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Biomedical subjects

O Adam

Publications and source records attributed to O Adam.

At least 55 records · Page 3Linked to original sources
PubMed1989

Lowering of plasma cholesterol in herbivores and omnivores by low molecular weight dextran.

Two rabbits and two home pigs were infused in a cross-over design with equal volumes, adapted to the plasma volumes of the animals, of dextran-40 and saline. The infusions resulted in a reduction of plasma cholesterol and control parameters, such as plasma protein, hemoglobin, and hematocrit. The reduction of hemoglobin and hematocrit was related to plasma expansion with both infusion regimens. With dextran-40 infusions the reduction of plasma protein was greater than hemodilution in both species (-18% in rabbits and -20% in home pigs), because of steric exclusion of the protein. Lowering of plasma cholesterol in rabbits was comparable to the reduction in plasma protein, whereas in home pigs the reduction of plasma cholesterol (-25%) surpassed that of plasma protein. Reports in the literature have shown that dextran infusions increase cholesterol concentration in liver cells, leading to a reduction of intestinal cholesterol resorption in omnivores. This dextran effect is supposed to be responsible for the observed additional reduction of plasma cholesterol levels in omnivores.

Animals↗
PubMed1988

[Spontaneous course of Wegener's granulomatosis].

Two cases of Wegener's granulomatosis are reported. During the 5 and 9 years course of the disease complete remissions and the disappearance of pulmonary opacities were found without specific treatment. Since 1970 cytotoxic drugs, e.g. cyclophosphamide, are frequently used for the treatment of Wegener's granulomatosis. The evaluation of the follow-up showed in these patients that in most cases the side-effects of the therapy, and not the primary disease, limited the life-expectancy. This especially applies for patients with mild forms of Wegener's granulomatosis, in which the initiation of a cytotoxic therapy should carefully be evaluated.

Aged↗
PubMed1987

[Secondary gout and pseudo-Bartter syndrome in females with laxative abuse].

Four females (27-54 y), presenting with a history of long-term laxative abuse, were admitted to the Medizinische Poliklinik for evaluation of generalized weakness. Laboratory findings revealed signs of Bartter's syndrome, including hypokalemia, systemic alkalosis and normal blood pressure. Three of the four females showed impaired renal function and elevated serum uric acid levels, two of them suffered from recurrent gouty attacks. In our patients the incidence of hyperuricemia and impaired renal function, as a consequence of chronic hypokalemia, was much higher than known from patients with Bartter's syndrome. Hyperuricemia is related to some pathophysiological features of Pseudo-Bartter's syndrome, (e.g. systemic alkalosis, elevated angiotensin) and combined with additional factors (e.g. catabolism, reduced plasma volume) may lead to gouty attacks. Gallstones were found in two of the four females. Long term surreptitious laxative ingestion frequently is observed in females. Hypokalemia, induced by the laxatives, causes reduced intestinal motility and leads to augmented laxative intake. These patients are prone to develop Pseudo-Bartter's syndrome, causing eventually a hyperuricemia and gouty attacks.

Adult↗
PubMed1986

[Comparison of the effect of linolenic acid and eicosapentaenoic acid on prostaglandin biosynthesis and thrombocyte function in humans].

Platelet aggregation, bleeding time, prostaglandin biosynthesis and plasma cholesterol fatty acids were investigated in 12 healthy females (25-32 years), who were given different amounts of linolenic acid (0%, 4%, 8%, 12%, 16% of total energy intake) or eicosapentaenoic acid (1.7%) with formula diets for 2 weeks each. Linolenic and eicosapentaenoic acids prolonged the bleeding time and inhibited platelet aggregation and prostaglandin biosynthesis. These effects became apparent after a linolenic acid intake of 12% of the energy intake. A decrease in PGE in 24 h urine was observed after intake of linolenic acid amounting to 8% of energy intake. Eicosapentaenoic acid influenced all parameters measured ten times more than linolenic acid. Linolenic acid intake had no effect on the ratio of linoleic/arachidonic acids in plasma cholesterol esters in contrast to in vitro findings. Thus energy intake comprising 1.7% of eicosapentaenoic acid is sufficient to affect thrombocyte function in man. The concomitant intake of linolenic-type fatty acids inhibits the biosynthesis of prostaglandins E2 and F2 alpha to different degrees.

