Biomedical subjects

A Gustafson

Publications and source records attributed to A Gustafson.

At least 91 records · Page 5Linked to original sources

PubMed1979

Treatment of hyperlipoproteinemia type II with etofibrate.

Seven patients with hyperlipoproteinemia (HLP) type II (four patients with type II A and three patients with type II B), who were experienced to be resistant to hypolipidemic drugs, were treated for 6 months with etofibrate, a double-ester of nicotinic acid and clofibrinic acid, at a dose of 0.3 g t.i.d. Mean serum cholesterol level decreased by up to 18% from a pre-treatment value of 7.7 +/- 1.4 mmol/l. The reduction of serum cholesterol was due both to a decrease in very low density (VLDL) and low density (LDL) lipoprotein cholesteral by 61 and 25%, respectively (after 6 months). Furthermore alpha-LP (HDL) cholesterol increased by 8%, (after 6 months). All seven patients had previously received clofibrate and had obtained a mean decrease in plasma cholesterol by 6%. There was a slight transient increase in S-ASAT and S-ALAT simultaneous with in increase in serum urate. However, these values returned after 3 months to pre-treatment level. No influence on glucose tolerance was recorded. There were no bothersome side effects except a transient discomfort in the form of flushing or acid indigestion which occurred after 1--2 months of treatment with etofibrate.

Body Weight↗

PubMed1979

Treatment of hyperlipoproteinemia (HLP) type II A with a new phenoxy-isobuturic acid derivative, procetofen.

Eleven patients with hyperlipoproteinemia (HLP) type II A, were treated for 3 months with a new compound, a phenoxy-isobuturic acid derivative, procetofen, at a dosage of 100 mg t.i.d. Mean plasma cholesterol decreased after 3 months by 25% from a pretreatment value of 10.3 +/- 0.7 mmol/l (p less than 0.001). The reduction of plasma cholesterol was apparently due not only to a decrease in LDL, as expressed from a marked reduction (15%) of the major LDL apolipoprotein moiety, apolipoprotein B, but also presumably to a decrease in VLDL as reflected from a marked reduction (45%, p less than 0.05) in plasma triglycerides. Furthermore, a marked favourable increase (28%, p less than 0.001) in HDL major apolipoprotein moiety, apolipoprotein A, was observed. No disagreeable side-effects were recorded, except for a skin rash in one patient.

Adult↗

PubMed1978

Release of cyclic AMP from thyroid cells in vitro.

Half lobes of mouse thyroid gland were incubated in vitro with TSH. They released cyclic AMP (cAMP) into the medium in amounts depending on the concentration of TSH. The release of cAMP was greatest during the first hour of incubation then it occurred at a lower rate. With an incubation time of 45 min the medium cAMP levels ranged from 43.0 +/- 11.9 pmole per mg tissue protein for controls to 296.5 +/- 29.2 pmole per mg tissue protein with 5 mU of TSH in the medium. The tissue cAMP level reached a maximum after 15--30 min of incubation with TSH, then it gradually decreased towards control level during 4 h of incubation. With 25 min of incubation the tissue cAMP level was 28.5 +/- 8.8 pmole per mg tissue protein for controls compared to 194.3 +/- 27.0 pmole per mg tissue protein with 5 mU TSH in the incubation medium. The release of thyroxine was of the same order during the later part of the 4 h incubation period compared to the first one. The results illustrate the quantitative importance of cAMP release, and the fact that in the later part of the incubaion period the cell content of cAMP was low while the release of thyroxine remained high.

Animals↗

PubMed1978

Electroimmunoassay, radioimmunoassay, and radial immunodiffusion assay evaluated for quantification of human apolipoprotein B.

