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Biomedical subjects

S J Wilson

Publications and source records attributed to S J Wilson.

At least 109 records · Page 6Linked to original sources
PubMed1993

Saccadic eye movement parameters in normal subjects.

The present study obtained saccadic eye movements from 122 normal subjects to establish normative values and test-retest reliability data, using a recently developed electrooculographic recording and analysis system. Factors that might affect saccade values, such as age, sex, and time of day when testing, were also assessed. Mean (+/- S.D.) peak velocity values over saccade angles of 15 degrees, 25 degrees and 35 degrees were in agreement with those previously reported. Repeat testing in 11 subjects on 4 separate occasions showed that saccade measurements were consistent across tests. Several saccade parameters were significantly negatively associated with age for 35 degrees saccades. The association between age and peak velocity was examined in greater detail over a range of saccade angles, and the greatest effect was observed for saccades of > or = to 35 degrees. Diurnal changes in performance were observed, with a tendency for slightly slower values in the early afternoon. There were no significant differences between males and females.

Adolescent↗
PubMed1993

Respiratory triggered imaging with an optical displacement sensor.

Motion of abdominal organs with respiration is a major problem in NMR spectroscopy and imaging thereof. Triggering each phase-encoding step with respiration or gating a number of phase-encoding steps is one approach to the problem. The design of a sensor for small animal experiments has not been as simple. An optical device, implemented with polymer optical fibres is described, along with associated hardware and electronics which can act as a trigger for small animal NMR experiments. A brief description of a similar device for human application is also given. 2DFT spin-echo and B0 susceptibility images, both triggered and untriggered, are presented to validate the technique.

Abdomen↗
PubMed1993

A method for the estimation of traces of chlorhexidine in water.

A simple method of estimating traces of chlorhexidine in water using bromothymol blue is described. The procedure involves the extraction of the chlorhexidine/bromothymol blue complex into carbon tetrachloride from a buffered neutral solution and measurement of the absorbances of the extracts in a spectrophotometer. The extracted complex has good colour stability, and the method is accurate, reproducible, and very sensitive, with concentrations of chlorhexidine down to 0.05 micrograms ml-1 measurable.

Bromthymol Blue↗
PubMed1993

The release of chlorhexidine from modified dental acrylic resin.

A method for the incorporation of chlorhexidine into acrylic resin using monomer together with the pattern of release of chlorhexidine from treated resin into water at 37 degrees C is described. Release from polished and unpolished resin, and from acrylic prepared by short-curing and dry-curing processes are investigated. The pattern of release in all cases was of an exponential nature, showing a rapid release within the first 10 days becoming almost constant at a level of 0.4-1.5 micrograms cm-2 at about 20 days. Release was still evident at the end of the test period in all cases. Release of chlorhexidine into water from the short-cure specimens was accompanied by release of monomer, evident from the odour of the test solutions, indicating that polymerization was not complete.

Acrylic Resins↗
PubMed1993

Diagnostic utility of postmortem blood cultures.

The autopsy is receiving renewed emphasis as a tool for quality assurance in clinical medicine. Postmortem blood cultures frequently are taken during the autopsy but are costly and of unclear diagnostic utility. To assess whether postmortem blood cultures contribute any useful information not already known from antemortem blood cultures, we compared positive postmortem blood cultures taken in 111 autopsies with the results of antemortem blood cultures. Of these, 60 (54%) of 111 had positive postmortem blood cultures despite a cause of death not related to an infectious cause. Of the 111 patients, 54 (49%) had antemortem blood cultures drawn in the 7 days before death, of which 34 (63%) of 54 were negative and 20 (37%) of 54 were positive. Of the 20 patients with true antemortem bacteremia/fungemia, seven (35%) had postmortem blood cultures that yielded the same organism, 10 (50%) yielded multiple organisms that were considered to be contaminants, and three (15%) yielded different organisms. These latter three cultures yielded microorganisms that were related to the patients' illness but did not provide additional information not already known from antemortem blood cultures or the patients' clinical or autopsy findings. Of the 91 patients who had no, negative, or contaminated antemortem blood cultures, 69 (76%) had postmortem blood cultures that yielded contaminants and 22 (24%) yielded microorganisms that were indeterminate as a cause of sepsis and, therefore, did not yield new or useful information. In summary, results of postmortem blood cultures rarely, if ever, provide information that is not already known, can be interpreted, provide new insights into pathophysiology, or detect errors in therapy.