Adult↗
PubMed1986

Effect of alpha-linolenic acid in the human diet on linoleic acid metabolism and prostaglandin biosynthesis.

The effect of dietary alpha-linolenic acid intake on linoleic acid metabolism and prostaglandin (PG) biosynthesis was investigated in two groups of six healthy females (25-32 yr). They were given isocaloric formula diets (FD) containing linoleic acid at a constant intake (4% of calories), with different amounts of alpha-linolenic acid: 0% (FD4/0), 4% (FD4/4), 8% (FD4/8) (group I) and 12% (FD4/12) or 16% (FD4/16) (group II); the diets were given for 2 weeks each. Comparing diet FD4/0 to FD4/16, enrichment of alpha-linolenic acid was greatest in cholesteryl esters (+6.8% in plasma, +7.1% in low density lipoproteins (LDL), +5.9% in high density lipoproteins (HDL)), less in phosphatidylcholine (+2.5% in plasma, +2.9% in LDL, +2.7% in HDL), and least in platelet lipids (+0.7%). The accumulation of alpha-linolenic acid was compensated by a decrease of oleic acid. Eicosapentaenoic acid (EPA), which was excluded from the diet, increased in all plasma lipids with augmented alpha-linolenic acid intake, indicating a chain elongation and desaturation of alpha-linolenic acid to EPA. However, even at the end of FD4/16, EPA was less than 2% of total fatty acids in all plasma lipids. Plasma linoleic acid levels were constant during all dietary regimes, according to the constant dietary intake of this fatty acid. No replacement of linoleic acid by alpha-linolenic acid could be observed. The percentage of arachidonic acid in all lipids was unaffected by alpha-linolenic acid intake. As arachidonic acid was not provided by the diet, it can be concluded that alpha-linolenic acid does not inhibit chain elongation and desaturation of linoleic acid to arachidonic acid in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Nutrition physiology studies with formula diets: metabolism of multiple unsaturated fatty acids and prostaglandin biosynthesis in the human].

Linoleic and linolenic acids are precursors for the biosynthesis of prostaglandins (PG) and related compounds. In man augmented linoleic acid intake results in stimulation of PG-biosynthesis, for PG originating from the kidney a stimulation only is found for PGE2. Dietary linolenic acid inhibits PG biosynthesis to a tenfold lesser degree than eicosapentaenoic acid. Renal PGE2 is depressed by linolenic acid intake, while no effect is found for PGF2 alpha up to 8 energy% of linolenic acid supply. Linoleic and linolenic acids additionally display effects on fatty acid metabolism. In contrast to the results of in vitro studies the supply with the precursor linoleic acid results in a decrease of arachidonic acid in cholesterolesters of plasma and in HDL-lecithin, while the intake of linolenic acid is without effect. From these data it is concluded that in vivo the conversion of linoleic to arachidonic acid occurs preferentially to the analogous conversion of linolenic to eicosapentaenoic acid.

Arachidonic Acid↗
PubMed1985

Prostaglandin formation and platelet aggregation during fasting and linoleic acid intake.

Prostaglandin formation, estimated by the determination of tetranorprostanedioic acid (TNPDA) in the urine, and platelet aggregation were investigated in seven healthy volunteers each day during fasting, and in three of them additionally during intake of carbohydrates (328kcal/day) or safflor oil (328 kcal, 20 g linoleic acid). Monitoring TNPDA in 8-h fractions of the urine showed a reduction during the night (23.00-07.00) by 70% on the average. During Days 1 and 2 of fasting the amount of TNPDA in 24-h urine was the same as under a conventional diet. On Day 3, TNPDA decreased in all experimental subjects to 162 micrograms/day on the average and was not changed by carbohydrate intake. A linoleic acid intake of 20 g/day increased TNPDA in 24-h urine to pre-experimental levels measured under free diet. Platelet aggregation did not change during the experiment. No relationship between prostaglandin formation and lipolysis in man was found.