We examined three immunoassay techniques for measuring apolipoprotein B in serum and major lipoprotein density fractions from normolipidemic and hyperlipoproteinemic persons, comparing values by electroimmunoassay, radioimmunoassay, and radial immunodiffusion assay with those determined gravimetrically. Electroimmunoassay is faster and simpler than radioimmunoassay, and equally precise (within- and between-assay coefficients of variation for both were 5 and 7%, respectively). All the immunoassays gave results that agreed with those by gravimetry for normolipidemic sera and the corresponding lipoprotein density fractions, but only electroimmunoassay results agreed with those by gravimetry for apolipoprotein B in lipoproteins of d less than 1.019 g/ml isolated from hypertriglyceridemic patients. Concentrations of apolipoprotein B in plasma, determined by electroimmunoassay in a population of normal persons and patients with primary hyperlipoproteinemias, were: normals, 980 +/- 200; type I, 700 +/- 160; type IIa, 2000 +/- 260; type IIb, 2180 +/- 300; type III, 1300 +/- 340; type IV, 1470 +/- 400; and type V, 1550 +/- 390 mg/liter (mean +/- SD). Lipoprotein density fractions from the hyperlipoproteinemic patients each had a characteristic distribution of free and associated forms of lipoprotein family B. The absolute concentration and distribution of apolipoprotein B between the free and associated forms of lipoprotein B may represent a useful indicator of the underlying biochemical defect(s).

Adult↗

PubMed1977

Serum lipids and lipoproteins during abstinence after heavy alcohol consumption in chronic alcoholics.

Serum lipids, liver function tests and liver histology were studied during a withdrawal period in sixty-one male chronic alcoholics with a well-documented earlier clinical history. In these alcoholics with a mean daily ethanol consumption of 340 g during the débauche, the FFA were initially high and decreased during the first week, concomitantly with an increase in serum triglycerides. 38% of the patients had a type IV hyperlipoproteinaemia with elevated serum triglycerides still after 17 days of abstinence. 51% were normolipidaemic at that time. The cholesterol content in the alpha-lipoproteins were initially elevated and normalized during the first week of abstinence. No relationships were observed between serum lipids and liver function tests or degree of liver steatosis or alcohol consumption. The present findings stress the importance of stating the duration of abstinence in studies of biochemical changes after withdrawal.

Adult↗

PubMed1977

Cardaic arrhythmias in chloral hydrate poisoning.

In three patients admitted to hospital after ingestion of an overdose of chloral hydrate, the ECG showed supreventricular and ventricular tachyarrhythmias. The possible mechanism for the arrhythmias may be an enhanced automaticity of supraventricular and ventricular pacemaker cells caused by metabolites of chloral hydrate. The ventricular arrhythmia responded to i.v. treatment with lignocaine in one patient, and to phenytoin in another in whom lignocaine failed to restore a normal sinus rhythm.

Adult↗

PubMed1977

Myocardial scintigraphy as a supplementary diagnostic tool in heart disease.

Myocardial scintigraphy with cesium-131 and thallium-201 was performed in 191 patients. Previous myocardial infarctions localized to the anterior and lateral wall of the left ventricle were correctly diagnosed with both radionuclides. Inferior and posterior infarctions were only detected when thallium was used. In patients with non-informative ECG changes like bundle branch block, non-specific ST-T changes or with atypical symptoms, myocardial imaging made an essential contribution to the establishment of a correct diagnosis. The potential value of myocardial imaging in patients with valvular heart disease and in cardiomyopathy is described.

Adolescent↗

PubMed1977

Cholesterol and DNA content in arterial tissue in severe obesity: their relation to some risk factors for ischaemic heart disease.

Arterial tissue was obtained from twelve severely obese patients during jejuno-ileal by-pass surgery. The arterial DNA content was inversely correlated with the sum of venous glucose values during an oral glucose tolerance test (rs = -0.72). This observation may have implications on the known relationship between decreased glucose tolerance and early manifestations of atherosclerosis.

Adult↗

PubMed1977

Studies in cholestasis of pregnancy. VI. Fatty acid composition of glycero-phospholipids before and after delivery.

