Search PubMed⌕ Search

Biomedical subjects

K Berg

Publications and source records attributed to K Berg.

At least 451 records · Page 25Linked to original sources
PubMed1980

Degradation of amyloid-related serum protein SAA by a component present in rabbit and human serum.

After incubation of protein SAA-containing rabbit serum at 37 degrees C overnight, the strength of the precipitation reaction against antiserum to SAA was decreased. This was at east partly due to enzymatic degradation of protein SAA. The enzymatic activity was not strongly associated with the SAA-high-density lipoprotein (HDL) complex, since it sedimented in the preparative ultracentrifuge at a density at which the SAA-HDL complex floats. The degrading component was obtained in concentrated form from rabbit and human sera by adsorption to Sepharose 4B. Degradation of human SAA by the human serum component was inhibited with disopropyl fluorophosphate, an inhibitor of serine proteases.

Amyloid↗
PubMed1980

Myofascial pain dysfunction (MPD) syndrome in twins.

The Myofascial Pain Dysfunction Syndrome (MPD) was investigated in 94 twin pairs (21 male pairs and 73 female pairs), who had not been selected with respect to MPD. The frequency of past and/or present symptoms was found to be 10% in males and 27% in females. No differences between monozygous (identical) and dizygous (non-identical) female twins was found in pair-wise concordance rates, the concordance rate being higher than expected to occur by chance in both twin types. The findings are compatible with the view that environmental influences give rise to this specific stress-reaction pattern.

Diseases in Twins↗
PubMed1980

Effect of gemfibrozil on serum lipid levels.

A short term investigation of the effect of Gemfibrozil in 1200 mg daily doses has been carried out in a group of 20 Swedish males, 9 Lp[a+] and 11 Lp[a-]. The effect of 8 weeks of treatment upon serum lipids resembled those found in previous trials, with a significant decrease in serum total cholesterol. In this series, even VLDL cholesterol and apoB levels decreased significantly. With the apparent exception of HDL cholesterol, there was no suggestion that Lp[a+] individuals responded less well to treatment than did Lp[a-] individuals.

Cholesterol↗
PubMed1980

Presence of "free" apoA-I in serum: implications for immunological quantification of HDL and its apoproteins.

Antibodies against purified apoA-I and apoA-II have been produced. Immunological studies revealed that apoA-I exists in serum as apoA-I bound in high density lipoprotein (HDL) particles containing apoA-II, apoC and apoE, in HDL particles deficient in apoA-II, and as apoA-I particles associated with some lipid, referred to as "free" apoA-I. ApoA-II was found only in HDL particles which also contained apoA-I. All apoA-I and apoA-II in the different HDL particles were immunologically detectable without delipidation. The concentration of "free" apoA-I in fresh serum was 10-30% of total apoA-I. "Free" apoA-I had electrophoretic mobility different from the other HDL particles. Following delipidation with 1, 1, 3, 3-tetramethylurea (TMU), or heating at 56 degrees C all apoA-I could be detected as "free" apoA-I. Storage at 37 degrees C for four weeks had a similar but weaker effect. Density gradient ultracentrifugation showed that the different HDL subclasses had different hydrated densities, and apart from differences in the apoprotein composition, they also differed in cholesterol concentration. Quantitative determination of apoA-I bound in HDL, "free" apoA-I, total apoA-I, apoA-II, and of apoA-I following delipidation with TMU, were performed in 100 sera from normal individuals. The correlation coefficient between total apoA-I ("free" plus HDL-bound) and apoA-I following delipidation was 0.81. Regression analysis between total apoA-I and apoA-II yielded a correlation coefficient of 0.43.

Animals↗
PubMed1979

Effect of smoking on serum levels of HDL apoproteins.

Quantitative determination of HDL apoproteins in serum from 97 healthy men showed a significantly lower apoA-I and apoA-II level in smokers than in non-smokers. Also a significant, negative correlation was found between the apoA-I or apoA-II levels, and the number of cigarettes smoked per day.

Adult↗
PubMed1979

High-density lipoprotein as carrier for amyloid-related protein SAA in rabbit serum.

