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Biomedical subjects

A Berg

Publications and source records attributed to A Berg.

At least 199 records · Page 11Linked to original sources
PubMed1993

Acute and delayed effects of prolonged exercise on serum lipoproteins. I. Composition and distribution of high density lipoprotein subfractions.

To investigate the effects of a single period of prolonged exercise on lipoprotein concentration and composition, the serum of 13 healthy, endurance-trained men was examined before and after (1 h, 20 h) a field test [running time, 130 (SD 7.4) min]. We found changes in composition of all of the lipoprotein fractions isolated. In detail, all very low density lipoprotein particle components were reduced after exercise; the most pronounced changes found were in the concentrations of phospholipids (PL) and triglycerides (TG) (PL, before vs 20 h after, P < 0.01; TG, before vs 20 h after, P < 0.01). The serum high density lipoprotein (HDL)-cholesterol mass was unchanged after exercise, but both HDL subfractions showed changes in composition. In HDL3 the relative amounts of cholesterol increased (unesterified free cholesterol; FC) before vs 20 h after, P < 0.05; cholesterylester (CE), before vs 20 h after, P < 0.01) and TG and PL decreased (TG and PL, before vs 20 h after, P < 0.05). The HDL2 particles became enriched in the relative amount of CE (before vs 20 h after, P < 0.01) and lost TG after exercise (before vs 20 h after, P < 0.01). The observation that all the changes in lipoprotein concentration and composition reached their maximal differences compared to the pre-exercise values 20 h afterwards would support the assumption that circulating lipoproteins play an important role in the regeneration period, refilling the intramuscular triglyceride stores.

Adult↗
PubMed1993

Acute and delayed effects of prolonged exercise on serum lipoproteins. II. Concentration and composition of low-density lipoprotein subfractions and very low-density lipoproteins.

To investigate the effects of a single period of prolonged exercise on lipoprotein concentration and composition, 13 healthy endurance-trained men were examined before and after (1 h, 20 h) a cross-country run [30 km, time: 130 (SD 7.4) min]. The data show that following acute exercise, serum triglyceride (TG) concentration were reduced (36%) as a consequence of a reduced number (31%) of very low density lipoprotein (VLDL) particles. Changes in composition of VLDL were present but less evident. In contrast to this, acute exercise did not induce significant changes in the average concentration of individual low-density lipoprotein (LDL) subfractions. However, changes in dense LDL [density (d) > 1.044 g.ml-1] concentration were significantly correlated to changes in serum TG: a reduction of dense LDL occurred in subjects with large reductions in serum TG. In addition, LDL composition changed significantly. Immediately (1 h) after exercise the TG content of all LDL subfractions was reduced. These reductions were significant in large (d = 1.006-1.037 g.ml-1) and small LDL (1.044-1.063 g.ml-1). It can be concluded therefore from our study that acute exercise primarily altered the composition of LDL subfractions while their concentration remained stable.

Adult↗
PubMed1993

Essential fatty acids in infantile seborrheic dermatitis.

BACKGROUND: In infantile seborrheic dermatitis (ISD) several different pathogenetic mechanisms have been proposed. OBJECTIVE: The purpose of the study was to investigate the importance of essential fatty acids (EFAs) and their metabolites in the origin of ISD. METHODS: The serum EFA patterns of 30 children with ISD, 1 to 6 months of age, were studied for 2 to 5 months. Blood samples were obtained at the time of diagnosis and after spontaneous recovery. Control samples were taken from age-matched healthy children. RESULTS: In children with active dermatitis levels of EFA 18:1w9 were increased and levels of 18:2w6 were decreased, whereas 20:4w6 levels remained normal. The rare fatty acid 20:2w6 was found in significant amounts in 20 patients, but at only barely detectable levels in the controls. All deviant values but the levels of 20:2w6 were normal at the time of recovery. Breast milk samples were obtained at the time of diagnosis from the patients' mothers and from a control group consisting of healthy nursing mothers. The EFA patterns were identical. The differences in EFA pattern between children with ISD and those free of skin disease were significant. The normalization of the deviation in ISD paralleled the recovery at any age it occurred. CONCLUSION: The laboratory findings suggest a transient impaired function of the enzyme delta-6-desaturase. The altered EFA pattern in ISD may be important in the pathogenesis of the disease.

Dermatitis, Seborrheic↗
PubMed1993

Prevention of endotoxin-induced monokine release by human low- and high-density lipoproteins and by apolipoprotein A-I.

