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S J Elliott

Publications and source records attributed to S J Elliott.

14 recordsLinked to original sources
PubMed1992

The contribution of increased collagen synthesis to human glomerulosclerosis: a quantitative analysis of alpha 2IV collagen mRNA expression by competitive polymerase chain reaction.

We previously reported that one of the main components of the sclerotic material in human glomerular diseases was type IV collagen. In this study we examined the contribution of increased synthesis to this process at the gene expression level. Sufficient material has not been available to study type IV collagen synthesis by normal or sclerotic glomeruli in humans. We took advantage of the availability of nephrectomy specimens from patients with renal carcinoma, and of the observation that approximately 50% of these patients develop varying degrees of glomerulosclerosis. We microdissected glomeruli from 10 patients and analyzed them using in situ reverse transcription coupled with polymerase chain reaction (PCR) analyses (in situ RT-PCR). alpha 2IV collagen mRNA, after reverse transcription into cDNA, was detected in all patients and appeared to be increased in those with glomerulosclerosis (n = 5). A competitive PCR assay was developed to quantitate this change. There was an average 3.7-fold increase in glomerular type IV collagen cDNA in patients with significant sclerosis. This change was not due to an increased number of glomerular cells. Thus, glomerulosclerosis in humans is associated with an elevation of glomerular type IV collagen gene expression, suggesting that increased synthesis of type IV collagen may represent one component of this process.

Adult↗
PubMed1992

Effect of oxidant stress on calcium signaling in vascular endothelial cells.

The endothelial cell is recognized as a critical modulator of blood vessel tone and reactivity. This regulatory function of endothelial cells occurs via synthesis and release of diffusible paracrine substances which induce contraction or relaxation of adjacent vascular smooth muscle. In response to stimulation by blood-borne agonists such as bradykinin or histamine, the endothelial cell utilizes cytosolic ionic Ca2+ as a trigger in the transduction of the stimulatory signal into a paracrine response. Considerable evidence has accumulated to indicate that various forms of biologically important oxidant stress alter vascular function in an endothelium-dependent manner. Further, oxidant stress is known to alter the mechanisms which govern Ca2+ homeostasis in the endothelial cell. Recently, we have described a model in which the oxidant tert-butylhydroperoxide is utilized to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. In this model, three temporal phases are evident and consist of (1) inhibition of the agonist-stimulated Ca2+ influx pathway, (2) inhibition of receptor-activated release of Ca2+ from internal stores and elevation of resting cytosolic free Ca2+ concentration, and (3) progressive increase in resting cytosolic Ca2+ concentration and loss of responsiveness to agonist stimulation. In this review, the mechanisms which characterize agonist-stimulated Ca2+ signaling in vascular endothelial cells, and the effects of oxidant stress on signal transduction will be described. The mechanisms potentially responsible for oxidant-induced inhibition of Ca2+ signaling will be considered.

Animals↗
PubMed1992

Ca2+ signaling mechanisms of vascular endothelial cells and their role in oxidant-induced endothelial cell dysfunction.

Endothelial cell function may be compromised in disease states as a result of oxidative injury, which may arise from a variety of sources. Oxidant stress appears to influence vascular reactivity and permeability via alteration in the production, release, or effect of endothelium-derived paracrine substances. An early event associated with endothelial cell dysfunction involves alteration in transmembrane signaling mechanisms. In particular, substantial evidence suggests that oxidant stress alters Ca2+ homeostatic mechanisms of the endothelial cell. Because an increase in the free cytosolic Ca2+ concentration ([Ca2+]i) of the endothelial cell is important for release of paracrine factors responsible for regulation of vascular tone and reactivity, oxidant stress-induced changes in Ca2+ signaling could explain much of the observed pathophysiology associated with oxidative injury. Under normal conditions, agonists such as bradykinin and ATP cause a biphasic increase in [Ca2+]i of the endothelial cell; an initial transient component reflects release of Ca2+ from internal stores, whereas a more long-lasting elevation in [Ca2+]i reflects Ca2+ influx from the extracellular space. After incubation with tert-butyl hydroperoxide, a time-dependent inhibition of the agonist-stimulated changes in [Ca2+]i is observed. The underlying molecular mechanisms associated with normal Ca2+ signaling and how these may be altered in the endothelial cell by oxidative stress is the subject of this review.

Animals↗
PubMed1992

Oxidant stress alters Na+ pump and Na(+)-K(+)-Cl- cotransporter activities in vascular endothelial cells.