Eight pregnant women, complaining of generalized pruritus with lipoprotein-X (LP-X) in their serum and diagnosed as cases of cholestasis of pregnancy (CP)--were studied during pregnancy and after delivery. Ten women with uncomplicated normal pregnancy served as controls. LP-X, liver function tests and relative fatty acid composition of serum lecithin (determined by gas-liquid chromatography, GLC) were followed. The fatty acid composition in liver and serum lecithin is determined by the synthesis pathways of lecithin in the liver. The faster and quantitatively dominating cytidine-diphosphate diglyceride pathway, pathway I, causes the appearance of lecithin with palmitic acid (16:0) in 1-position and oleic (18:1) or linoleic (18:2) acid in 2-position, while pathway II, with methylation of phosphatidyl-ethanolamine (cephalin) preferentially cases the appearance of lecithin with stearic acid (18:0) in 1-position and arachidonic acid (20:4) in 2-position. Pathway I is enchanced by oestrogenic and pathway II by cholestatic influence. During pregnancy women with CP were characterized in their serum lecithin fatty acid composition by a high palmitic (16:0) and a high oleic (18:1) acid content, in agreement with earlier studies. After delivery, in women with prior CP a decrease in palmitic (16:0) and linoleic (18:2) acids and an increase in stearic (18:0) acid, was interpreted as decreased influence on the major lecithin synthesis pathway I and an enhancement of pathway II. In addition, after delivery in the lactating mother, serum lecithin fatty acid composition data revealed an essential fatty acid (EFA) "consumption." It was earlier shown, that women with previous CP (when studied 8--21 months after delivery) had as judged from their serum lecithin fatty acid composition, a "basic metabolic defect," expressing presumably as estrogen enhanced pathway II of liver lecithin synthesis. In the present study, soon after delivery (on day 4--8) women with prior CP showed, however, less pathway II influence than women with a prior normal pregnancy. This was interpreted as a presistence of the cholestatic influence on liver lecithin synthesis pathways at this short time after delivery. Serum lecithin fatty acid composition appears to be a sensitive variable for the evaluation of metabolic influences in the liver.

Adult↗

PubMed1977

Isolation and partial characterization of a glycine- and serine-rich polypeptide from human serum high-density lipoproteins (HDL).

Lately, several minor polypeptides characterized by a high content of glycine and serum have been described in human serum lipoproteins. By column chromatography we have isolated a glycine- and serine-rich polypeptide from totally delipidized high-density lipoproteins, apo-HDL. The partial characterization of this polypeptide by total amino acid composition and by immunology utilizing monospecific antisera to polypeptides of human serum lipoproteins, would indicate a unique polypeptide. This low molecular weight (4900 Daltons) glycine- and serine-rich polypeptide was characterized by a mobility on polyacrylamide gel electrophoresis, similar to that of polypeptide. A-I, a blocked NH2-terminal amino acid and a terminal COOH-fragment consisting of R-Ser-Ala-Gly-Gly. There are similarities between this polypeptide and the protein moiety of a cholesterol ester-rich lipoprotein fraction, HDLsup, obtained by in vitro incubation of HDL subfractions and described in earlier publications by our group. The identity between these two polypeptides, cannot be confirmed by the present study.

Amino Acids↗

PubMed1977

Treatment of oral estramustine phosphate (Estracyt) in prostatic carcinoma: influences on lipid and carbohydrate metabolism.

Estramustine phosphate (Estracyt), a combination of estradiol and nitrogen mustard given to males with prostatic carcinoma, had the same effect on serum lipids, lipoproteins, and serum phosphoglyceride fatty acid composition as ethynyl estradiol (Etivex). The characteristic effects on serum lipids caused by both drugs, i.e., a reduction in serum cholesterol and an increase in serum phospholipids, were apparently expressions for reduced low density lipoproteins and increased alpha-lipoproteins. Serum lecithin fatty acid composition revealed during the administration of both drugs a characteristic increase in palmitic acid (16:0) and a decrease in stearic acid (18:0), interpreted as evidence for a cholestatic, although subclinical, liver involvement. Similar changes have earlier been revealed in women given ethynyl estradiol; however, the increase in serum triglycerides and very low density lipoprotein cholesterol in young women was not duplicated in aged males with prostatic carcinoma. Furthermore, in aged males, the administration of these estrogens did not change carbohydrate metabolism but did produce an increase in adipose tissue lipoprotein lipase.

