University of Arkansas for Medical Sciences

About: University of Arkansas for Medical Sciences is a education organization based out in Little Rock, Arkansas, United States. It is known for research contribution in the topics: Population & Health care. The organization has 14077 authors who have published 26012 publications receiving 973592 citations. The organization is also known as: UAMS.

Delivered Oxygen Concentrations Using Low-Flow and High-Flow Nasal Cannulas

Abstract: INTRODUCTION: Nasal cannulas are commonly used to deliver oxygen in acute and chronic care settings; however, there are few data available on delivered fraction of inspired oxygen (FIO2). The purposes of this study were to determine the delivered FIO2 on human subjects using low-flow and high-flow nasal cannulas, and to determine the effects of mouth-closed and mouth-open breathing on FIO2. METHODS: We measured the pharyngeal FIO2 delivered by adult nasal cannulas at 1–6 L/min and high-flow nasal cannulas at 6–15 L/min consecutively in 10 normal subjects. Oxygen was initiated at 1 L/min, with the subject at rest, followed by a period of rapid breathing. Gas samples were aspirated from a nasal catheter positioned with the tip behind the uvula. This process was repeated at each liter flow. Mean, standard deviation, and range were calculated at each liter flow. FIO2 during mouth-open and mouth-closed breathing were compared using the dependent t test for paired values, to determine if there were significant differences. RESULTS: The mean resting FIO2 ranged from 0.26–0.54 at 1–6 L/min to 0.54–0.75 at 6–15 L/min. During rapid breathing the mean FIO2 ranged from 0.24–0.45 at 1–6 L/min to 0.49–0.72 at 6–15 L/min. The mean FIO2 increased with increasing flow rates. The standard deviation (±0.04–0.15) and range were large, and FIO2 varied widely within and between subjects. FIO2 during mouth-open breathing was significantly (p CONCLUSIONS: FIO2 increased with increasing flow. Subjects who breathed with their mouths open attained a significantly higher FIO2, compared to those who breathed with their mouths closed.

Mechanisms of DNA Damage, DNA Hypomethylation, and Tumor Progression in the Folate/Methyl-Deficient Rat Model of Hepatocarcinogenesis

Abstract: Using the folate/methyl-deficient rat model of hepatocarcinogenesis, we obtained evidence that may provide new insights into a major unresolved paradox in DNA methylation and cancer research: the mechanistic basis for genome-wide hypomethylation despite an increase in DNA methyltransferase activity and gene-specific regional hypermethylation. Previous studies revealed that the methyltransferase binds with higher affinity to DNA strand breaks, gaps, abasic sites, and uracil than it does to its cognate hemimethylated CpG sites, consistent with its ancestral function as a DNA repair enzyme. These same DNA lesions are an early occurrence in models of folate and methyl deficiency and are often present in human preneoplastic cells. We hypothesized that the high-affinity binding of the maintenance DNA methyltransferase to unrepaired lesions in DNA could sequester available enzyme away from the replication fork and promote passive replication-dependent demethylation. In support of this possibility, we found that lesion-containing DNA is less efficiently methylated than lesion-free DNA from folate/methyl-deficient rats and that an increase in DNA strand breaks precedes DNA hypomethylation. Despite an adaptive increase in DNA methyltransferase activity, hemimethylated DNA from folate/methyl-deficient rats is progressively replaced by double-stranded unmethylated DNA that is resistant to remethylation with dietary methyl repletion. In promoter regions, the inappropriate binding of the DNA methyltransferase to unrepaired lesions or mispairs may promote local histone deacetylation, methylation, and regional hypermethylation associated with tumor suppressor gene silencing. These insights in an experimental model are consistent with the possibility that DNA lesions may be a necessary prerequisite for the disruption of normal DNA methylation patterns in preneoplastic and neoplastic cells.