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W Richmond

Publications and source records attributed to W Richmond.

65 records · Page 4Linked to original sources

Use of cholesterol oxidase for assay of total and free cholesterol in serum by continuous-flow analysis.

Idescribe an assay for total cholesterol in serum, with use of the AutoAnalyzer ii (Technicon), in which cholesterol esters are saponified by alkali, cholesterol is held in aqueous micellar solution with a surfactant (Triton X-100) and oxidized by cholesterol oxidase, and the hydrogen peroxide produced is measured by chelation with Ti4+ and xylenol orange. An assay for free cholesterol in serum, based on similar principles, is also described, and the two can be run simultaneously on a dual-channel AutoAnalyzer II. Standard solutions of cholesterol in isopropanol have poorer carryover characteristics than sera, and therefore do not reach the same continuous-flow steady state as sera of equivalent concentrations. Consequent potential calibration errors are avoided by using micellar solutions of cholesterol containing albumin for standardization. The formation of cholesterol peroxide in solutions of cholesterol in isopropanol is demonstrated, and this constitutes another potential source of error in the calibration of enzymic cholesterol assays. In analyzing patients' sera, results of the total cholesterol assay correlate well with those of a mechanized method in which cholesterol esterase and cholesterol oxidase are used; an automated Abell method, calibrated with solutions of cholesterol in isopropanol, gave slightly higher values. Determinations of the ratio of free cholesterol to total cholesterol by our automated cholesterol exidase assays given values that agree well with published results in which digitonin precipitation is used.

Autoanalysis↗

Insulin resistance, cardiovascular risk factors and ultrasonically measured early arterial disease in normotensive Type 2 diabetic subjects.

BACKGROUND: The objective of the study was to examine the relationship between serum fasting insulin, insulin sensitivity S(i), cardiovascular risk factors, and asymptomatic early atherosclerosis in normotensive Type 2 diabetic subjects. METHODS: Specific insulin was measured using an enzyme-linked immunosorbent assay (ELISA) and insulin sensitivity was assessed with an insulin-modified frequently sampled intravenous glucose tolerance test (FSIVGTT). Early atherosclerotic change was assessed using carotid intima media thickness (IMT) and an arterial ultrasound score (AUS) measured by high-resolution B-mode ultrasound. RESULTS: On bivariate analysis, there was a positive correlation between S(i) and high density lipoprotein (HDL) cholesterol (r(s)=0.27, p<0.05), and a negative correlation between S(i) and body mass index (BMI) (r(s)=-0.42, p<0.001), HbA(1c) (r(s)=-0.29, p<0.05) and serum triglyceride (r(s)=-0.30, p<0.05). There was a positive correlation between carotid IMT and age (r(s)=0.41, p<0.0005), and a positive association with male sex (p<0.0001) as well as with smoking (p<0.0001). However, we found no correlation between carotid IMT and fasting specific insulin (r(s)=-0.04) or S(i) (r(s)=-0.08). On multiple regression analyses, only age and serum triglycerides appeared to be significant independent variables with respect to carotid IMT whereas age, male sex and smoking emerged jointly significant with respect to AUS. There were no independent associations between carotid IMT or AUS with other variables including using either fasting specific insulin or S(i) as markers on insulin resistance separately. CONCLUSION: Carotid IMT and AUS in Type 2 diabetes are closely associated with age, male sex and smoking. The relationships between serum insulin and insulin resistance with ultrasonically measured early arterial disease in Type 2 diabetes remain unclear.

Analysis of Variance↗

Left atrial receptor inhibition of cardiac efferent vagal activity in the dog.

1. The tachycardia produced by atrial receptor stimulation has been reported to be 'solely' due to an increased sympathetic activity, but not inhibitable by propranolol. We examined the effect of left atrial balloon inflation in chloralose-anaesthetized dogs on heart rate with and without propranolol (1.0 mg/kg) and on the activity in single cardiac efferent fibres of the vagus nerve. 2. Propranolol reduced the cardiac response to balloon inflation by one-third, but did not abolish the tachycardia. Efferent cardiac vagal activity was 3.8 +/- 0.4 spikes/s and 2.3 +/- 0.7 spikes/s prior to and during balloon inflation respectively. 3. It was concluded that the left atrial receptors produce a tachycardia by decreasing cardiac parasympathetic and increasing sympathetic efferent activities.

Action Potentials↗

Blood rheology and cardiovascular risk factors in type 1 diabetes: relationship with microalbuminuria.

Whole blood and plasma viscosity, erythrocyte aggregation and deformability, plasma fibrinogen, lipids, lipoproteins, apolipoproteins, and measures of blood glucose control were compared between 21 Type 1 diabetic patients with microalbuminuria (overnight albumin excretion rate 30-200 micrograms min-1) and 21 patients with albumin excretion below this range matched for age, sex, and duration of diabetes. Patients with microalbuminuria had significantly higher glycosylated haemoglobin (9.4 +/- 1.6 (+/- SD) vs 7.9 +/- 1.8% (normal range 5.0 to 7.6%)), total-cholesterol (5.6 +/- 1.1 vs 4.6 +/- 1.3 mmol l-1), apolipoprotein B (0.82 +/- 0.21 vs 0.66 +/- 0.14 g l-1), and apolipoprotein B:A1 ratio (0.58 +/- 0.18 vs 0.50 +/- 0.15) than those without microalbuminuria (all p less than 0.05). HDL-cholesterol was also raised (1.71 +/- 0.46 vs 1.43 +/- 0.37 mmol l-1, p less than 0.05). Lipoprotein(a) concentration was possibly higher in the microalbuminuric group (median (95% Cl) 105 (82-140) vs 72 (52-114) mg l-1, p = 0.06). No differences were seen in any of the rheological measurements. These results confirm the presence of potentially atherogenic lipoprotein changes in Type 1 diabetic patients with microalbuminuria, but suggest that altered blood rheology does not predate the development of nephropathy.

Adult↗