Biomedical subjects

K Hirschberg

Publications and source records attributed to K Hirschberg.

24 records · Page 2Linked to original sources

PubMed1985

A liver-function test using 15N-labelled ammonium chloride.

Malfunction of the liver involves disturbances of urea synthesis and ammonia detoxification. These phenomena became apparent, especially during ammonia loading of patients. The functional state of the liver can be assessed by oral administration of 15NH4Cl and subsequent analysis of 15N-urea and 15N-ammonia in urine by emission spectrometry. Clinical tests based on the ratio of the excess abundances of 15N-ammonia to 15N-urea excreted in urine 3 h after oral administration gave values for patients with liver disease which differed significantly from those for healthy subjects. Absorption disturbances, which often accompany liver diseases, do not influence the effectiveness of the method.

Aged↗

PubMed1985

Nuclear medicine liver function tests for pregnant women and children. 1. Breath tests with 14C-methacetin and 13C-methacetin.

Stable isotopes, such as 13C, should be substituted for the long-lived radionuclide 14C in the 14C breath test when doing liver function tests in children and pregnant women. For comparison 13C, 15N-methacetin and 14C-methacetin were synthesized as suitable diagnostic agents. Methods are described for the measurement of 14C and 13C in the breath. After oral administration of labelled methacetin to healthy subjects and patients with liver diseases a good correspondence between 13C- and 14C-measurements in the same subject on the one hand, and a good discrimination between controls and patients on the other hand were shown. Findings with regard to 14C measurements in urine are discussed supporting the supposed advantage of 13C-methacetin over 14C-methacetin application.

Acetamides↗

PubMed1985

Adenine therapy in Lesch-Nyhan syndrome.

In a 7-year-old patient with Lesch-Nyhan syndrome (LNS) the 15N excess frequency was determined in the excreted uric acid after oral application of 27 mg 15N glycine/kg body weight, using emission spectrometry. Incorporation of glycine into uric acid was considerably increased in untreated LNS in comparison with the control. This was due to the extremely increased endogenous de novo synthesis of purine. Allopurinol therapy caused only a gradual decrease of uric acid excretion. The pattern of purine excretion changed in favour of the better soluble oxipurines hypoxanthine and xanthine, by competitive inhibition of xanthine oxidase. In LNS, however, allopurinol had no uricostatic effect. Therapy with adenine is an alternative to influence the de novo synthesis. After adenine application a decrease of the cumulative 15N uric acid excretion occurs and the percentual proportion of 15N uric acid in total 15N excretion decreases. These changes are due to an inhibition of de novo purine biosynthesis. Adenine, however, must be applied in combination with allopurinol in order to avoid the formation of nephrotoxic 2,8-dioxiadenine by xanthine oxidase. Adenine therapy led to an improvement of the clinical course. No side-effects were observed.

Adenine↗

PubMed1984

[Protein turnover in liver failure--determination using the stable isotope 15N].

The 15N-tracer technique gives new opportunities to medical research for investigation of normal and pathological nitrogen metabolism. Analysis of 15N kinetic data derived from total nitrogen excretion in the urine allows to calculate quantitatively certain parameters of protein synthesis and protein metabolism. At the same time analysis of serum samples will allow measurement of 15N-nitrogen incorporation into particular protein or non-protein fractions of the plasma. In the study reported here patients with different liver parenchyme lesions (acute hepatitis, chronic active hepatitis, biliary obstruction, cirrhosis of the liver, hepatic coma) were investigated with a standardized 15N-tracer method developed by us. It could be shown, that protein turnover in patients with liver insufficiency is significantly decreased as compared to healthy persons. Decrease of protein synthesis is associated with a still more pronounced decrease of protein catabolism. There are significant differences in dynamics of 15N in patients with hepatic coma as compared to other patients with liver parenchyme disease without portal encephalopathy. Nevertheless, even in hepatic coma 15N incorporation into plasma proteins can be shown. Differences in the 15N elimination kinetics of the non-protein pool between patients with chronic active hepatitis, biliary obstruction and hepatic coma could be found.

Adolescent↗

PubMed1983

Combination estrogen and progestogen replacement therapy does not adversely affect coagulation.

Coagulation and fibrinolysis profiles of naturally menopausal women receiving conjugated estrogens (0.625 or 1.25 mg for 21 of 28 days) and medroxyprogesterone acetate (10 mg for seven of 28 days) for 18 months were compared with those of similar women receiving no hormone therapy. Tests indicative of the dynamics of the coagulation cascade, ongoing intravascular coagulation, and anticoagulation were performed. Hormone therapy had no effect on prothrombin times, activated partial thromboplastin times, or thrombin times. There was no evidence of intravascular coagulation in any of the groups as assessed by platelet counts, fibrinogen antigen and activity, and fibrin degradation products. Antithrombin III antigen and activity, alpha 1-antitrypsin antigen, and alpha 2-macroglobulin antigen, the natural inhibitors of coagulation, were also unaffected by hormone therapy. Plasminogen antigen levels were unaffected, but plasminogen activity was enhanced in the hormone-treated groups, suggesting a stimulatory effect on fibrinolysis. These data indicate that in terms of the coagulation system, healthy women can safely use a combined regimen of conjugated estrogens and medroxyprogesterone acetate.

Androstenedione↗

PubMedDate not supplied

Retinoic acid enhances histamine content and H1 receptor expression in human neuroblastoma cell line Paju.

BACKGROUND: A human neuroblastoma cell line (Paju) was induced by retinoic acid (RA) to differentiate into neuron-like cells. MATERIALS AND METHODS: We studied the expression and the possible role of histamine receptors H1 and H2 in retinoic-acid mediated differentiation by semiquantitative RT-PCR. We studied the effect of exogeneously added RA on the morphological change of the human neuroblastoma cell line and the differentiation was followed by vimentine, glial fibrillary acidic protein (GFAP) and neurofilament (NF) immunostaining. We monitored the change of the histidine decarboxylase (HDC) expression and the histamine content during the RA treatment by immunoblot and flow cytometry methods. RESULTS: Our data showed that H1 and H2 histamine receptors are present on Paju cells. Ten nM RA markedly increased the H1 receptor expression of these cells, while the H2 expression was unchanged. CONCLUSION: In the RA-treated Paju cells, the histamine content increased compared to the untreated cells, suggesting that neuroblastoma-derived histamine is involved in the regulation of RA-induced in vitro differentiation by H1 receptors.

Cell Differentiation↗