We have previously shown that oxidant stress activates Ca(2+)-dependent K+ efflux in pulmonary vascular endothelial cells. The present study was performed to determine the effect of oxidant stress on Na+ and K+ homeostasis using the radiotracers, 22Na+ and 86Rb+. Cellular ion contents at equilibrium were determined after incubation of cells with tert-butyl hydroperoxide (t-BOOH; 0.4 mM) for various durations. Cell content of 86Rb+ was unchanged through incubation periods of 2 h but was significantly decreased at 3 h, whereas cell content of 22Na+ progressively increased with increasing incubation duration. The effect of t-BOOH on Na+ pump and Na(+)-K(+)-Cl- cotransporter activities was examined via measurement of 86Rb+ influx in the absence or presence of ouabain and bumetanide, respectively. Oxidant stress time dependently increased ouabain-sensitive 86Rb+ influx, with little alteration in specific ouabain binding. In contrast, bumetanide-sensitive 86Rb+ influx was decreased by incubation with the oxidant. These findings suggest that the oxidant-induced increase in cellular Na+ content is associated with increased plasmalemmal Na(+)-K(+)-adenosinetriphosphatase activity. Furthermore, inward ion movement via the bumetanide-sensitive pathway is decreased, suggesting that oxidant stress inhibits the Na(+)-K(+)-Cl- cotransporter.

Adenine↗
PubMed1991

Production of type 1 fimbriae by Escherichia coli HB101.

Escherichia coli HB101 is frequently used as a host in the cloning of bacterial virulence genes because of its reported lack of virulence determinants such as fimbriae, adhesins and haemagglutinins. However, passage of HB101 in standing broth culture rapidly induced the production of fimbriae which mediated adhesion to HEp-2 cells and mannose-sensitive haemagglutination of human and guinea-pig erythrocytes. Fimbrial serology, morphology and pilin molecular mass of 18 kDa were consistent with those of type 1 fimbriae.

Animals↗
PubMed1991

Oxidative stress inhibits bradykinin-stimulated 45Ca2+ flux in pulmonary vascular endothelial cells.

The effects of oxidant stress and altered glutathione reductase activity on agonist-induced flux of Ca2+ were studied in cultured calf pulmonary artery endothelial cells using radioisotopic 45Ca2+. Bradykinin-stimulated uptake of 45Ca2+ was determined after cells were incubated with the membrane-permeant oxidant t-butylhydroperoxide (0.4 mM) for various durations. t-Butylhydroperoxide increased uptake of 45Ca2+ under basal conditions and significantly decreased bradykinin-stimulated uptake in a time-dependent manner through incubation periods of 2 h. Preincubation of cells with 1,3-bis(chloroethyl)-1-nitrosourea markedly reduced bradykinin-stimulated uptake in cells subsequently treated with t-butylhydroperoxide. Bradykinin-stimulated efflux of 45Ca2+ and 86Rb+ was examined in control and oxidant-stressed endothelial cells. t-Butylhydroperoxide initially decreased bradykinin-stimulated efflux of 45Ca2+ but had no effect on 86Rb+ efflux. After more prolonged incubation with the oxidant, stimulated 45Ca2+ efflux was further inhibited, and basal efflux of 86Rb+ was increased to a rate similar to that observed with bradykinin stimulation. Elevated basal 86Rb+ efflux was blocked by tetrabutylammonium chloride, a selective inhibitor of Ca2(+)-dependent K+ channels in endothelial cells. These findings, together with our previously described results using fura-2, suggest that oxidant stress initially inhibits bradykinin-stimulated Ca2+ influx and later inhibits stimulated Ca2+ efflux. Finally, cytosolic free Ca2+ concentration becomes persistently elevated and is associated with elevated basal efflux of K+ via the Ca2(+)-dependent K+ channel.

Animals↗
PubMed1990

Carmustine augments the effects of tert-butyl hydroperoxide on calcium signaling in cultured pulmonary artery endothelial cells.

The effects of oxidant stress and inhibition of glutathione reductase on the bradykinin-stimulated changes in cytosolic free Ca2+ concentration ([Ca2+]i) of calf pulmonary artery endothelial cells were determined using the intracellular fluorescent probe, fura-2. Changes in [Ca2+]i upon stimulation with bradykinin were measured after incubation of cells with the chemical oxidant tert-butyl hydroperoxide (0.4 mM) for various times. After 60 min, bradykinin-stimulated Ca2+ influx was significantly decreased. With more prolonged incubations with the peroxide, bradykinin had little effect on cytosolic calcium concentration. Preincubation of cells with the glutathione reductase inhibitor, carmustine, led to elevated basal [Ca2+]i, yet the cells remained responsive to bradykinin. However, incubation of carmustine-treated cells with tert-butyl hydroperoxide for 30 min dramatically reduced both bradykinin-stimulated release of Ca2+ from internal stores and influx of Ca2+ from the extracellular space. These results suggest that inhibition of glutathione reductase alters cytosolic Ca2+ homeostasis and enhances the effects of oxidative stress on signal transduction in vascular endothelial cells.

