Biomedical subjects

A B Sullivan

Publications and source records attributed to A B Sullivan.

4 recordsLinked to original sources

PubMed2003

Preferential flow path development and its influence on long-term PRB performance: column study.

The operating life of an Fe(0)-based permeable reactive barrier (PRB) is limited due to chemical reactions of Fe(0) in groundwater. The relative contributions from mineral precipitation, gas production, and microbial activity to the degradation of PRB performance have been uncertain. In this controlled field study, nitrate-rich, site groundwater was treated by Fe(0) in large-volume, flow-through columns to monitor the changes in chemical and hydraulic parameters over time. Tracer tests showed a close relationship between hydraulic residence time and pH measurements. The ionic profiles suggest that mineral precipitation and accumulation is the primary mechanism for pore clogging around the inlet of the column. Accumulated N(2) gas generated by biotic processes also affected the hydraulics although the effects were secondary to that of mineral precipitation. Quantitative estimates indicate a porosity reduction of up to 45.3% near the column inlet over 72 days of operation under accelerated flow conditions. According to this study, preferential flow through a PRB at a site with similar groundwater chemistry should be detected over approximately 1 year of operation. During the early operation of a PRB, pH is a key indicator for monitoring the change in hydraulic residence time resulting from heterogeneity development. If the surrounding native material is more conductive than the clogged Fe-media, groundwater bypass may render the PRB ineffective for treating contaminated groundwater.

Chemical Precipitation↗

PubMed1997

Estrogen-receptor-mediated inhibition of human endothelial cell apoptosis. Estradiol as a survival factor.

BACKGROUND: A series of studies was performed to examine the ability of estradiol (E2) to protect endothelial cells from apoptosis. METHODS AND RESULTS: Light and transmission electron microscopy demonstrated typical features of apoptosis in human umbilical vein endothelial cells (HUVEC) exposed to tumor necrosis factor-alpha (TNF-alpha). Northern and Western blot analyses revealed induction of message and protein for the interleukin-1 beta converting enzyme (ICE), which has been shown to mediate apoptosis induced by TNF-alpha. Immunofluorescent staining of HUVEC colocalized ICE expression to apoptotic HUVEC. Direct cell counting demonstrated a significant decrease in total endothelial cell number after 24 hours of TNF-alpha exposure and a dose-dependent reversal of the effect of TNF-alpha with E2 treatment. This protective effect was abrogated by an estrogen-receptor antagonist. Fluorescence-activated cell sorting analysis revealed 39.3% apoptosis after 24 hours of TNF-alpha exposure. Treatment with E2 resulted in a 50% decrease in apoptosis. Similarly, viability assays revealed 35 +/- 4% cell death after TNF-alpha exposure. Simultaneous treatment with E2 resulted in a dose-dependent reduction of cell death to a minimum of 18 +/- 2%. The protective effect of E2 was nullified by a specific estrogen-receptor antagonist. CONCLUSIONS: E2 treatment resulted in a dose-dependent, receptor-mediated inhibition of TNF-alpha-induced endothelial cell apoptosis. These studies indicate that E2 may also serve a maintenance function in preventing endothelial cell death after noxious stimuli and suggest that the ICE pathway may mediate cytokine-induced apoptosis in endothelial cells. Preservation of endothelial integrity represents another mechanism that may account for the atheroprotective effect of estrogen.

Apoptosis↗

PubMed1997

Vascular endothelial growth factor inhibits endothelial cell apoptosis induced by tumor necrosis factor-alpha: balance between growth and death signals.

A series of experiments was performed to determine whether vascular endothelial growth factor (VEGF), in addition to its endothelial cell specific mitogenic activity, can also protect endothelial cells from toxin-induced programmed cell death. Apoptosis was induced in endothelial cell culture with tumor necrosis factor-alpha (TNF-alpha). Simultaneous exposure of endothelial cells to VEGF resulted in a dose dependent inhibition of apoptosis when evaluated by: (1) direct counting of cells with morphologic features of apoptosis after acridine orange staining; (2) analysis of DNA fragmentation by (a) agarose gel electrophoresis and (b) fluorescence activated cell sorting (FACS); and (3) viability assays dependent upon mitochondrial function. Induction of fibronectin and beta 3 integrin expression in endothelial cells by VEGF suggests that altered adhesion molecule expression may explain this survival effect.

Animals↗

PubMed1997

Frequent short rest breaks from computer work: effects on productivity and well-being at two field sites.

Computer operators at two work sites (n = 73, n = 19) were prompted to take three 30-s and one 3-min break from computer work each hour in addition to conventional rest breaks. Some operators were asked to perform stretching exercises during the short breaks. Mood state and musculoskeletal discomfort were assessed at each work site over a 2- or 3-week baseline period and a 4- or 6-week treatment period, respectively. Operator productivity measures were obtained from company records. Operators complied with about half of the added breaks but favoured 3-min breaks over 30-s breaks. No improvement in productivity or well-being was found at the larger work site. At the smaller work site, productivity, eye, leg and foot comfort all improved when the short breaks included stretching exercises. These results provide evidence that frequent short breaks from continuous computer-mediated work can benefit worker productivity and well-being when the breaks integrate with task demands.

Adult↗