Adult↗
PubMed1985

[The effect of linoleic acid intake on its concentration and resultant products in individual plasma lipids in humans].

Dietary linoleic acid enrichment in different plasma lipids was investigated in six healthy females. They were given formula diets (FD) containing no arachidonic acid, and providing a linoleic acid supply of 0% (FD0), 4% (FD4) or 20% (FD20) of total energy intake. At the end of each two weeks FD period fatty acid distribution was determined in cholesterol esters (CE) and in lecithin of LDL and HDL. The increase of linoleic acid in CE was twice that found in the lecithin of LDL and HDL. Comparing FD0 and FD20 the increase of linoleic acid in CE of LDL and HDL was 34%, and in lecithin 15%. Simultaneously oleic acid was lowered in CE (-17%) and in lecithin (-8%) of LDL and HDL. Comparing FD0 and FD20 arachidonic acid, which derives from linoleic acid, was lowered with increased linoleic acid intake in LDL-CE (-5%) and in HDL-lecithin (-8%), while no effect was found in LDL-lecithin. Our results demonstrate that dietary linoleic acid enrichment occurs preferentially in CE of LDL and HDL, but does not lead to an increase of arachidonic acid in plasma lipids. However, a decrease was found for arachidonic acid in HDL-lecithin, while in LDL-lecithin no effect could be observed. From this it is concluded that incorporation and metabolism of linoleic acid in different plasma lipids is not identical, although lipid exchange and lipid transfer have been shown for most lipoprotein fractions.

Adult↗
PubMed1985

A combination of plastic and plaster of Paris (Kombigips) in fracture treatment.

A new model of plaster bandage with combination of gypsum and plastics is presented and its economic use is compared with traditional technics. "Kombigips" in 12 patients was more efficient in staging of fracture healing than traditional plaster bandages, because the X-ray properties of "Kombigips" are more profitable. "Kombigips" is much more cheaper than use of pure plastic bandages and nearly as cheap as use of traditional plaster bandages.

Adolescent↗
PubMed1984

Antiasthmatic effects of onion extracts--detection of benzyl- and other isothiocyanates (mustard oils) as antiasthmatic compounds of plant origin.

Previous studies showed the inhibitory effects of crude ethanolic onion extracts (COE) on allergic skin reactions in man as well as on allergen-induced bronchial asthma in man and guinea-pigs. Work is in progress in order to identify both the mode of action of COE and the active substance(s). The present study describes asthma-protective effects of isothiocyanates. Groups of at least 5 guinea-pigs sensitized to ovalbumin were challenged twice (time 0 and 10 min) by the inhalation of ovalbumin 30 min after oral treatment with increasing doses of the agent tested or control solutions. Bronchial obstruction (BO) was measured by whole body plethysmography. Chloroform extracts of onions showed similar protective effects on BO as COE. The water-soluble fraction of COE was inactive. Benzyl-isothiocyanate (BITC) was identified as one component of onion lipids by combined gas chromatography/mass spectrometry. BITC inhibited BO in a dose-dependent fashion: 150 mg/kg: 89%; 75 mg/kg: 76%; 30 mg/kg: 66%; 15 mg/kg: 49%. Ethyl-isothiocyanate and allyl-isothiocyanate showed similar effects; p-hydroxy-benzyl-isothiocyanate, a very unstable mustard oil, was ineffective. Additional experiments showed no antagonistic effects of COE on histamine- or acetylcholine-induced BO. The antiasthmatic effects of onions and - perhaps - other plants may be mediated at least in part by isothiocyanates.

Administration, Oral↗
PubMed1984

Effect of different linoleic acid intakes on prostaglandin biosynthesis and kidney function in man.

