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Biomedical subjects

K Berg

Publications and source records attributed to K Berg.

At least 487 records · Page 27Linked to original sources
PubMed1977

Interaction of isolated Lp(a) lipoprotein with calcium ions and glycosaminoglycans in vitro.

The interaction between the lipoprotein carrying the Lp(a) antigen, i.e. the Lp(a) lipoprotein, and agarose gels substituted with glycosaminoglycans, as well as the precipitation of the Lp(a) lipoprotein by Ca++ were studied. Comparisons between Lp(a) lipoprotein and other serum lipoproteins were conducted. Very low density lipoprotein (VLDL) and low density lipoprotein (LDL) were bound to the tested glycosaminoglycans at low ionic strength of sodium chloride, but no binding was found with the Lp(a) lipoprotein. However, Ca++ as a divalent buffer cation gave a precipitating Ca++-Lp(a) lipoprotein complex even at a physiological Ca++ concentration. VLDL and LDL were not precipitated under these conditions. These findings may be of interest in relation to the previously reported higher frequency of the phenotype Lp(a+) in subjects with coronary heart disease.

Agar↗
PubMed1977

Leukaemia-associated antigen (LAA) in proliferative blood disorders.

Serum leukaemia associated antigen (LAA) was found in 41-75% of patients with acute leukaemia or chronic myelogenous leukaemia, but in only 12% of persons suffering from chronic lymphocytic leukaemia. LAA was present in detectable amounts in 1% of healthy blood donors. Thus LAA is truly leukaemia associated rather than leukaemia specific. Occurrence of LAA in the serum of a leukaemia patient may signal a serious turn of the disease.

Adolescent↗
PubMed1977

Human leukaemia associated antigen (LAA): occurrence and characteristics.

Serum leukaemia-associated antigen (LAA) is identified as an oncofetal antigen (or antigens) since it is present in fetal liver and in amniotic fluid. Although it is mainly found in patients with proliferative haematological disorders, particularly acute leukaemias and chronic myelogenous leukaemia, LAA is occasionally present in sera from healthy people. In protein fractionation experiments, LAA behaves as a distinct population of molecules and has the characteristics of an alpha2-beta-globulin, not carrying any lipids. The origin of LAA in haematological disorders is unknown. Its presence does not correlate with high white blood cell count, although antibody to LAA has been raised in animals injected with blast cells from leukaemia patients. LAA is distinct from alpha-fetoprotein, and we have observed a reaction of immunological non-identity between LAA and ferritin. This is of considerable interest since ferritin has been reported to be immunologically closely related to alpha2H-globulin which may occur in the same categories of patients as LAA. It is preliminary concluded that LAA as defined by our antisera may be different from alpha2H-globulin and ferritin.

Amniotic Fluid↗
PubMed1977

A linkage study of rabbit serum high density lipoprotein (HDL) allotypes.

Close linkage between the two allotypic systems of rabbit serum high density lipoprotein (HDL), Hl 1 and R 67, has been confidently excluded, the recombination fraction being at least 0-20. No suggestion of linkage between either HDL allotype and the immunoglobulin allotypes a1a2a3/b4b9, or the red blood cell system (RBC) ADF was obtained. Close linkage was confidently excluded for the Hl 1-ADF, Hl 1-a1a2a3, R 67-ADF, R 67-a1a2a3, R 67-b4b9, a1a2a3-b4b9, and b4b9-ADF relationships.

Animals↗
PubMed1977

Effector cell involved in cell-mediated cytotoxicity to cells infected with herpes simplex virus type 1.

Experiments were performed to analyze the characteristics of the effector cells involved in cell-mediated killing of herpes-infected fibroblasts. Effector cells were fractionated according to adherence and phagocytic properties, and lymphocytes were depleted of T-cells, and EA- and EAC- (antibody-coated bovine erythrocytes and bovine erythrocytes coated with rabbit anti-bovine antibodies and C5-deficient mouse serum, respectively) rosette-forming cells by differential centrifugation. Column passage was used as an alternative to depletion of B-cells and F(c)-receptor-positive cells. Antibody-dependent, cell-mediated cytotoxicity was found to be associated with nonphagocytic cells carrying low-avidity F(c) receptors. Some of these had surface immunoglobulin; others lacked both B- and T-cell markers. Low levels of killing were found without addition of anti-herpes antibody to the test system, and this killing seemed to depend on cells belonging to the same subpopulation as the antibody-dependent effector cells.

