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Biomedical subjects

A Nauman

Publications and source records attributed to A Nauman.

At least 19 recordsLinked to original sources
PubMed2001

Type I 5'-iodothyronine deiodinase activity and mRNA are remarkably reduced in renal clear cell carcinoma.

The purpose of this study was to compare thyroid hormone metabolism between non-cancerous tumor-surrounding human kidney tissues and renal clear cell carcinomas (RCCC). The material consisted of samples taken from 10 RCCC patients of both sexes and three grades of differentiation, G1 to G3. We showed that, similar to rat tissue, type I 5' monodeiodinase (5'DI) expression is heterogeneous within the human kidney. We also found a poor correlation between 5'DI activity and mRNA level in non-cancerous tumor-surrounding tissue suggesting significant post-transcriptional regulation of 5'DI expression by an unidentified process in the human kidney. In all RCCC tissues both 5'DI activity and mRNA levels were undetectable. This suggests either loss of human 5'DI gene expression during neoplastic transformation or the origination of RCCC from a tubular cell type that does not express 5'DI.

Adenocarcinoma, Clear Cell↗
PubMed2000

Expression of thyroid hormone receptors is disturbed in human renal clear cell carcinoma.

Human renal clear cell carcinoma (RCCC) accounts for up to 2% of human cancers. To find out if thyroid hormone (T3) and its receptors (TRs) play a role in tumorigenesis of RCCC, the expression of TRs was evaluated on mRNA and protein level. It was found that TRalpha (both alpha1 and alpha2) mRNA amount was significantly decreased in tumors while compared with healthy kidney tissue, and this decrease was deepest in G1 (well differentiated) RCCCs. In contrast, TRalpha1 protein was 1.6x overexpressed in tumors. TRbeta1 mRNA amount was overexpressed in 30% and significantly decreased in 70% of examined tumors. On the protein level, TRbeta1 amount was 1.7x lower in tumors than in healthy controls.

Adenocarcinoma, Clear Cell↗
PubMed1995

The deiodination of thyroxine to triiodothyronine in the testes of patients with prostate cancer.

Until recently metabolism and expression of thyroid hormones was considered not to occur in the tissues of the testes. Lately, specific receptors for triiodothyronine have been found in the nuclei of human testicular cells which shows that testicular tissue requires hormonal action [9]. The aim of the present study was to evaluate if the prohormone thyroxine is converted into triiodothyronine within human testes (resected because of prostatic carcinoma) and if hormonal therapy with dihydrostilbestrol (DES), a testosterone antagonist, affects production of the active thyroid hormone. Our earlier studies showed a complete lack of iodothyronine 5'-deiodinase activity in prostatic carcinoma (PC) [7]. The present material consisted of testes from 21 patients with PCs. According to Whitmore's classification 13 patients were at stage C with mean PSA of 70.15 ng/ml and 8 were at stage D with mean PSA of 308.73 ng/ml. Before castration 6 patients (3 stage C and 3 stage D) were pretreated with 3 mg DES daily for 3 days. The resected testes were homogenized and ultracentrifuged. The obtained microsomal fraction was the source of thyroxine 5'-deiodinase (T4-5'-D). In 15 patients, in whom the primary approach was surgical, the specific T4-5'-D activity was not different between stage C and D patients (mean +/- SD): 19.52 +/- 12.55 vs. 22.07 +/- 12.68 fmol de novo produced triiodothyronine/min/mg of microsomal protein, respectively. However, in 6 patients pretreated with DES the activity was significantly decreased, regardless of the degree of differentiation of the prostate carcinoma: 0.70 +/- 0.68 fmol T3/min/mg for stage C and 2.6 +/- 4.5 fmol/min/mg for stage D patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Pharmacologic effect of excess iodine on type I thyroxine 5'-deiodinase activity in rat thyroid].

Many mechanism may participate in the inhibition of thyroid function by excess of iodine. The present study was aimed at answering the question, whether the excess of iodine influences the activity of type I thyroxine 5'-deiodinase. To 40 female rats fed with standard diet a dose of 42 micrograms of iodine daily was administered into the stomach through the gastric tube. Control group consisting of 10 rats received standard diet only. Part of the animals was sacrificed after each of the consecutive time intervals (2, 4, 7 and 14 days of treatment with iodine) and the activity of deiodinase in the thyroid as well as the blood serum levels of hormones, T3 and T4, were determined. A decrease in the activity of deiodinase in comparison with control group was observed during the whole experiment, the highest inhibition occurring after 4 days of treatment with iodine. A fall in the concentration of T3 was observed after the second and fourth dose of iodine, with no change in T4 concentration. The results of the experiments indicate that the excess of iodine inhibits the activity of type I thyroxine 5'-deiodinase in the thyroid.

Animals↗
PubMed1987

Decrease of rat-liver-T4-5'-deiodinase activity during chronical isoprenaline beta-action in vivo.

Pure adrenergic beta-action, brought about by long-term adrenaline + regitine application in rats, was able to increase liver T4-5'-deiodinase activity for 8 h (Nauman et al. 1984a). Long-term isoprenaline application without alpha-blocking yielded contrary results. One of the compensatory mechanism to be probably blamed could have been the very high endogenous adrenaline-levels (Porta et al. 1985). Simultaneous treatment with isoprenaline and alpha-methyltyrosinemethylester did not settle the problem since even then deiodinase activity was still drastically decreased. Two more components have been found which could very well be the reason for that "paradox beta-action" in vivo, namely very low glucose and insulin levels, both of which are known to influence deiodinase activity. In vivo--contrary to in vitro--it is seemingly not possible that catecholaminergic beta-action could increase the peripheral production of T3 unless general alpha-blocking took place.