Prostaglandin (PG) biosynthesis and kidney function was investigated in 24 adults (23 to 32 yr) during isocaloric formula diet periods, for 2 wk each, providing a linoleic acid supply of 0, 3, 3.5, 4, 6, 8, 13, 17, 18, or 20% of total energy intake. Total protein intake (15 energy %) was constant, as well as 5 g NaCl, 3 g KCl, and 0.6 g cholesterol per 2200 kcal formula diet. The amount of PG metabolites, PG-E, sodium, and creatinine in 24-h urine increased with augmented linoleic acid intake. Comparing a linoleic acid intake of 0 and 20 energy %, an increase of sodium (8%) and creatinine (16%) in 24-h urine was found on the 5th day of high linoleic acid supply. Coincidently a stimulated PG biosynthesis could be measured. Potassium, water, and PG-F excretion showed no relation to linoleic acid intake. It is concluded that linoleic acid in the diet stimulates PG-E biosynthesis in man, leading to effects in systems which control renal function, and may have clinical relevance for the sodium and potassium balance in man.

Adult↗
PubMed1982

Prostaglandin formation in man during intake of different amounts of linoleic acid in formula diets.

Prostaglandin formation in healthy female volunteers was investigated during intake of different amounts of linoleic acid in liquid formula diets (LFD). The average amounts of the metabolites convertible to tetranorprostanedioic acid (TNPDA) were 123 +/- 5.2 (x +/- SEM), 175 +/- 7.0 and 352 +/- 10.8 microgram/day, during 2-week periods with a linoleic acid supply of 0, 4 or 20% of energy, respectively. The day-by-day variations in prostaglandin formation were less than the changes observed due to different amounts of linoleic acid. High linoleic acid intake was followed by an increase of TNPDA in the urine after 3-4 days, which was more pronounced when the linoleic acid intake during the period before had been low. In all persons, the highest amount of TNPDA, 411 +/- 13.2 microgram/day, was found between days 5 and 10 of high linoleic acid intake. From day 11 through day 14 an average of 372 +/- 14.3 microgram/day was found and the values were lower in 5 of 6 persons as compared to the values found between days 5 and 10. At the end of the experiment with LFD providing a linoleic acid supply of 0, 4 or 20% of energy, the percentage of cholesteryl linoleate in plasma increased (35 +/- 1.8, 48 +/- 1.0, 63 +/- 0.6) while those of cholesterylarachidonate decreased (14 +/- 1.0, 10 +/- 0.6, 8 +/- 0.6). During the periods without linoleic acid intake the TNPDA excretion was lowest in all persons. A reduction in linoleic acid supply resulted in a decrease of urinary TNPDA within 1 day.

Adult↗
PubMed1980

[Clinical significance of essential fatty acids (author's transl)].

Essential fatty acids are important constituents of human nutrition. They lower cholesterol and phospholipid levels in serum. They are structural parts of cell membranes, affecting the function of membrane-bound enzymes and transport systems and modulating cellular immune response. Prostaglandins, prostacyclin and thromboxane, the metabolites of essential fatty acids, are active compounds in the cardio-vascular system, the lung, in the uro-genital and gastro-intestinal tract, in the inflammatory response and platelet aggregation.

Cardiovascular Physiological Phenomena↗
PubMed1980

[Platelet aggregation and prostaglandin turnover in man during defined linoleic acid supply with formula diets (author's transl)].

A report is given on changes of platelet aggregation and prostaglandin turnover during a cross-over experiment with six female volunteers being given a linoleic acid supply with formula diets of 0 g or 50 g daily. Collagen- and ADP-induced platelet aggregation was determined with a Borne-type aggregometer. Prostaglandin turnover was measured by analyzing the excretion of a joint derivative of prostaglandin metabolites, tetranorprostanedioic acid, in urine. With a linoleic acid supply of 50 g daily we found an increase of tetranorprostanedioic acid in urine, while platelet aggregation decreased. When the experimental subjects came from a conventional diet (linoleic acid intake 20 g daily) these changes were seen later than after a linoleic acid free formula diet. A linoleic acid-deficient formula diet caused a fall in prostaglandin turnover within 24 hr. ADP-induced platelet aggregation was unchanged after 1 week, while collagen-induced platelet aggregation was increased after 1 and 3 weeks of linoleic acid-deficient diet. These results clearly demonstrate the influence of nutrition on platelet aggregation.

Adult↗