Autopsy↗
PubMed1992

Early stages of myogenesis in a large mammal: formation of successive generations of myotubes in sheep tibialis cranialis muscle.

The generation of myotubes was studied in the tibialis cranialis muscle in the sheep hindlimb from the earliest stage of primary myotube formation until a stage shortly before muscle fascicles began to segregate. Primary myotubes were first seen on embryonic day 32 (E32) and reached their maximum number by E38. Small numbers of secondary myotubes were first identified at E38, and secondary myotube numbers continued to increase during the period of study. The ratio of adult muscle fibre to primary myotube numbers was approximately 70:1, making it seem unlikely that every later generation myotube used a primary myotube as scaffold for its formation, as described in small mammals. By E62, some secondary myotubes were supporting the formation of a third generation of myotubes. Experiments with diffusible dye markers showed that primary myotubes extended from tendon to tendon of the muscle, whereas most adult fibres ran for only part of the muscle length, terminating with myo-myonal attachments to other muscle fibres in a series arrangement. Acetylcholinesterase (AChE) and acetylcholine receptor (AChR) aggregations appeared in multiple bands across the muscle shortly after formation of the primary generation of myotubes was complete. The number of bands and their pattern of distribution across the muscle as they were first formed was the same as in the adult. Primary myotubes teased from early muscles had multiple focal AChE and AChR deposits regularly spaced along their lengths. We suggest that the secondary generation of myotubes forms at endplate sites in a series arrangement along the length of single primary myotubes, and that tertiary and possibly later generations of myotubes in their turn use the earlier generation myofibres as a scaffold. Although the fundamental cellular mechanisms appear to be similar, the process of muscle fibre generation in large mammalian muscles is more complex than that described from previous studies in small laboratory rodents.

Acetylcholinesterase↗
PubMed1992

Effect of inhaled platelet-activating factor on bronchial inflammation in atopic non-asthmatic subjects.

We have investigated the effect of inhaled platelet-activating factor (PAF) on bronchial mucosal inflammation in 6 atopic non-asthmatic subjects in a double-blind, placebo-controlled, randomised and crossover study. On 2 study periods at least 4 weeks apart, fiberoptic bronchoscopy was performed 24 h after inhalation of either 200 micrograms PAF or methacholine (control) to obtain endobronchial biopsies. Immunocytochemistry using antibodies for trypase (AA1) and eosinophil cationic protein (EG2) was performed to enumerate mast cells and eosinophils, respectively, in the bronchial submucosa. Median values of AA1+ cells and EG2+ cells did not differ significantly after inhalation of PAF or control (23.8 vs. 39 and 6 vs. 8/mm2, respectively, PAF vs. control, non-significant). Our findings suggest that within 24 h of inhaling a bronchoconstrictor dose of PAF, this agonist does not induce bronchial hyperresponsiveness or mucosal inflammation in atopic non-asthmatic subjects. However, because of the small number of subjects studied, these preliminary data should be interpreted with caution.

Administration, Inhalation↗
PubMed1992

Effect of an inhaled corticosteroid on airway inflammation and symptoms in asthma.

The effect of inhaled corticosteroid therapy on airway mucosal inflammation was investigated in 10 symptomatic atopic asthmatic patients treated with inhaled albuterol and whose disease severity required preventative antiinflammatory treatment. Endobronchial biopsies were obtained by fiberoptic bronchoscopy before and after 6 wk of therapy with inhaled beclomethasone dipropionate (2,000 micrograms/day for 2 wk followed by 1,000 micrograms/day for 4 wk). Following treatment, there was a significant increase in mean morning peak expiratory flow (p less than 0.05) and baseline FEV1 measured on the day of methacholine challenge (p less than 0.05) and a decrease in asthma symptoms (p less than 0.01), peak expiratory flow variation (p less than 0.05), and albuterol usage (p less than 0.05). This was accompanied by a sevenfold decrease in airway responsiveness (p = 0.001). The clinical improvement in asthma was associated with a significant (p less than 0.05) reduction in epithelial and mucosal mast cells and eosinophils and submucosal T lymphocytes, but electron microscopy did not identify any changes in the extent of mast cell and eosinophil degranulation following treatment. Because of the association between the decrease in inflammatory cell numbers and the improvement in all the measured clinical and physiologic indices of asthma, we suggest that the beneficial effect of inhaled corticosteroids in asthma may be attributed to their antiinflammatory action in the bronchial mucosa.