Interaction of endotoxin (lipopolysaccharide [LPS]) with human lipoproteins is known to prevent the LPS-induced activation of human monocytes and release of cytokines (monokines). LPS was exposed to lipoprotein classes separated by ultracentrifugation and to apolipoprotein A-I. Then monocytes were added, and the LPS activation of monocytes was determined by measuring the induced monokines. Failure of LPS to induce monokine release was called LPS inactivation caused by lipoproteins or apolipoproteins. The LPS inactivation is shown to be a function of low-density lipoproteins. High-density lipoproteins inactivate LPS to a much lesser extent. The very-low-density lipoproteins cannot inactivate LPS. Lipid components seemed not absolutely required for LPS inactivation, because purified human apolipoprotein A-I without its physiological lipid complement also inhibits LPS-induced monokine release.

Adult↗
PubMed1993

Accumulation of "small dense" low density lipoproteins (LDL) in a homozygous patients with familial defective apolipoprotein B-100 results from heterogenous interaction of LDL subfractions with the LDL receptor.

The interaction of LDL and LDL subfractions from a patient homozygous for familial defective apoB-100 (FDB) has been studied. His LDL cholesterol ranged from 2.65 to 3.34 g/liter. In cultured fibroblasts, binding, internalization, and degradation of the patient's LDL was diminished, but not completely abolished. The patient's apolipoprotein E concentration was low, and the amount of apolipoprotein E associated with LDL was not elevated over normal. LDL were separated into six subfractions: LDL-1 (1.019-1.031 kg/liter), LDL-2 (1.031-1.034 kg/liter), LDL-3 (1.034-1.037 kg/liter), LDL-4 (1.037-1.040 kg/liter), LDL-5 (1.040-1.044 kg/liter), and LDL-6 (> 1.044 kg/liter). LDL-5 and LDL-6 selectively accumulated in the patient's plasma. Concentrations of LDL-1 to 3 were normal. The LDL receptor-mediated uptake of LDL-1 and LDL-2 could not be distinguished from normal LDL. LDL-3 and LDL-4 displayed reduced uptake; LDL-5 and LDL-6 were completely defective in binding. When apolipoprotein E-containing particles were removed by immunoabsorption before preparing subfractions, LDL-3 and LDL-4, but not LDL-1 and LDL-2, retained some receptor binding activity. We conclude that in FDB, LDL-1 and LDL-2 contain sufficient apolipoprotein E to warrant normal cellular uptake. In LDL-3 and LDL-4, the defective apoB-100 itself displays some receptor binding; LDL-5 and LDL-6 are inable to interact with LDL receptors and accumulate in plasma.

Adolescent↗
PubMed1993

Malnutrition and "nutrition engineering" in low-income countries: a rejoinder.

Malnutrition cannot be reduced to any single causality. While the political economy explanation is correct, suffering must be addressed in the short term by the available technical solutions. More work is needed on both the long-term causes of malnutrition and on methods of prophylaxis and treatment for nutritional diseases.

Developing Countries↗
PubMed1993

Clinical features in 28 consecutive cases of laboratory confirmed massive poisoning with carbamazepine alone.

A retrospective study of consecutive cases of massive carbamazepine poisoning treated in an intensive care unit during the period 1981-1991 was performed, mainly to determine whether serum carbamazepine levels were predictive of toxicity. Out of a total of 51 admissions with a diagnosis of carbamazepine self-poisoning, 28 (25 patients) were included. The reasons for exclusion were coingestion of other drugs (11 cases), incorrect diagnosis or inadequate information (6 cases), a peak observed serum concentration of carbamazepine below 76 mumol/L [18 mg/L] (4 cases), and lack of any documented serum carbamazepine assay (2 cases). The peak serum concentrations ranged from 78 to 285 mumol/L [18.4 to 67.4 mg/L]. It was found that serum levels equal to or above 170 mumol/L [40 mg/L] were significantly associated with an increased risk of serious complications such as coma, seizures, respiratory failure and cardiac conduction defects. In 60% of the 10 patients with a serum level > or = 170 mumol/L at least two of these symptoms occurred, in 50% at least three, and in 40% all four. There were two fatalities. Among the 16 patients (18 admissions) with a serum carbamazepine concentration below 170 mumol/L, only one was comatose and none had any of the other severe symptoms. It is concluded that serum carbamazepine levels accurately predict the severity of toxicity in massive carbamazepine poisoning in adults.