In this study present evidence that SAA is complexed to high density lipoprotein (HDL) in rabbit serum and is co-isolated with HDL apoproteins. The binding of SAA to HDL seems to be quite strong, judged from affinity chromatography experiments. The studies did not reveal any interaction between SAA and albumin, and there was no evidence that SAA could complex to itself. By isolation of HDL apoproteins, SAA seems to behave like other known apoproteins and may be characterized as an apoprotein that is present in normal serum in very low concentration but increases in concentration under different unphysiological circumstances.

Amyloid↗
PubMed1979

Human leucocyte interferon: analysis of effect on MLC and effector cell generation.

Mixed lymphocyte cultures (MLC) showed decreased thymidine incorporation when interferon (IF) had been added to the culture medium. The cell-mediated lympholysis (CML) potential generated in mixed lymphocyte cultures grown in the presence of IF was substantially augmented at a certain concentration range. Highly purified leucocyte IF also had this effect, whereas mock preparations did not. The CML-augmenting property was found in the antiviral fraction after separation of semipurified leucocyte IF (by the method of Dahl & Degree). The possibility that the effects were due to a shift in kinetics after culturing in the presence of IF has been excluded. The killer-enhancing properties of IF did not seem to be due to an enhanced expression of histocompatibility antigens, the selective inhibition of CML suppressor cells, or a change in the specificity of recognized target cells. The results of secondary in vitro MLC-CML experiments, in which primary MLC had been carried out in the presence or absence of IF, indicated that the compound acts (in vitro) through preferential selection of cells that are less sensitive to inhibition by IF and more likely to kill.

Cells, Cultured↗
PubMed1979

Lp(a) phenotypes, other lipoprotein parameters, and a family history of coronary heart disease in middle-aged males.

In a study of 95 presumably healthy, 40-42-year old males from Northen Sweden, the Lp(a) phenotype distribution differed between those who had, and those who did not have one or more close relatives (parent or sib) with coronary heart disease. In the former group, 60% of the males were Lp(a+), as opposed to 28% in the latter group. Thus, in the homogeneous population sample studied, analysis of the normal inherited Lp(a) variation permitted the identification of distinct subpopulations, with respect to familial occurrence of coronary heart disease. None of a series of other parameters distinguished such sub-populations. The results reported are in agreement with our previous finding of a close association between phenotype Lp(a+) and risk of contracting coronary heart disease.

Adult↗
PubMed1979

Confirmation of an influence of the inherited Lp(a) variation on serum insulin and glucose levels.

Previously reported analyses on three different series of people suggested that fasting serum insulin levels are lower in males with (high levels of) serum Lp(a) lipoprotein (Lp(a+)) than in males without detectable Lp(a) lipoprotein (Lp(a-)). The same was observed during an oral glucose tolerance test. Also, blood glucose concentrations tended to be lower in males with high levels of Lp(a) lipoprotein than in those in whose serum no Lp(a) lipoprotein could be detected. In this paper, we present data which appear to confirm the previously reported results. A significant correlation was found between the fasting triglyceride level and the sum of insulin values determined during the oral glucose tolerance test in healthy Lp(a-) but not in Lp(a+) individuals. The present data, together with those previously reported on an effect of the Lp(a) locus on serum lipid levels and on propensity to contract coronary heart disease, indicate that the genetically determined Lp(a) lipoprotein may be of considerable clinical importance.

Adult↗
PubMed1979

Insulin response to an oral glucose load in relation to Lp(a)/pre-beta 1-lipoprotein levels in non-diabetic patients with peripheral vascular disease and in controls.

An oral glucose tolerance test (OGTT) was performed in 21 patients with previously known or recently detected peripheral vascular disease as well as in 16 age-matched controls. The angiographic results and the results in a physiological investigation were used to classify patients with high and low stenosis and normal controls, respectively. No significant differences in mean levels of insulin and blood glucose were found between patients with high and low stenosis, respectively, or between normal controls and (a) the whole group of patients with high stenosis, (b) only those with high stenosis who had not undergone arterial surgery. However, individuals with high amounts of Lp(a) lipoprotein were found to have significantly lower insulin mean levels during the OGTT and an even lower mean fasting level as compared to individuals without detectable Lp(a) lipoprotein. In the group of individuals with high amounts of Lp(a) lipoprotein, the glucose mean levels were also significantly lower, during a part of the OGTT. These findings are in agreement with previous results and suggest that inherited metabolic differences exist between individuals with high and zero or low levels of Lp(a) lipoprotein.

Aged↗