Administration, Inhalation↗
PubMed1992

Selective eosinophil leukocyte recruitment by transendothelial migration and not by leukocyte-endothelial cell adhesion.

Eosinophil infiltration is the hallmark of allergic inflammatory events. However, the mechanisms governing the influx of eosinophils into the tissue at a site of an allergic reaction remains unclear. We have examined the interactions of eosinophils and neutrophils isolated from the same atopic donor with cultured human umbilical vein endothelial cell (EC) monolayers in the search for a mechanism for this selective eosinophil recruitment. First, the adherence of eosinophils and neutrophils to ECs stimulated with lipopolysaccharide, interleukin (IL)-1 alpha, and tumor necrosis factor-alpha were compared. Each mediator induced a similar dose-dependent enhancement of eosinophil adhesiveness for both eosinophils and neutrophils. Thus, although cytokine activation of ECs in the vasculature adjacent to an inflammatory site probably serves as an important focusing mechanism for the extravasation of inflammatory cells at this site, there does not appear to be any selective EC-dependent mechanism for eosinophil recruitment. Little or no effect on eosinophil and neutrophil adherence was observed with IL-3, IL-5, granulocyte/macrophage colony-stimulating factor, platelet-activating factor (PAF), leukotriene B4, or histamine. Second, the migration of eosinophils and neutrophils through an EC monolayer in response to chemoattractants was examined. PAF was found to selectively enhance eosinophil transendothelial migration at doses of 10(-7) to 10(-10) M, with optimal effect at 10(-8) M. This effect was gradient dependent and could be inhibited by WEB 2086, a specific PAF inhibitor. These results suggest that localized production of PAF may be a prime factor in the events leading to eosinophil accumulation at allergic inflammatory sites, and that selectivity for eosinophil recruitment occurs at the stage of transendothelial cell migration under the influence of cell-specific chemoattractants.

Amitrole↗
PubMed1992

The expression of leukocyte-endothelial adhesion molecules is increased in perennial allergic rhinitis.

Accumulating evidence supports the importance of leukocyte-endothelial cell adhesion molecule (CAM) expression as an initiating process in tissue inflammation. To investigate the relevance of CAM expression to allergic airways inflammation, nasal biopsies from patients with perennial allergic rhinitis (n = 8) and from nonatopic healthy volunteers (n = 8) were immunostained with monoclonal antibodies directed against the CAMs, intercellular adhesion molecule-1 (ICAM-1), endothelial cell adhesion molecule-1 (ELAM-1), and vascular cell adhesion molecule-1 (VCAM-1). The endothelial staining of these CAMs was related to the number of vessels within each biopsy, delineated by a monoclonal antibody against Ulex europaeus-1 lectin bound to endothelial cells, and to the number of tissue leukocytes staining for one of the ligands of ICAM-1, the beta 2 integrin, lymphocyte function-associated antigen (LFA-1). Expression of CAMs was related to the number of infiltrating neutrophils, eosinophils, and lymphocytes identified immunohistochemically within the biopsies. ICAM-1 was the most prominent CAM present on the endothelium of the normal nasal mucosa, with less expression of ELAM-1 and only minimal or absent expression of VCAM-1. In perennial rhinitis, both ICAM-1 (P less than 0.05) and VCAM-1 (P less than 0.01) expression on endothelial cells were increased and were positively correlated in their level of expression (P less than 0.002). The number of tissue LFA-1-positive cells was significantly greater (P less than 0.05) in the biopsies from the perennial rhinitics (median, 27.3/mm2) than from the healthy controls (median, 5.3 cells/mm2). LFA-1 expression significantly correlated with the number of ICAM-1-positive vessels (P less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Bronchial mucosal manifestations of atopy: a comparison of markers of inflammation between atopic asthmatics, atopic nonasthmatics and healthy controls.

