PubMed Health⌕ Search

Biomedical subjects

A Gustafson

Publications and source records attributed to A Gustafson.

At least 37 records · Page 2Linked to original sources
PubMed1989

Occupational lead exposure and pituitary function.

Twenty-five moderately exposed lead workers (mean blood-lead level 1.9 mumol/l) had lower plasma levels of follicle stimulating hormone than 25 individually matched controls without occupational lead exposure (blood-lead level 0.2 mumol/l). In addition, the ten most heavily exposed individuals had higher levels of thyroid stimulating hormone, and the 14 workers under the age of 40 had decreased plasma levels of luteinizing hormone and serum levels of cortisol, as compared to the controls. All values were within "normal" reference limits. There was no significant change of the plasma testosterone level. These data indicate a complex effect on the endocrine system by moderate lead exposure, possibly mediated by changes at the hypothalamic-pituitary level. Besides the effect on hormone levels, there was also a decrease in plasma selenium level for the lead exposed workers.

Adult↗
PubMed1989

Studies on blood viscosity during the menstrual cycle and in the postmenopausal period in healthy women.

Blood viscosity was measured in 14 healthy, menstruating women, aged 17-51 years and in 10 healthy, postmenopausal women, aged 55-64 years. The fertile women were studied once a week during a normal menstrual cycle and the postmenopausal women twice with an interval of 2 weeks. Blood viscosity was measured at natural hematocrit as well as at hematocrit 45%. In the postmenopausal women no changes in blood viscosity were found. In the fertile women, blood viscosity at hematocrit 45% was lowest at the start of the menstrual bleeding and increased to a peak at day 7 (p less than 0.01), with a similar pattern when measured at natural hematocrit. Plasma viscosity also had its lowest value at the onset of menstrual bleeding, increasing to a maximum at day 21. Changes in plasma triglycerides, but not in fibrinogen or cholesterol, seemed to contribute to this increase. Plasma factors only partly explained the variations in blood viscosity, and changes in red cell properties were also found to be of importance. The clinical significance of these rheological changes remains to be established, but at least theoretically there may be an increased risk for thromboembolism, e.g. at surgery, during days 5-15 of the cycle. In studies on blood flow and rheological conditions in fertile women, it seems advisable to standardize for time in the menstrual cycle.

Adult↗
PubMed1988

Diagnosis and management of acute aortic dissection, clinical and radiological follow-up.

A clinical series of acute aortic dissections is presented. Twenty cases were of type A and 10 of type B. Acute severe chest pain was common, in type A also blood pressure difference between the arms and aortic regurgitation. The diagnosis was established by echocardiography, computerized tomography and/or aortography. Antihypertensive therapy was instituted immediately after diagnosis and was in type A cases followed by acute surgery unless definite contraindications existed. Of 14 surgically treated type A patients 13 survived the operation. On follow-up 1.5-3.5 years later, 12 patients were still alive and doing well, but the false channel remained open in all cases where it had not been resected totally. Only one of six conservatively treated type A patients survived. Type B dissections were operated on only if conservative therapy failed. Four of five conservatively and two of five surgically treated type B patients survived.

Adult↗
PubMed1988

Determinants of kallikrein proteolysis of apolipoprotein B-100 in human blood plasma.

The formation of apolipoprotein B-74, a fragment of apolipoprotein B-100, in blood plasma in vitro is shown to occur only at temperatures below 15 degrees C, and is promoted by exposure to glass and other surfaces known to activate factor XII. Removal of C-I esterase inhibitor from plasma permits formation of apolipoprotein B-74 at room temperature. These observations are consistent with conversion of prekallikrein to kallikrein by factor XII, and with evidence that kallikrein proteolysis in vitro is activated in the cold by alteration of its binding to C-I esterase inhibitor. Since the two proteolytic fragments of apolipoprotein B-100 produced by kallikrein digestion are identical to apolipoproteins B-74 and B-26, it is concluded that apolipoproteins B-74 and B-26 are in-vitro products produced in low density lipoproteins of normal plasma in the cold by kallikrein.

Anticoagulants↗
PubMed1988

Lipid metabolism in patients with chronic renal failure in the predialytic phase.

CRF is accompanied by characteristic alterations of lipoprotein metabolism with a retarded catabolism of triglyceride-rich lipoproteins as a prominent feature. Further investigation of the lipoprotein profile of CRF could provide information on the fundamental pathophysiological processes responsible for these disturbances and their possible clinical significance.

Apolipoproteins↗
PubMed1988

Fatty acid composition in plasma and platelet phospholipid in hypothyroid patients before and after 1-thyroxine substitution.

