Search PubMed⌕ Search

Biomedical subjects

J Savory

Publications and source records attributed to J Savory.

At least 91 records · Page 5Linked to original sources
PubMed1985

Evaluation of a bromocresol purple method for the determination of albumin adapted to the DuPont aca discrete clinical analyzer.

We evaluated a new method for the determination of albumin on the DuPont aca discrete clinical analyzer that utilized an albumin selective dye, bromocresol purple (BCP). This dye minimizes globulin interference that occurs with bromocresol green (BCG) methods that have long (greater than 30 s) incubation times. Good correlation was observed between the new BCP method and two methods which do not show significant globulin interference: an immunological method and a rapid BCG method. Comparisons with alternate BCG methods (SMA 12/60, SMAC, and the aca) were generally not as good. The albumin results by the BCP method on specimens with elevated globulins were similar to results from the immunological and rapid BCG methods. The reference interval was 34-50 g/L. The between-day coefficient of variation ranged from 0.9 to 3.5% at three evaluation sites on 2 levels of 8 different control materials. The method was linear between 6-70 g/L. No interference was observed from hemoglobin at levels less than or equal to 5.00 g/L or from bilirubin at levels less than 342 mumol/L. Also, no interference was observed from nine common drugs that are known to bind to albumin. These studies show that accuracy, reproducibility and linearity of the BCP albumin method on the aca are acceptable for clinical use.

Autoanalysis↗
PubMed1985

Aluminium toxicity in chronic renal insufficiency.

Aluminium is a ubiquitous element in the environment and has been demonstrated to be toxic, especially in individuals with impaired renal function. Not much is known about the biochemistry of aluminium and the mechanisms of its toxic effects. Most of the interest in aluminium has been in the clinical setting of the haemodialysis unit. Here aluminium toxicity occurs due to contamination of dialysis solutions, and treatment of the patients with aluminium-containing phosphate binding gels. Aluminium has been shown to be the major contributor to the dialysis encephalopathy syndrome and an osteomalacic component of dialysis osteodystrophy. Other clinical disturbances associated with aluminium toxicity are a microcytic anaemia and metastatic extraskeletal calcification. Aluminium overload can be treated effectively by chelation therapy with desferrioxamine and haemodialysis. Aluminium is readily transferred from the dialysate to the patient's bloodstream during haemodialysis. Once transferred, the aluminium is tightly bound to non-dialysable plasma constituents. Very low concentrations of dialysate aluminium in the range of 10-15 micrograms/l are recommended to guard against toxic effects. Very few studies have been directed towards the separation of the various plasma species which bind aluminium. Gel filtration chromatography has been used to identify five major fractions, one of which is of low molecular weight and the others appear to be protein-aluminium complexes. Recommendations on aluminium monitoring have been published and provide 'safe' and toxic concentrations. Also, the frequency of monitoring has been addressed. Major problems exist with the analytical methods for measuring aluminium which result from inaccurate techniques and contamination difficulties. The most widely used analytical technique is electrothermal atomic absorption spectrometry which can provide reliable measurements in the hands of a careful analyst.

Aluminum↗
PubMed1985

Water content of aluminum, dialysis dementia, and osteomalacia.

In the presence of normal renal function, a high concentration of aluminum in drinking water has been implicated as a factor in the etiology of a neurological syndrome in one specific geographical area. The role of aluminum as a toxic agent in other neurological disorders, where renal function is normal, is controversial. Aluminum is absorbed from the gastrointestinal tract and is normally excreted by the kidneys in the urine. In patients with chronic renal failure, aluminum appears to be of proven toxicological importance. In these patients the accumulation of aluminum in tissues causes an encephalopathy (dialysis encephalopathy or dialysis dementia), a specific form of metabolic bone disease (osteomalacic dialysis osteodystrophy), and an anemia and also plays an etiological role in some of the other complications associated with end-stage chronic renal disease. A failure in the normal renal excretory mechanism accounts for the tissue accumulation in chronic renal failure. The majority of chronic renal failure patients who develop aluminum toxicity are on long-term treatment with either hemo- or peritoneal dialysis; some patients develop toxicity who are only on treatment with aluminum-containing phosphate-binding agents. Aluminum in the dialysate appears to be the major source of the metal in chronic renal failure patients who develop aluminum toxicity. The aluminum content of the dialysate depends primarily on the content of the water with which it is prepared; there may be some contribution from the chemicals used in the concentrate which is added to the water. Some domestic tap-water supplies contain aluminum in high concentration, either naturally or because aluminum has been added as a flocculant in the purification process.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1985

Evaluation of equilibrium gel filtration chromatography for the study of protein binding of aluminum in normal and uremic sera.

Normal and uremic serum samples were chromatographed on a gel filtration column and fractions were analyzed for protein and aluminum content. Whereas much of the aluminum in the serum samples eluted with protein, a significant fraction appeared to be associated with low molecular weight species. Analysis of column fractions for aluminum binding by a competitive binding assay indicated no aluminum-binding serum constituents in these later eluting fractions. Uremic serum appeared, however, to contain aluminum-binding constituents of a lower molecular weight than in normal serum.

Aluminum↗
PubMed1984

Quantitative study of aluminum binding to human serum albumin and transferrin by a chelex competitive binding assay.

Binding of aluminum to human serum albumin and transferrin was investigated using a competitive binding assay incorporating a cation exchange resin, chelex. Both albumin and transferrin were found to produce linear Scatchard plots of aluminum binding data over the aluminum and protein concentration ranges found in humans. Binding constants measured for albumin and transferrin were 1.96 and 0.515 microM, respectively.

Aluminum↗
PubMed1984

Acute electrophysiologic effects of bethanidine sulfate in patients with ventricular tachycardia or fibrillation.