We studied the role of atopy, as defined by positive skin tests to common inhalant allergens, in allergic bronchial inflammation. Endobronchial biopsies were taken via the fibreoptic bronchoscope in 13 symptomatic atopic asthmatics, 10 atopic nonasthmatics, and 7 normals. The numbers of mast cells, identified in the submucosa by immunohistochemistry using the AA1 monoclonal antibody against tryptase, were no different between the three groups, but electron microscopy showed that mast cell degranulation, although less marked in atopic nonasthmatics, was a feature of atopy in general. The numbers of eosinophils, identified by immunohistochemical staining using the monoclonal anti-eosinophil cationic protein antibody, EG2, were greatest in the asthmatics, low or absent in the normals and intermediate in the atopic nonasthmatics. In both atopic groups eosinophils showed ultrastructural features of degranulation. Measurements of subepithelial basement membrane thickness on electron micrographs showed that the collagen layer was thickest in the asthmatics, intermediate in the atopic nonasthmatics and thinnest in the normals. The results suggest that airways eosinophilia and degranulation of eosinophils and mast cells, as well as increased subepithelial collagen deposition, are a feature of atopy in general and suggest that the degree of change may determine the clinical expression of this immune disorder.

Adult↗
PubMed1991

Inhibition of replicon initiation in human cells following stabilization of topoisomerase-DNA cleavable complexes.

Diploid human fibroblast strains were treated for 10 min with inhibitors of type I and type II DNA topoisomerases, and after removal of the inhibitors, the rate of initiation of DNA synthesis at replicon origins was determined. By alkaline elution chromatography, 4'-(9-acridinylamino)methanesulfon-m-anisidide (amsacrine), an inhibitor of DNA topoisomerase II, was shown to produce DNA strand breaks. These strand breaks are thought to reflect drug-induced stabilization of topoisomerase-DNA cleavable complexes. Removal of the drug led to a rapid resealing of the strand breaks by dissociation of the complexes. Velocity sedimentation analysis was used to quantify the effects of amsacrine treatment on DNA replication. It was demonstrated that transient exposure to low concentrations of amsacrine inhibited replicon initiation but did not substantially affect DNA chainelongation within operating replicons. Maximal inhibition of replicon initiation occurred 20 to 30 min after drug treatment, and the initiation rate recovered 30 to 90 min later. Ataxia telangiectasia cells displayed normal levels of amsacrine-induced DNA strand breaks during stabilization of cleavable complexes but failed to downregulate replicon initiation after exposure to the topoisomerase inhibitor. Thus, inhibition of replicon initiation in response to DNA damage appears to be an active process which requires a gene product which is defective or missing in ataxia telangiectasia cells. In normal human fibroblasts, the inhibition of DNA topoisomerase I by camptothecin produced reversible DNA strand breaks. Transient exposure to this drug also inhibited replicon initiation. These results suggest that the cellular response pathway which downregulates replicon initiation following genotoxic damage may respond to perturbations of chromatin structure which accompany stabilization of topoisomerase-DNA cleavable complexes.

Amsacrine↗
PubMed1990

DNA repair endonuclease activity during synchronous growth of diploid human fibroblasts.

DNA-repair endonuclease activity in response to UV-induced DNA damage was quantified in diploid human fibroblasts after synchronizing cell cultures to selected stages of the cell cycle. Incubation of irradiated cells with aphidicolin, an inhibitor of DNA polymerases alpha and delta, delayed the sealing of repair patches and allowed estimation of rates of strand incision by the repair endonuclease. The apparent Vmax for endonucleolytic incision and Km for substrate utilization were determined by Lineweaver-Burk and Eadie-Hofstee analyses. For cells passing through G1, S or G2, Vmax for reparative incision was, respectively, 7.6, 8.4 and 8.4 breaks/10(10) Da per min, suggesting that there was little variation in incision activity during these cell-cycle phases. The Km values of 2.4-3.1 J/m2 for these cells indicate that the nucleotidyl DNA excision-repair pathway operates with maximal effectiveness after low fluences of UV that are in the shoulder region of survival curves. Fibroblasts in mitosis demonstrated a severe attenuation of reparative incision. Rates of incision were 11% of those seen in G2 cells. Disruption of nuclear structure during mitosis may reduce the effective concentration of endonuclease in the vicinity of damaged chromatin. The extreme condensation of chromatin during mitosis also may restrict the accessibility of reparative endonuclease to sites of DNA damage. Confluence-arrested fibroblasts in G0 expressed endonuclease activity with Vmax of 5.5 breaks/10(10) Da per min and a Km of 5.5 J/m2. The greater condensation of chromatin in quiescent cells may restrict the accessibility of endonuclease to dimers and so explain the elevated Km. When fibroblasts were synchronized by serum-deprivation, little variation in reparative endonuclease activity was discerned as released cells transited from early G1 through late G1 and early S. Proliferating fibroblasts in G1 were shown to express comparatively high numbers of reparative incision events in the absence of aphidicolin which was normally used to inhibit DNA polymerases and hold repair patches open. It was calculated that in G0, S and G2 phase cells, single-strand breaks at sites of repair remained open for 30, 19 and 14 sec, respectively. In G1 phase cells, repair sites remained open for 126 sec. Addition of deoxyribonucleosides to G1 cells reduced this time to 42 sec suggesting that the slower rate of synthesis and ligation of repair patches in G1 was due to a relative deficiency of deoxyribonucleotidyl precursors for DNA polymerase.(ABSTRACT TRUNCATED AT 400 WORDS)