Adipose Tissue↗

PubMed1976

Studies on an additional pre-beta-lipoprotein, sinking pre-beta (SPB). I. Isolation and characterization.

The occurrence on cellulose acetate and agarose gel electrophoresis of additional bands with the mobility of pre-beta-lipoprotein (LP) has recently been linked to ischemic heart disease (IHD). In the present study, one of these additional pre-beta-LP fractions, earlier designated as 'pre-beta-LP' and now defined on agarose gel electrophoresis, was isolated by preparative ultracentrifugation and gel filtration. The characterization of this pre-beta-1-LP revealed a 'sinking pre-beta-LP' (SPB) of density 1.050-1.080 g/ml. SPB shared its major antigenic determinant with low-density lipoproteins (LDL) and resembled closely LDL with regard to its lipid composition. Specific anti-LP(a) serum confirmed the presence of LP(a) antigen in the purified SPB preparation.

Electrophoresis, Agar Gel↗

PubMed1976

Studies in diabetic pregnancy. I. Serum lipids.

The serum lipid values at different stages of pregnancy in twenty-six pregnany diabetic women attending a special antenatal clinic at the Department of Obstetrics and Gynecology, were compared with the corresponding values in four control series composed of non-diabetic pregnant women. Control series were studied at weeks 10, 22, 34 and after delivery, respectively. Serum triglycerides were higher in the diabetic women at week 10 (p less than 0.01), week 34 (p less than 0.05) and after delivery (p less than 0.05). Furthermore, in the diabetic women, infant birth weights were correlated (r=0.52, p=0.05) with maternal serum triglyceride values at week 31. Women with the highest serum triglyceride values (greater than 250 mg/100 ml) were delivered of infants with a higher birth weight (p less than 0.05) than those women with lower serum triglyceride values (less than 250 mg/100 ml). Intra-uterine deaths (n=4) were not related to maternal serum triglyceride values, but mean blood glucose values (during the whole pregnancy) were higher (p less than 0.001) in mothers with intra-uterine deaths. Elevated plasma free fatty acids (FFA) in the diabetic mother would be a possible cause for elevated serum triglycerides through increased liver triglyceride synthesis, while in the fetus an excess of plasma FFA (passing through the placental barrier) together with normal or elevated plasma insulin would be a likely explanation for increased triglyceride synthesis in adipose tissue and thereby of increased fat depots and body weight.

Birth Weight↗

PubMed1976

Studies on human serum high-density lipoproteins. VI. Studies on a cholesterol ester-releasing reaction in vitro.

High-density lipoproteins (HDL) turn turbid during in vitro incubation, concomitant with the formation of a cholesterol ester-rich lipoprotein, designated HDL-sup. The increase in turbidity (A) formed in relation to incubation time (t) is an asymptotic function: A=Uo(1 - e-k1t), where Uo is the amount of HDL with the property of releasing HDL-sup and k1 the velocity constant of the reaction. The increase in turbidity and formation of HDL-sup was not related to cholesterol ester content of the incubated fraction nor to exogenous factors like bacterial growth. The in vitro incubation was accompanied by a cholesterol esterification with a mean production of 8 nmol cholesterol ester/mg HDL protein, but also by a more pronounced degradation of phosphatidyl choline, 148 nmol/mg HDL protein. These data indicate that the lipid changes are induced by a two-step lecithin:cholesterol acyltransfer (LCAT) reaction. This reaction caused in HDL lipids a consumption of surface material and an increase in 'lipid core', presumably leading to a weakening and disruption of the lipoprotein surface with a recombination of 'lipid core' material in the form of HDL-sup.