Animals↗
PubMed1990

Housing satisfaction, preference and need among the chronically mentally disabled in Hamilton, Ontario.

This paper examines housing satisfaction, preference and need among a sample of the CMD in Hamilton, Ontario. The research goes beyond simply documenting the gap in housing supply by examining issues of housing quality as expressed by clients themselves. Survey data were obtained in two rounds of interviews from 66 clients attached to three aftercare programmes. Various indicators were consistent in showing a relatively high level of satisfaction with the current living situation. At the same time, clients reported major housing difficulties due to lack of appropriate and affordable accommodation, unacceptable conditions and financial constraints. Housing satisfaction was a significant correlate of scores of coping indices. There was considerable variability in satisfaction within groups of the sample defined in terms of type of housing, location and living arrangement. Data on preferences and expressed needs correspond quite closely with normative prescriptions for a continuum of housing options ranging from restricted congregate care to autonomous individual living situations. These findings underline the heterogeneity of the CMD and their needs.

Adaptation, Psychological↗
PubMed1990

Parameter interpolation in speech synthesis.

A comparison has been made of the transition properties of six types of speech synthesizer parameters: serial resonance, prediction coefficients, reflection coefficients, area functions, parallel resonance, and, finally, a simple set of articulatory parameters. The first four synthesizers are formally equivalent and can be made to produce identical steady-state sounds (targets). The last two involve approximations, but achieve similar targets. Formant paths between targets will differ according to the parameter type used during interpolation. Each type was tested on nonsense words spanning a wide range of parameter values. Linear interpolation of synthesizer parameters was used to determine a path between target values. The resultant data were then converted to formant values and plotted as a spectrographic (frequency versus time) representation. Small differences in formant frequency (versus linear transitions of formant frequency and bandwidth) were common, and some quite large differences in formant bandwidths were observed in certain cases.

Communication Devices for People with Disabilities↗
PubMed1989

Effect of t-butyl-hydroperoxide on bradykinin-stimulated changes in cytosolic calcium in vascular endothelial cells.

The effect of oxidant stress on agonist-induced changes in endothelial cell cytosolic free Ca2+ (Ca2+i) was measured using the fluorescent probe, fura-2. Cultured vascular endothelial cells were loaded with fura-2 via the acetoxymethyl ester form, fura-2/AM, before incubation with t-butyl-hydroperoxide (0.4 mM). Bradykinin-stimulated changes in (Ca2+i) were measured in cells exposed to the hydroperoxide for 0, 30, 60, 120, and 180 min. Incubation of cells with the oxidant initially (within 30 min) diminished the peak rise in (Ca2+i) that occurs after stimulation with bradykinin. Experiments conducted with cells in a Ca2+-free buffer indicated that t-butyl-hydroperoxide inhibited bradykinin-stimulated Ca2+ influx from the extracellular space and had little effect on agonist-induced release of Ca2+ from internal stores. At the later incubation periods (greater than 60 min), basal (Ca2+i) progressively rose and the peak response to bradykinin progressively decreased. After 180 min, the cells appeared unable to maintain steady-state with respect to Ca2+ flux. These alterations in Ca2+ homeostasis occurred before detectable changes in the ability of the cells to exclude trypan blue. These results suggest that oxidant stress alters the change in Ca2+i of vascular endothelial cells following stimulation with vasoactive agents.

Animals↗
PubMed1985

Hematuria after renal allograft biopsy: treatment with aminocaproic acid.

Aminocaproic acid (EACA) was used in 2 patients with cadaveric renal allografts because gross hematuria developed after percutaneous renal biopsies. Marked improvement was noted within twelve hours with no recurrence after discontinuation of EACA. EACA was effective in moderate renal failure.

Adolescent↗
PubMed1985

Clinical presentation and management of Pseudomonas osteomyelitis.

To determine the incidence and clinical characteristics of Pseudomonas aeruginosa osteomyelitis in children, the records of 144 hospitalized patients under 19 years of age were reviewed; 104 fulfilled the study criteria for the diagnosis of acute or chronic osteomyelitis. Pseudomonas aeruginosa was recovered from 10.6 percent of the children and was the second most common pathogen isolated. In comparison to children with staphylococcal infections, patients with pseudomonal osteomyelitis were significantly older, gave an antecedent history of penetrating trauma, and lacked clinical and laboratory evidence of systemic illness. The data collected in this study suggest that osteomyelitis due to Pseudomonas aeruginosa is a distinct entity with clinical features differing from those of Staphylococcus aureus. Management should be directed at adequate surgical debridement followed by 10 to 21 days of antimicrobial therapy.

Adolescent↗