Aphidicolin↗
PubMed1990

Quantitation of mast cells and eosinophils in the bronchial mucosa of symptomatic atopic asthmatics and healthy control subjects using immunohistochemistry.

We have used fiberoptic bronchoscopy to obtain endobronchial biopsies in which mast cells and eosinophils were enumerated using monoclonal antibodies directed against mast cell tryptase (AA1) and the eosinophil cationic protein (EG2). Eleven symptomatic atopic asthmatics treated with beta 2-agonists alone and six normal subjects were studied. Over a period of 2 wk prior to bronchoscopy, patients recorded asthma symptom scores, bronchodilator usage, and twice-daily peak expiratory flow. Five days before bronchoscopy, methacholine responsiveness was assessed. Two biopsies were taken from the subcarinae, one of which was processed into araldite for immunostaining by the streptavidin biotin immunoperoxidase method and the other into Spurr resin for electron microscopy. The number of AA1 staining mast cells present in the bronchial mucosa was not significantly different in the epithelium or submucosa between the asthmatic and the normal subjects. However, in the biopsies from asthmatics, there were significantly greater numbers of EG2-staining eosinophils in the epithelium (median, 1.2/mm versus zero; p less than 0.005) and in the submucosa (median, 50/mm2 versus 1/mm2; p less than 0.001). Electron microscopy showed morphologic features of mast cell and eosinophil degranulation in the asthmatics. No correlation could be established between mast cell or eosinophil numbers and indices of disease activity of PC20 methacholine, which points to the complexity of mechanisms responsible for the symptoms and the airway hyperresponsiveness of asthma.

Adult↗
PubMed1989

Appendicectomy stumps: 'to bury or not to bury'.

A prospective randomized trial of 130 patients was carried out to compare simple ligature with invagination of the appendix stump. There were 64 and 66 patients, respectively, in the two groups and they were well matched for age, sex, weight and severity of appendicitis. One patient in the invagination group developed wound infection but there was no infection in the other group. This difference was not statistically significant (P greater than 0.5) and there was no evidence of adhesive ileus in either group after a mean follow-up period of nine months. We recommend simple ligature of the appendix stump as a safe procedure.

Appendectomy↗
PubMed1988

A comparison of the specificity of phosphatidylcholine synthesis by human fetal lung maintained in either organ or organotypic culture.

Human fetal lung (14-18 weeks gestation) was maintained in either organ or organotypic culture. By 4 days in organ culture or 14 days in organotypic culture, epithelial cells within both culture systems exhibited well-developed apical microvilli and possessed numerous intracellular lamellar bodies characteristic of surfactant phospholipid stores. However, analysis of the pattern of synthesis of individual molecular species of phosphatidylcholine by [14C]choline incorporation and reversed-phase h.p.l.c. showed that this apparent maturation was not paralleled by an increased synthesis of the dipalmitoyl species in either culture system. By contrast, the fractional synthesis of dipalmitoyl phosphatidylcholine, expressed as a percentage of total [14C]choline incorporation, decreased with time in both organ and organotypic culture. Moreover, these fractions were not significantly different from those measured in parallel monolayer cultures of mixed human fetal lung cells that displayed mainly fibroblast morphology. These results suggest that the synthesis pattern of phosphatidylcholine species by lung cells in culture is determined principally by their incubation conditions and not by their state of apparent maturation.

Cells, Cultured↗