Adolescent↗
PubMed1992

Distribution of lipoprotein species (LpA-I, LpA-I:A-II) in serum and HDL subfractions of untrained and trained normolipemic men.

The distribution of lipoprotein species (LpA-I, LpA-I:A-II) in serum and within HDL subfractions (HDL2b, HDL2a, HDL3) was examined in 26 sedentary and 19 endurance trained normolipemic male individuals. The concentrations of lipids and apolipoproteins in serum and HDL subfractions and the concentrations of LpA-I and LpA-I:A-II were determined. Significant differences (Mann-Whitney-U-test) were found in serum concentrations of apoB (P < 0.05), apoA-II (P < 0.01) and LpA-I:A-II (P < 0.001). In HDL3 apoA-II concentration was significantly lower in the trained group (P < 0.05) but in HDL2 subclasses the concentrations of apoA-I and apoA-II did not differ between the groups. Despite similar concentrations of the two apolipoproteins, there were difference in the distribution of lipoprotein species within HDL2 subfractions. The concentrations of LpA-I did not differ, but the concentrations of LpA-I:A-II particles were higher in the trained group. Untrained and trained had similar concentrations of apoA-II (in HDL2b) but obviously more apoA-II containing particles and this leads to the assumption that within HDL2 of endurance trained individuals LpA-I:A-II particles have a lower apoA-II content compared with particles of untrained individuals. The data emphasize, that normolipemic individuals of different maximum oxygen uptake have a different distribution and composition of lipoprotein species (LpA-I, LpA-I:A-II).

Adult↗
PubMed1992

A semiautomated, 96-well plate assay for collagen synthesis.

We have established a rapid method for the measurement of collagen synthesis in large numbers of cell cultures. 3H-labeled collagen in microwell cultures was salt precipitated, harvested, and washed using a commercially available cell harvester and the filtered collagen was directly counted. The cell number could then be assessed either by methylene blue staining or by dissolving the cells in NaOH and estimating the protein content with bicinchoninic acid. In all of these procedures, the samples remain in microtiter plates, thus ensuring that minimal amounts of reagents are used and minimizing the amount of manipulation necessary. The intergroup variability is 3 to 9% and the recovery of 3H-labeled collagen is greater than 90%. Using this method, large numbers of samples can be assessed for collagen synthesis quickly, conveniently, and for minimal cost.

Animals↗
PubMed1992

Probucol, incorporated into LDL particles in vivo, inhibits generation of lipid peroxides more effectively than endogenous antioxidants alone.

One of the first steps in lipid autoxidation leads to the generation of lipid peroxides (LPO). The time course of LPO generation during Cu++ catalyzed oxidation of LDL before and after treatment with probucol was determined in this study. Before analysis the samples had been stored for about 3 years at -20 degrees C. The results show that in LDL samples without probucol the total antioxidative potential had been depleted during the long-term storage. In contrast, LDL containing probucol showed almost no signs of lipid autoxidation. In addition, the ratio of vitamin E to cholesterol was significantly higher in serum samples containing probucol. We conclude that, in vivo, probucol is incorporated into LDL particles in concentrations high enough to inhibit even early steps of lipid autoxidation.

Antioxidants↗
PubMed1992

Low density lipoproteins inhibit endotoxin activation of monocytes.

Human serum and low density lipoproteins (LDLs) were shown to inactivate endotoxin (lipopolysaccharide [LPS]) by testing the effect of LPS interactions with serum or LDL on the activation of human monocytes. Sera and LDL preparations from four patients with familial hypercholesterolemia were used to demonstrate the inhibition of LPS from inducing interleukin-1 release. Before LDL removal by immunoapheresis, the patients' sera were able to inactive approximately fivefold more LPS than after LDL removal. The LPS-inactivating capacity lost during apheresis could essentially be retrieved in the LDL-rich eluate from the immunoadsorption columns. Because patients were treated frequently with immunoapheresis, their LDL levels before LDL removal were not markedly elevated. These patients' sera before LDL removal were shown to inactivate amounts of LPS comparable to those inactivated by the sera from three healthy volunteers. LDL prepared by ultracentrifugation showed similar LPS inactivation as LDL prepared by immunoapheresis. We conclude that the inhibition of LPS-induced monocyte activation by human serum is dependent to a large extent on the LDL fraction. LDLs were demonstrated to inhibit LPS from inducing interleukin-1 release by human monocytes.

Adult↗