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Biomedical subjects

P E Langton

Publications and source records attributed to P E Langton.

7 recordsLinked to original sources
PubMed2001

A simple assay for a human serum phospholipase A2 that is associated with high-density lipoproteins.

Phospholipase A2 (PLA2) activity is usually assayed with expensive radioactive or chromogenic substrates unsuitable for performing large numbers of assays. We have designed a simple microplate assay for human serum PLA2 using the chromogenic substrate 4-nitro-3-octanoyloxy-benzoic acid. Using this substrate, serum PLA2 activity was similar to that measured with the previously characterized chromogenic phospholipid substrate 1,2-bis-heptanoylthio-glycerophosphocholine. However, the assay described here appears to be more sensitive. The mean PLA2 activity in serum from healthy volunteers (n = 30) measured by this assay was 10.4 +/- 1.6 micromol x h(-1) x ml(-1). The assay is reproducible and is suitable for the analysis of large numbers of samples in a clinical setting. We have also demonstrated that 94% of the PLA2 activity in normal human serum is associated with high-density lipoproteins and that serum PLA2 activity is positively correlated with the lipoprotein parameters total triglyceride (P < 0.0001), total cholesterol (P < 0.0001), and atherogenic index (P = 0.008). The serum PLA2 activity was calcium dependent and was inhibited by the serine protease inhibitor 3,4-dichloroisocoumarin (EC(50) = 0.4 mM). The PLA2 activity characterized here is unlikely to be due to plasma platelet-activating factor acetylhydrolase or low molecular weight His-Asp sPLA2, and may represent a new sPLA2 type.

Chromatography, Gel↗
PubMed2000

Changing the site of delivery of thrombolytic treatment for acute myocardial infarction from the coronary care unit to the emergency department greatly reduces door to needle time.

OBJECTIVE: To quantify the change in door to needle time when delivery of thrombolytic treatment of acute myocardial infarction was changed from the coronary care unit to the emergency department. DESIGN: A comparative observational study using prospectively collected data. SETTING: Coronary care unit and emergency department of an Australian teaching hospital. PARTICIPANTS: 89 patients receiving thrombolysis in coronary care unit between June 1994 and January 1996, and 100 patients treated in the emergency department between April 1997 and May 1998. INTERVENTIONS: From April 1997, by agreement between cardiology and emergency medicine, all patients with acute myocardial infarction receiving thrombolysis were treated by emergency physicians in the emergency department. MAIN OUTCOME MEASURE: Door to needle time measured from time of arrival at the hospital to start of thrombolysis. Other outcomes included pain to needle time and mortality. RESULTS: Median door to needle times were less for patients treated in the emergency department than in the coronary care unit (37 minutes, 95% confidence interval (CI) 33 to 44 v 80 minutes, 95% CI 70 to 89, respectively; p < 0.0001). Door to needle time was under 60 minutes in 83% of emergency department patients and 26% of coronary care unit patients (57% difference, 95% CI 45% to 69%; p < 0.0001). Median pain to needle time was less for emergency department patients than for coronary care unit patients (161 minutes, 95% CI 142 to 177 v 195 minutes, 95% CI 180 to 209; p = 0.004); times of less than 90 minutes occurred in 18% of emergency department patients v 1% of coronary care unit patients (17% difference, 95% CI 9% to 25%; p < 0.05). Overall mortality was similar in patients treated in the emergency department and the coronary care unit. CONCLUSIONS: With a collaborative interdepartmental approach, thrombolytic treatment of acute myocardial infarction was more rapid in the emergency department, without compromising patient safety. This should improve the outcome in patients with infarcts treated with thrombolytic agents.

Adult↗
PubMed1999

Differential expression of neutrophil adhesion molecules during coronary artery surgery with cardiopulmonary bypass.

BACKGROUND: Activation of neutrophil adhesion molecules and subsequent neutrophil adhesion to vascular endothelium are key events initiating inflammatory organ dysfunction after cardiopulmonary bypass and ischemic reperfusion. OBJECTIVES: We sought to characterize neutrophil integrin CD11b and L-selectin activation associated with coronary artery bypass graft surgery and to determine whether neutrophil activation contributes to their sequestration on postbypass reperfusion. METHODS: Twenty patients undergoing routine coronary artery bypass were studied. Heparinized whole blood was simultaneously sampled from a central venous line, aorta, coronary sinus, and right and left atrium before, during, and up to 20 minutes after cardiopulmonary bypass. Neutrophil counts were obtained, and neutrophil CD11b and L-selectin expression was determined by flow cytometric analysis in whole blood. RESULTS: CD11b expression on circulating neutrophils increased during cardiopulmonary bypass, peaking at 145% of baseline level after release of the aortic clamp and then declined by 20 minutes after bypass (analysis of variance, P =.003). No change in neutrophil L-selectin expression was observed during cardiopulmonary bypass. Neutrophils responded to ex vivo stimulation by C5a and leukotriene B(4) during cardiopulmonary bypass but not at 24 hours after the operation. After reperfusion, neutrophil loss, but not local activation, was demonstrated in the coronary and pulmonary circulations. CONCLUSIONS: Upregulated CD11b expression on neutrophils is likely to contribute to neutrophil sequestration in the heart and lungs after bypass, but neutrophil activation may be limited by their reduced responsiveness to agonist stimulation. CD11b represents a potential therapeutic target for diminishing inflammation after cardiac operations.

CD11 Antigens↗