Biomedical subjects
Publications and source records attributed to N Zöllner.
In a patient with upper abdominal pain real-time sonography produced the first relevant sign of a space-occupying gastric lesion. Final diagnosis was gastric hemangiopericytoma.
Lipogenesis has been investigated in diploid fibroblasts derived from patients with familial hypertriglyceridaemia (FHT) and compared with cells from healthy persons. There was no difference in acetyl-CoA carboxylase activity in both cell types. Incorporation of [2-14C]-acetate into triglyceride fatty acids was slightly increased (34%) by the FHT lines. Addition of triiodothyronine caused a marked rise in [2-14C]-acetate incorporation by the FHT lines whereas the normal lines exhibited only control values. Maximal rise in [2-14C]-acetate incorporation was obtained with 5 micrograms/ml for 72 h. Under these conditions, acetate incorporation by the FHT lines was 220% of the controls, compared with 94% by the normal lines. Measurements of acetyl-CoA carboxylase specific activity supported the results obtained with measurements of acetate incorporation into triglyceride fatty acids. Individual FHT lines differ much in their quantitative answer to thyroid hormones, although the described effects were obtained with all eight lines under study. Insulin increased acetyl-CoA carboxylase activity and incorporation of [2-14C]-acetate in lipids in both cell types, but with no difference between normal and FHT lines. The results seem to reflect a higher lipogenic capacity of the hypertriglyceridaemic fibroblasts compared with normal cells.
The regulation of triacylglycerol synthesis by various long-chain fatty acids was studied using primary cultures of hepatocytes. The activity of diacylglycerol acyltransferase was measured after 72-h incubation with various fatty acids in equimolar concentrations (0.5 mM): oleate, linoleate, linolenate, palmitate, stearate and arachidonate increased enzyme activity to 191%, 161%, 148%, 124%, 116% and 114%, respectively, compared to controls. Cellular triacylglycerol levels showed the same changes, suggesting a regulatory function of diacylglycerol acyltransferase in triacylglycerol synthesis. Elaidate lowered the enzyme activity by 57%. The addition of different fatty acids to the incubation medium did not influence the distribution of enzyme activity in the 30 000 x g pellet which was routinely discarded and the microsomal fraction (105 000 x g), where the enzyme was predominantly localized (91%). The release of lactate dehydrogenase into the culture medium of hepatocyte monolayers as well as ketone body production was not affected by any of the fatty acids.
In this clinical evaluation it could be demonstrated that the appearance of ossification centers in the developing hand can be shown in transmission sonography as well as in roentgenography.
In Real-time Sonography slice-thickness artifacts may lead to misinterpretation, mainly in cystic organs. With in vitro studies it was possible to show the mechanism of this artifact, which is based on beam thickness.
Bow-shaped artifacts can often be seen in B-mode-ultrasound examinations. In order to find out the origin of these artifacts, water tank experiments were carried out and compared with in vivo observations. The studies showed that bow-shaped artifacts are caused by beam breadth, and that their shape is influenced by the type of the B-mode-instrument, the adjustment of the machine, and by the shape of the reflector. In vitro and in vivo, bow-shaped artifacts arise at strong reflectors and are visible in regions of low echogeneity. In vivo bow-shaped artifacts may imitate pathological findings such as septa or sludge.
The effects of a fixed combination of 100 mg allopurinol and 20 mg benzbromarone (Acifugan) on plasma and urinary uric acid were compared with those of 300 mg allopurinol alone during standardized dietary conditions (purine-free, isoenergetic formula diet with addition of 2 g ribonucleic acid per day). In addition, the components of the fixed combination were given separately. Diet and ribonucleic acid were taken by healthy volunteers for periods of 14 days, drugs were added from day 8 to day 14. Steady state uric acid values before and during drug ingestion were compared intraindividually to calculate drug effects. The fall of plasma uric acid was not significantly different during treatment with 300 mg allopurinol as compared with combined low dose treatment. Renal uric acid excretion was decreased by 56 and 23%, respectively. Comparing combined low dose treatment with the cumulative effects of its constituents it was found that combined treatment was less effective. With combined low dose treatment there is no need to observe prophylactic measures concerning complications at the site of the urinary tract. Compared with monotherapy with 300 mg allopurinol there is no advantage. However, the frequencies of side effects, which are not dose-dependent, will be cumulative with combined treatment, which is probably a major disadvantage. Combined treatment should not be used therefore with the exception of proven inefficiency of monotherapy.
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Bilateral carpal tunnel syndrome was observed in a 39-year-old female with gout. Until now carpal tunnel syndrome caused by gout has not been observed in females. Due to marked clinical symptoms neurolysis on the right side had to be performed. The course of the left hand affection was observed while on conservative treatment with a xanthine oxidase inhibitor. As such therapy is possible and successful, it is mandatory to diagnose carpal tunnel syndrome early in gout. Histology showed the cause of carpal tunnel syndrome to be uric acid tendovaginitis.
Pool size, turnover, and excretion of uric acid were investigated in three normal subjects both during purine-free, isoenergetic liquid formula diet and during additional purine administration by use of isotope dilution techniques. The fractional turnover of the uric acid pool was increased during dietary purine administration suggesting an increased total body uric acid clearance as a result of the increase in renal clearance. Fractional turnover increased more in the female subject than in males, while pool size was increased less. It can be calculated from the results obtained that endogenous uric acid synthesis is not inhibited by dietary purines.
The pathways of purine biosynthesis and degradation have been elucidated during the last 30 years; the regulation of the mechanisms involved is not yet fully understood, particularly with respect to quantitative aspects. Research into inborn errors of purine metabolism has provided valuable insights into purine synthesis and salvage pathways. Nutrition experiments using purine-free formula diets and supplements with defined purine sources permit precise descriptions of the influence of various dietary purines on uric acid formation. Supplements of dietary purines produce dose-proportional increases in plasma uric acid concentrations, uric acid pool size and renal uric acid excretion. The magnitude of these increases depends on the type of purine compound administered, which may limit the value of food tables for human dietetics. Purine content of food must be related not only to weight but also to energy and to protein, particularly if new foodstuffs or a vegetarian diet are ingested. Dietary purines appear to influence the biosynthesis of pyrimidines. In contrast to dietary purines, pyrimidines in the diet, if administered as nucleosides or nucleotides, are utilized in animals for the synthesis of nucleic acids. Much further work is necessary for a better understanding of the inter-relationships of purine and pyrimidine metabolism.
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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.
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Three elderly patients are reported, in whom serologically confirmed recent infectious mononucleosis is followed by fatal lymphoproliferation (case 1), by acute monocytic leukemia (case 2), and by acute probably monocytic leukemia (case 3).
Sixty-two subjects from 23 families were evaluated by serum lipid analyses and tissue culture biochemistry in skin fibroblasts. In 53 cases from 19 families with proven familial hypercholesterolemia (FHC), fibroblast cultures were successful. In 45 of these cases (85%) the clinical diagnosis of hyper- or normocholesterolemia was in accordance with the tissue culture findings. Four patients 2-38 years old, had hypercholesterolemia but normal tissue culture results. Four patients, 18-44 years old, had normal serum cholesterol levels for their age and sex, but were heterozygotes according to tissue culture results. In the remaining four families only the propositus had hypercholesterolemia. All members of the families including the propositus had normal tissue culture determinations indicating that not all cases of idiopathic hypercholesterolemia are due to the Goldstein-Brown mechanism of defective LDL receptor function.