Publications by authors named "Douglas Mason"

We study the threshold for chaos and its relation to thermalization in the 1D mean-field Bose-Hubbard model, which, in particular, describes atoms in optical lattices. We identify the threshold for chaos, which is finite in the thermodynamic limit, and show that it is indeed a precursor of thermalization. Far above the threshold, the state of the system after relaxation is governed by the usual laws of statistical mechanics.

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Purpose: Eritoran (E5564) is a glycophospholipid that acts as a toll-like receptor 4 (TLR4) antagonist that is being tested as a treatment for severe sepsis and septic shock. In the blood, eritoran binds to plasma lipoproteins altering its pharmacokinetic and pharmacodynamic (PD) effects in vivo. The purpose of this study was to determine the influence of changes in plasma cholesterol and triglyceride concentrations on the plasma pharmacokinetics and ex vivo activity of eritoran following single intravenous bolus dosing of eritoran to healthy female rabbits fed either a regular chow diet or a cholesterol-enriched diet.

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In contrast to rodent cells, normal human fibroblasts are generally resistant to neoplastic transformation in vitro. Here, we report the derivation and characterization of a spontaneously transformed cell line from normal human IMR90 fibroblasts transduced with E1A and Ras oncogenes. Unlike the parental, non-tumorigenic E1A/Ras-expressing IMR90 cells, these spontaneously transformed cells displayed aberrant growth potential in vitro and were capable of tumorigenesis in vivo.

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Several studies have shown that forced expression of oncogenic H-ras can induce a senescence-like permanent growth arrest in normal cells. Here we report that expression of oncogenic H-ras in human osteosarcoma U2OS cells also resulted in a senescence-like flat and enlarged cell morphology and permanent growth arrest. In contrast to normal human fibroblasts, U2OS cells were arrested independently of the p16 and ARF tumor suppressors.

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Senescence irreversibly arrests the proliferation of cells that have sustained significant cellular stress. Replicative senescence, due to the shortening and dysfunction of telomeres, appears to provide a barrier to the immortalization of cells and development of cancer. In normal human fibroblasts, senescence induced by oncogenic H-ras displays a nearly identical cellular phenotype to that of replicative senescence, suggesting the activation of a common senescence mechanism.

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Telomerase is a ribonucleoprotein enzyme responsible for the addition of telomeres onto the ends of chromosomes. Short or dysfunctional telomeres can lead to cell growth arrest, apoptosis, and genomic instability. Telomerase uses its RNA subunit to copy a short template region for telomere synthesis.

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The objective of this study was to determine the agreement between cardiac output measured by central (cranial vena cava) versus peripheral (cephalic vein) venous injection of lithium chloride for lithium-dilution cardiac output (LiDCO) determination in the dog. Five dogs (2 males, 3 females), anesthetized with halothane, were used. With each dog, 12 alternating central and peripheral LiDCO measurements were made, resulting in 10 paired comparisons.

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Objectives: To assess the effect of increasing serum lithium concentrations on lithium dilution cardiac output (LiDCO) determination and to determine the ability to predict the serum lithium concentration from the cumulative lithium chloride dosage.

Animals: 10 dogs (7 males, 3 females).

Procedure: Cardiac output (CO) was determined in anesthetized dogs by measuring LiDCO and thermodilution cardiac output (TDCO).

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