Ten patients with a history of ventricular tachycardia or ventricular fibrillation underwent electrophysiologic study with programmed stimulation before and 90 minutes after oral administration of bethanidine sulfate, 20 mg/kg. Mean plasma bethanidine concentration was 2.62 +/- 2.2 (+/- SD) micrograms/ml at the start of repeat testing. This dose of bethanidine produced no effect on sinus node function, atrioventricular conduction, or atrial or ventricular refractoriness. Ventricular tachycardia or fibrillation, inducible in all patients during the control study, could still be initiated by ventricular stimulation in 9 of 10 patients after bethanidine. Bethanidine suppressed the ability to initiate an arrhythmia in one patient with ventricular fibrillation during control stimulation. Orthostatic hypotension was seen in all patients despite pretreatment with the tricyclic antidepressant, protriptyline, 15 mg every 8 hours. The results suggest that bethanidine has few electrophysiologic effects and is of limited efficacy during electrophysiologic testing in patients with life-threatening ventricular arrhythmias.

Aged↗
PubMed1984

Electrothermal atomic absorption spectrometric determination of aluminum in serum with a new technique for protein precipitation.

We have studied the electrothermal atomic absorption measurement of aluminum in serum samples by direct analysis with standard additions and the use of a matrix modifier. We have also measured aluminum by analysis of the supernate after pretreatment of serum with concentrated nitric acid to precipitate proteins, and have compared the results obtained by these two techniques. Both appear to eliminate interferences arising from the serum matrix. We quantified the aluminum by utilizing a stabilized temperature (L'vov) platform. Within-run precision (CV) for the standard-additions method was 16.6% (means = 6.5 micrograms/L) and 6.0% (means = 86.8 micrograms/L) and for the protein precipitation method was 10.1% (means = 10.9 micrograms/L) and 4.2% (means = 88.5 micrograms/L). Linearity of the standard curve extended from 0 to 120 micrograms/L for the standard-additions method and from 0 to 100 micrograms/L for the protein precipitation method. Samples from 38 patients were analyzed by both techniques, and linear regression analysis yielded the equation y (protein precipitation) = 1.02 X (standard additions) + 2.04.

Aluminum↗
PubMed1984

Improved liquid-chromatographic determination of 3-methoxy-4-hydroxyphenylethyleneglycol in urine with electrochemical detection.

In this improved method for quantifying 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) in urine, after a multistep extraction of MHPG and internal standard (iso-MHPG) from 3.0 mL of urine, the compounds are separated on a C18 reversed-phase column and quantified by use of an electro-chemical detector. The isocratic chromatographic separation takes about 16 min. The mobile phase is phosphate buffer/acetonitrile (88/12 by vol), the flow rate 0.7 mL/min. Recycling the mobile phase and automating the sample injection make possible the unattended assay of more than 70 samples per day. The within-run precision of the method is excellent (CV 1.8%) at a mean concentration of 1.1 mg/L.

Antidepressive Agents↗
PubMed1984

Specific affinity-chromatographic measurement of glycated hemoglobins in uremic patients.

The clinical utility of glycated hemoglobin measurements in renal failure is controversial, given numerous earlier studies showing no correlation between glycated hemoglobin and other indicators of blood glucose control in uremic subjects. This problem is attributable, in part, to analytical interferences from carbamylated hemoglobins. We report use of a specific affinity method to measure glycated hemoglobins in a group of uremic patients, diabetic and nondiabetic, undergoing treatment by continuous ambulatory peritoneal dialysis. Concentrations of glycated hemoglobins correlated significantly with values for fasting plasma glucose (r = 0.52, n = 17, p less than 0.05) in these patients and with mean glucose measurements in five diabetic patients who used home glucose monitoring (r = 0.91, p less than 0.05). Contrary to studies with ion-exchange chromatography, our measurements of glycated hemoglobin showed no positive correlation with concentrations of urea in serum. In a separate group of patients, we found that hemodialysis sessions produced no acute effect on glycated hemoglobin. Measurements of glycated hemoglobins by analytically specific methods may thus better reflect long-term control of blood glucose in renal dialysis.

Blood Glucose↗
PubMed1983

Measurement of plasma prostaglandin E2 using capillary gas chromatography negative ion chemical ionization mass spectrometry.

A stable isotope dilution assay for the measurement of plasma prostaglandin E2 (PGE2) employing capillary column gas chromatography-negative ion chemical ionization mass spectrometry (GC-NICIMS) is described. PGE2 was extracted from plasma using C18 and silica SEP-PAKS. Further purification and separation was accomplished by thin layer chromatography. The prostaglandin was analyzed as its pentafluorobenzyl ester-methoxime-trimethyl-silyl ether, using fragment ions at m/e 524 (protium) and m/e 528 (deuterium) for quantitation. The mean plasma concentration of PGE2 determined in 8 healthy volunteers was 2.8 +/- 2.0 pg/ml.

Adult↗
PubMed1983

Determination of bethanidine in plasma by liquid-chromatography with a microbore reversed-phase column.

In this novel method for quantifying bethanidine in plasma, after a multi-step extraction of bethanidine and internal standard from 2.0 mL of plasma, the drugs are separated on a "microbore" C18 reversed-phase column and quantified by their ultraviolet absorbance at 210 nm. The isocratic chromatographic separation takes about 15 min with use of an ion-pairing regent in the mobile phase (acetate buffer/acetonitrile, 9/1 by vol) and a flow rate of 0.25 mL/min. Sensitivity is increased relative to conventional columns, and solvent consumption is reduced by 90%. The standard curve is linear to at least 5 mg/L, and the detection limit is 0.02 mg/L. The within-run precision of the method is excellent (CV 4%) at a midrange concentration of 1.25 mg/L.

Bethanidine↗