B-Lymphocytes↗
PubMed1977

Serum immunoglobulins and organ non-specific antibodies in diseases of the liver.

Serum immunoglobulins and C3 levels, auto-antibodies to smooth muscle (SMA), mitochondria (MA), and nuclei (ANA), rheumatoid factors (RF), HB-antigen and HB-antibody were studied in 9 groups of liver disease. Hypergammaglobulinaemia was a prominent feature in most groups, IgG being particularly raised in active chronic hepatitis, IgM in primary biliary cirrhosis, and IgA in alcoholic liver disease, respectively. IgE was often increased in alcoholic liver disease and was frequently low in hepatic tumours, whereas IgD showed no typical pattern in any liver disorder. SMA was most frequently found in active chronic hepatitis (68%), and MA in primary biliary cirrhosis (58%), while ANA was detected in 50% of the patients with active chronic hepatitis. However, a pronounced over-lap of tissue antibodies was observed among the various groups of liver disease, particularly in active chronic hepatitis and primary biliary cirrhosis. The concurrent presence of SMA and ANA was most frequent in active chronic hepatitis. It was not excluded that antibody titres might have provided better diagnostic discrimination, since titration of antibodies was not performed. Low C3 levels in active chronic hepatitis were correlated with low levels of other liver-synthetized proteins, and no evidence was found of increased consumption by immunologic reactions.

Acute Disease↗
PubMed1977

Purification of human interferons by antibody affinity chromatography.

Human Leukocyte Interferon, Human Fibroblast Interferon and Namalva-interferon was purified on an antibody affinity colomn up to 2-20 X 10 IFU/mg protein with recoveries in the 80-120% range. The colomn was made by coupling highly absorped anti-leukocyte interferon immunoglobulins to Sepharose 4B. The absorption was performed by means of crude human leukocyte interferon covalently bound to Sepharose 4B.

Antibodies↗
PubMed1976

Serum-high-density-lipoprotein and atherosclerotic heart-disease.

Serum-high-density-lipoprotein (H.D.L.) concentrations were determined in 49 men who had had a myocardial infarction and in 102 healthy, middle-aged men, all from Northern Sweden. A quantitative immunological assay based on a monospecific antiserum to the main polypeptide (apoprotein A-I) of H.D.L. was used. The mean H.D.L. concentration was significantly lower in the men with coronary heart-disease than in the controls. The results accord with the hypothesis that high levels of H.D.L. to some extent protect against ischaemic heart-disease.

Adult↗
PubMed1976

Genetic variation in serum low density lipoproteins and lipid levels in man.

Combined data from 10 different populations indicate that the serum cholesterol and triglyceride levels are higher in Ag(x-) than in Ag(x+) individuals. Although the differences were relatively small, they became more pronounced with increasing age. The Ag(x) antigen, which is associated with the serum low density lipoprotein, is genetically controlled and the present study therefore has revealed a small but significant effect of a single autosomal locus on lipids implicated in the pathogenesis of atherosclerosis. No explanation of the higher cholesterol and triglyceride levels in Ag(x-) than in Ag(x+) persons is apparent.

Age Factors↗
PubMed1976

Pre-beta1-lipoprotein and Lp(a) antigen in relation to triglyceride levels and insulin release following an oral glucose load in middle-aged males.

A series of 30 previously investigated and presumably healthy middle-aged males have been studied, following an oral glucose tolerance test (OGTT). The insulin mean value 120 min after the start of the OGTT was found to be significantly lower in persons possessing the pre-beta1-lipoprotein (pre-beta1 +) and Lp(a) antigen, than in those who were pre-beta1-/Lp(a-). At 60 min during the OGTT, triglyceride and insulin correlated significantly in pre-beta1-/Lp(a-) individuals, but not in pre-beta1 + or Lp (a+) individuals; on the other hand, insulin correlated significantly with blood glucose at this time in the pre-beta1 + and Lp(a+) individuals, but not in the pre-beta1-/Lp(a-). These findings may reflect an important biochemical difference between the two subpopulations.