The relative concentration of fatty acids in plasma and platelet phospholipids (phosphatidylcholine) was determined in 11 patients with overt hypothyroidism (S-TSH greater than 80 mU/l) before and after 1-thyroxine substitution therapy. During therapy, the linoleic (C18:2) acid content decreased (p less than 0.01) whereas longer and more desaturated fatty acids, including arachidonic (C20:4) acid, increased (p less than 0.01) in plasma phospholipids. Also, oleic (C18:1) acid decreased (p less than 0.01) while the major saturated fatty acids, palmitic (C16:0) and stearic (C18:0) acids, were stable. In platelet membrane phospholipids, a similar reciprocal change in the relative content of linoleic (C18:2) and arachidonic (C20:4) acids, respectively, occurred. In plasma, these changes in linoleic and arachidonic acids were found to be inversely correlated (r = 0.56, p less than 0.05). The change in the linoleic acid content in plasma was also correlated to that in platelets (r = 0.64, p less than 0.05). Thus, we have found that thyroid hormones positively influence the conversion of linoleic acid to longer and more polyunsaturated fatty acids in a way that affects fatty acid composition not only in plasma but also in platelet membrane phospholipids.

Adult↗
PubMed1987

Small effect on plasma selenium level by occupational lead exposure.

Selenium level in plasma (P-Se) was slightly, but statistically significantly (2p = 0.02) lower in 25 lead-exposed secondary smelter workers (P-Se 1.09 +/- 0.02 mumol l-1, mean +/- SEM; blood lead level, B-Pb, 1.9 +/- 0.1 mumol l-1) than in 25 matched controls (P-Se 1.16 +/- 0.03 mumol l-1; B-Pb 0.2 +/- 0.01 mumol l-1). Further, there was a significant negative (2p = 0.02) correlation (r = -0.33) between B-Pb and P-Se. The data indicate a minor interaction, in humans, between occupational lead exposure and selenium status.

Adult↗
PubMed1987

Serum apolipoprotein profile of patients with chronic renal failure.

Serum concentrations of apolipoproteins A-I, A-II, B, C-I, C-II, C-III and E were determined by electroimmunoassay in 56 patients with chronic renal failure (CRF) in the predialytic phase. The results were compared with those obtained in asymptomatic normolipidemic subjects, patients with type IV hyperlipoproteinemia, and patients with type II diabetes mellitus. CRF patients had reduced concentrations of ApoA-I and ApoA-II, normal levels of ApoB and ApoC-I, and increased concentrations of ApoC-II and, in particular, of ApoC-III. There was a significant reduction in the levels of ApoE, especially in male patients. In comparison with type IV, hyperlipoproteinemic patients, CRF patients had lower concentrations of ApoA-I, ApoA-II, ApoB, ApoC-I and, particularly, ApoE; there was no difference in ApoC-III levels reflecting the hypertriglyceridemia common to both disorders. Similar but less marked differences were also found in comparison with type II diabetics. The findings suggest that in CRF, the accumulation of ApoC-III-enriched lipoprotein particles accompanied by a moderate hypertriglyceridemia may be caused more probably by an impaired catabolism than overproduction of triglyceride-rich lipoproteins. CRF patients with vascular disease tended to have higher serum concentrations of triglycerides, cholesterol and ApoB and lower ApoA-I/ApoC-III and ApoA-I/ApoB ratios than patients without vascular disease.

Adult↗
PubMed1987

Reduced high density lipoproteins as a risk factor after acute myocardial infarction.

In a group of normocholesterolemic, non-diabetic middle-aged males surviving an acute myocardial infarction for 4 +/- 2 years (mean +/- SD), we have previously described a low apolipoprotein A-I and a deficient fibrinolytic activity as two major characteristics. In the present study we have followed morbidity and mortality risk factors for five years in these males. Mortality was 40% in a hypertensive group and 16% in a normotensive group. In the normotensive group mortality was related to reinfarction. Furthermore, patients with a poor prognosis in the normotensive group had lower high density lipoprotein (HDL) cholesterol and lower apolipoprotein A-I concentration in plasma than patients with a good prognosis. Unexpectedly, in the hypertensive group death was related to a low (p less than 0.05) cortisol concentration in urine. It is concluded that a low HDL level may be a bad prognostic sign in males who have sustained an acute myocardial infarction and show no evidence of other risk factors, such as diabetes, hypercholesterolemia or hypertension.

Apolipoprotein A-I↗
PubMed1986

Scission of human apolipoprotein B-100 by kallikrein: characterization of the cleavage site.

Low density lipoprotein (LDL) from human plasma was digested with the specific endoprotease, kallikrein. Apolipoprotein B-100, the protein moiety of LDL, was cleaved by kallikrein into two fragments (K1 and K2) which we have compared to the naturally occurring fragments, B-74 and B-26. We have found that K1 and K2 precisely match B-74 and B-26 with respect to molecular weight, stoichiometry, and amino terminal amino acid sequence. These findings provide strong evidence that kallikrein is the agent responsible for the formation of B-74 and B-26 in human LDL.