Amino Acids↗

PubMed1976

Studies on an additional pre-beta-lipoprotein, sinking pre-beta (SPB). II. Fatty acid composition of lipid moieties.

The appearance of additional lipoprotein fractions with pre-beta-mobility on cellulose acetate and agarose gel electrophoresis has recently been linked with the early occurrence of ischemic heart disease (IHD). One of these fractions, designated sinking pre-beta-lipoprotein (SPB) has been isolated, purified, and identififed as synonymous with LP(a). In the present study, the lipid moieties of this lipoprotein fraction were further characterized as to their fatty acid composition. These were almost identical to those of low-density lipoprotein (LDL) lipid moieties. The acute influence on fatty acid composition of SPB lipid moieties, 5 hr after a linoleic acid-rich test meal, was a 40% increase in triglyceride linoleic acid content and only minor changes in phosphoglyceride fatty acids. Data speak against an actual conversion of chylomicron remnants into SPB but would allow a certain exchange of lipid moiety among chylomicrons, SPB, and LDL. It is therefore suggested that the origin of the SPB presumably synonymous with LP(a) is the same as for LDL: the liver.

Chromatography, Gas↗

PubMed1976

Studies on human serum high-density lipoproteins. V. Isolation and characterization of a cholesterol ester-rich lipoprotein after in vitro incubation.

Purified high-density lipoprotein (HDL), obtained by preparative ultracentrifugation at density 1.063-1.19 g/ml in the cold, were subfractionated by hydroxyl apatite column chromatography. Two of the obtained subfractions (subfractions II and III) turned turbid after incubation at 37 degrees C for 12 h. The turbid material was recovered in the supernatant of D 1.006 g/ml after centriguation at 30,000 g for 2 h. The lipoprotein fraction causing the turbidity was composed of 94% cholesterol ester and 2% apolipoprotein (by weight). On polyacrylamide gel electrophoresis the apolipoprotein moiety appeared as one polypeptide with the electrophoretic mobility of polypeptide A-I, revealed a blocked NH2-terminal amino acid, and had a total amino acid composition that differed from that of A-I and of the arginine-rich polypeptide.

Amino Acids↗

PubMed1976

On the occurrence of lipoprotein-x in non-hemolytic jaundice.

In cholestasis, serum lipids are altered. The alterations could at least partially be ascribed to the occurrence of an abnormal lipoprotein, LP-X. In 103 patients with jaundice, out of whom 16 had extra-hepatic cholestasis, the presence of LP-X was tested and semi-quantificated (by visual grading) utilizing an immunological technique. In extra-hepatic cholestasis, all patients showed LP-X in serum, while in intra-hepatic drug-induced cholestasis 87% revealed this phenomenon. At the initial stage of acute hepatitis, in drug-induced cholestasis, and in extra-hepatic cholestasis, the semi-quantificated LP-X correlated with alkaline phosphatase values. In extra-hepatic cholestasis, LP-X disappeared soon after the obstruction was relieved by operation.

Bilirubin↗

PubMed1976

Acute poisoning with dextropropoxyphene. Clinical symptoms and plasma concentrations.

Out of 14 cases of poisoning assumed to be due to dextropropoxyphene-containing drugs, propoxyphene and its main metabolite norpropoxyphene could be demonstrated in 11. The concentrations of the drugs were determined shortly after admission and then after 2, 4, 6 and 10 hours (in four cases also after 16 hours). The highest plasma concentration of propoxyphene, 0.74 mug/ml, was found in one case of fatal poisoning. Another patient with a plasma concentration of 0.51 mug/ml showed signs of severe respiratory depression but survived after respirator therapy. In the patients with lower plasma concentrations the poisoning had a benign course. In most cases the plasma concentration of norpropoxyphene exceeded that of propoxyphene even in the first blood sample.

Acidosis↗