Antigens↗
PubMed1976

Genetic lipoprotein variation and lipid levels in man.

Analyses of 12 population samples have revealed that the total serum cholesterol level is significantly higher in Lp(a +) than in Lp(a -) individuals. The difference is more pronounced in middle-aged and other people than in young persons, and the difference between Lp(a +) and Lp(a -) individuals is larger when LDL cholesterol rather than total serum cholesterol is considered. Lp(a -) individuals have a significantly higher triglyceride level than Lp(a +) individuals. The Lp(a) variation is genetically controlled. Thus, the present study has revealed a small but significant effect of a single, autosomal locus on lipids implicated in atherosclerosis. An association between the phenotype Lp(a +) and coronary heart disease has been demonstrated previously.

Adolescent↗
PubMed1976

The inheritance of hyperlipoproteinaemia with xanthomatosis. A study of 132 kindreds.

In a study of xanthomatosis kindreds in the county of Ostfold, Norway, 95 % of the living first degree relatives of the probands were investigated. Hyperlipoproteinaemia (lipid values above the 95th percentile) was present in 40.8 % of 554 first degree relatives of probands with xanthomatosis. The distribution curve was bimodal for cholesterol and LDL cholesterol concentrations, but not for triglyceride concentration within the different categories of families. The IIA lipoprotein pattern was the most frequent lipoprotein abnormality, in probands as well as in affected first degree relatives. However, IIB and IV lipoprotein patterns were also found in affected family members, irrespective of the pattern in the probands. About 93% of the xanthomatosis subjects had a lipoprotein disorder segregating as an autosomal dominant; the remaining 7 % were sporadic cases and/or had a multifactorially determined xanthomatosis. More sibs that offspring were affected; this was particularly pronounced for males with a IIA lipoprotein pattern. The genetic analysis gave no reason to suspect that hypercholesterolaemia with a IIA pattern is not the same disease as hypercholesterolaemia with a IIB pattern. However, a significant number of xanthomatosis patients had more than one type of hyperlipoproteinaemia. The frequency of the xanthomatosis trait was estimated to be 3.2/1000, and the ascertainment probability 0.6. The prevalence of familial hypercholesterolaemia with xanthomatosis was estimated to be 2.2/1000 and the multiple type hyperlipoproteinaemia with xanthomatosis had a frequency of 1.0/1000.

Chromosome Aberrations↗
PubMed1976

Cerebellar ataxia and hypergonadotropic hypogonadism in two kindreds. Chance concurrence, pleiotropism or linkage?

Two kindreds with Marinesco-Sjögren's syndrome in three sibships are described. In five of the six affected, but in none of the unaffected sibs, a hypergonadotropic hypogonadism was observed. In one of the kindreds a high degree of inbreeding was revealed, and inbreeding likely also existed in the other kindred. The two families were not related. Marinesco-Sjögren's syndrome is known to be a distinct clinical entity, governed by autosomal recessive inheritance, and this also applies to hypergonadotropic hypogonadism. Several heredo-degenerative nervous disorders are accompanied by a hypogonadotropic hypogonadism, which is believed to be secondary to the neurological disorder, as in traumatic paraplegia. A hypergonadotropic hypoganadism cannot readily be explained in this way. We consider genetic linkage between two independent disorders as the most likely explanation for the observed concurrence.

Adolescent↗
PubMed1976

Further evidence for the existence of genetically determined metabolic differences between Lp(a+) and Lp(a-) individuals.

Thirty, presumably healthy, middle-aged males from Northern Sweden were studied in September 1973 and again in February 1975. Mean fasting cholesterol and triglyceride concentrations were significantly higher at the latter investigation than they were at the former in the total group and in the Lp(a+) group, but not among those who were Lp(a-). Furthermore, estimation of free thyroxine factor yielded significantly higher results in the Lp(a-) than in the Lp(a+) group. In a previous paper, we reported significant differences between Lp(a+) and Lp(a-) individuals with respect to the relationships between insulin level and blood glucose concentration, and between insulin level and fasting triglyceride concentration. The combined results of the present and previous studies suggest that inherited metabolic differences exist between Lp(a+) and Lp(a-) individuals. In view of the association which has been found between the phenotype Lp(a+) and coronary heart disease it seems plausible that these differences may be of clinical importance.

Antigens↗