-bromodeoxyuridine for 3 consecutive days. The vascular density and the number of neuroprogenitors were analyzed.

No abstract

Changes in brain amino acid uptake and metabolism have been proposed as a possible etiological factor in hepatic encephalopathy. By use of a brain dialysis technique (a thin tube implanted in the brain of the living animal), the extracellular amino acid concentrations in the striatum of portacaval (PC)-shunted and sham-operated rats were measured. Leucine, phenylalanine, methionine, and glutamine were increased two- to sixfold in the PC-shunted rats, whilst no changes were seen for GABA, valine, glutamate, or isoleucine, confirming previous reports. Aspartate levels were 350% higher in the PC-shunted rats, and this rise, as well as that of phenylalanine, was significantly correlated with the lower motor activity observed in the PC-shunted rats, suggesting a possible importance of these amino acids in the etiology of hepatic encephalopathy. The amino acid concentrations measured in whole blood demonstrated the well-known pattern of low levels of branched-chain amino acids and increased concentrations of phenylalanine, glutamine, and histidine.