Amino Acid Sequence↗
PubMed1986

Influence of treatment with diethylstilbestrol for carcinoma of prostate on platelet aggregation and plasma lipoproteins.

Treatment of prostatic carcinoma with estrogens is accompanied by an increased risk for thromboembolic and cardiovascular complications. The underlying mechanisms are still unknown. Patients treated with diethylstilbestrol (DES) were compared with patients given no estrogen treatment regarding factors (platelet aggregation in vitro and plasma lipoproteins) that have been suggested to contribute to increased thrombogenesis and cardiovascular risk. The results do not show any increase in in vitro platelet aggregation in patients treated with DES compared with those given no treatment. This indicates that hyperaggregability does not contribute to the increased incidence in thromboembolic events seen in DES-treated patients. This is in contrast to the increased platelet aggregation previously described in patients treated with polyestradiolphosphate + etinylestradiol. The changes in plasma lipoproteins observed during DES-treatment are generally considered beneficial from an atherogenic point of view and do not appear to cause the elevated incidence of cardiovascular disease in these patients.

Aged↗
PubMed1986

Plasma lipoproteins and fatty acid composition during a moderate eicosapentaenoic acid diet.

The effect of a diet rich in marine fatty acids, especially eicosapentaenoic acid, on plasma lipids (total plasma cholesterol, HDL cholesterol, total triglycerides and apolipoproteins A and B) and fatty acid composition in plasma phosphatidylcholine (PC) was studied in 10 healthy men. They were maintained for 11 weeks on their normal diet which was partly replaced by 150-200 g of fatty fish per day. In the same individuals this diet had previously caused a delay in primary haemostasis and a decrease in platelet aggregability similar to that caused by acetylsalicylic acid, a known inhibitor of thromboxane A2 formation. Apart from its effect on haemostasis, the fish diet substantially reduced serum triglycerides (by 43%, p less than 0.01) but caused no changes in total plasma or HDL cholesterol or apolipoproteins A and B. After three weeks on the diet the proportion of plasma PC omega-3 polyunsaturated fatty acids increased (C20:5 and C22:6) and omega-6 fatty acids decreased (C18:2 and C20:3). The relative plasma PC content of arachidonic acid was unaffected throughout. These alterations in plasma PC fatty acid composition were principally in accordance with those seen in platelet membrane PC. There was a linear correlation between the content of omega-3 and of omega-6 fatty acids in plasma PC with that of platelet PC as well as in predominate individual fatty acids of the two series. Six weeks after the volunteers had resumed their usual diet, total triglycerides and the fatty acid composition of plasma PC had returned to the original state.

Adult↗
PubMed1985

Stimulation of cyclic adenosine 3',5'-monophosphate formation in rabbit choroid plexus by beta-receptor agonists and vasoactive intestinal polypeptide.

The formation of cyclic adenosine 3',5'-monophosphate (cAMP) was determined in blood-free choroid plexus homogenates from all ventricles of rabbit using a competitive protein binding technique. Previous stimulation of the intact plexus tissue in vitro with sympathomimetic drugs or vasoactive intestinal polypeptide (VIP) leads to increased local synthesis of cAMP. Tests with selective beta-receptor agonists and antagonists suggested that beta 1-receptors predominate, which is consistent with studies of sympathomimetic effects on cerebrospinal fluid production in vivo.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

Apolipoproteins A-I, A-II and E in cholestatic liver disease.

Apolipoproteins A-I, A-II and E were determined in the plasma of nine patients (five females, four males) with cholestatic liver disease (eight patients with primary biliary cirrhosis and one patient with sclerosing cholangitis). Plasma concentrations were measured by electroimmunoassay in the fasting state, postprandially after ingestion of either 100 g fat as whipping cream or a light mixed meal with or without addition of wheat fibre. Concentrations of apolipoproteins A-I and A-II were low in patients with cholestatic liver disease and A-I levels correlated inversely with the severity of liver disease as measured by bilirubin levels (r = -0.66). No changes in plasma apolipoprotein A-I, A-II or E concentrations occurred postprandially. There was an inverse correlation between plasma concentrations of apolipoproteins A-I and E (p less than 0.05, r = -0.68). A close relation existed between the ratio of apolipoprotein E to apolipoprotein A-I and plasma bile salt concentration (r = 0.80, p less than 0.01) and serum bilirubin (r = 0.76, p less than 0.01). This implies that in cholestatic liver disease apolipoprotein E and A-I levels reflect the degree of cholestasis.

Adult↗