Animals↗
PubMed1986

Failure of bone marrow cryopreservation in chronic granulocytic leukemia: relation to excessive granulo-macrophagic progenitor pool.

Autologous bone marrow transplantation (ABMT) in chronic granulocytic leukemia (CGL) aims at reversing the acute or acceleration phases by injection of stem cells collected during the chronic phase. This study was designed to explain an unusual rate of delayed engraftment (50%) in our experience of ABMT in CGL patients. We investigated all the factors possibly responsible for abnormal perpetuation of aplasia following infusion of cryopreserved marrow stem cells. The study of CFU-gm recovery in 41 bags of frozen marrow from 25 patients revealed an overall deficiency with a mean CFU-gm recovery of 55 +/- 38% in CGL patients versus 73 +/- 15% in the control group (p less than 0.001). Our data also showed an inverse linear relation (r = -0.40, p less than 0.05) between CFU-gm concentration and recovery after freezing. A good CFU-gm recovery (greater than or equal to = 50%) was observed in 70% of cases when the concentration was less than 3700 CFU-gm/ml as compared to 30% of cases when the concentration was over 3700 CFU-gm/ml (p less than 0.001). The lack of improvement by diluting rich CFU-gm marrows to reduce CFU-gm concentration/ml, as well as the absence of relationship between CFU-gm recovery after freezing and nucleated cells concentration, suggest a particular fragility of CGL stem cells to freezing, probably related to their excessive amplification. At the present time, we strongly recommend that the highest possible dose of progenitor cells be cryopreserved, preferably at a low concentration, in patients with CGL, and particular attention devoted to the freezing procedure in each individual patient, with numerous appropriate efficiency tests.

Bone Marrow Cells↗
PubMed1984

The effect of adrenaline pretreatment on the in vitro generation of 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine (reverse T3) in rat liver preparation.

The effects of adrenaline (A) on liver T3 and rT3 neogenesis from T4 were studied in Wistar rats. The animals were implanted subcutaneously either with A or placebo (P) especially coated tablets which linearly released the hormone. The serum A values 6 hrs after implantation of 7.5, 15.0 and 45.0 mg tablets were 6.5 +/- 1.31, 6.8 +/- 1.8 and 16.4 +/- 1.9 ng/ml, respectively vs 4.4 +/- 2.5 ng/ml seen in P pretreated group. The output rates of A were 0.11 (7.5 mg), 0.18 (15 mg) and 0.52 microgram/ml (45 mg). The pretreatment with A led to hyperglycemia and the "low T3 syndrome". Neogenesis of T3 from T4 in medium containing liver microsomes of P pretreated rats was 5.49 +/- 0.25 pmol of T3/mg protein/min and decreased in A pretreated rats to 3.82 +/- 0.17, 3.12 +/- 0.27 and 3.06 +/- 0.11 pmol of T3/mg of protein/min. Neogenesis of rT3 from T4 in microsomes from P group was 1.52 +/- 0.09 pmol rT3/mg protein/min and increased after A to 2.71 +/- 0.11, 2.60 +/- 0.21 and 2.21 +/- 0.34 pmol of rT3/mg protein/min thus showing no dose dependency. Enrichment of microsomes medium with cytosol either from P or A pretreated rats had no effect on T3 generation thus excluding effect of A on cytosolic cofactor. Although cytosol further increased rT3 neogenesis this was seen regardless of whether cytosol was obtained from A or P implanted rats. It is concluded that A decreases the activity of T4-5'-deiodinase in liver, and possibly increases the activity of T4-5-deiodinase.

Animals↗
PubMed1980

In vivo and in vitro effects of adrenaline on conversion of thyroxine to triiodothyronine and to reverse-triiodothyronine in dog liver and heart.

Infusion of adrenaline in healthy dogs in a dose simulating spontaneous release of the catecholamine during experimental myocardial infarction produced a significant decrease in the conversion of thyroxine (T4) to triiodothyronine (T3) and a moderate increase in the conversion of T4 to reverse-triiodothyronine (rT3). Similar changes in deiodination of T4 to T3 and to rT3 were also observed when adrenaline was added in vitro to liver and heart homogenates. These results are consistent with a direct effect of adrenaline on T4 deiodination as degradation of exogenous T4, T3 and rT3 was only slightly increased under the experimental condition employed. The present study suggests that increased tissue exposure to adrenaline might contribute to the hormonal changes seen in at least some case of the 'low T3 syndrome'.

Animals↗
PubMed1979

Effects of beta-blocking agent Metipranolol on metabolic variables in patients with ischemic heart disease, hyperkinetic syndrome, hyperthyreosis and in healthy subjects.

Metabolic effects of Metipranolol, a new beta adrenergic blocking agent, have been studied in patients with ischemic heart disease, hyperkinetic syndrome, hyperthyreosis and in healthy subjects. Administration of the drug (30 mg per day for one week) resulted in the decrease of noradrenaline excretion, blood free fatty acid level, and in lowering of blood pressure and heart rate, particularly in patients with ischemic heart disease and hyperkinetic syndrome. These alterations were accompanied by alleviation of clinical symptoms. It is suggested that Metipranolol by suppressing the activity of sympathetic nervous system and thereby diminishing lypolysis, exerts favourable clinical effects, most probably related to diminution of myocardial oxygen consumption.

Adrenergic beta-Antagonists↗
PubMed1978

Evidence for the detrimental effect of adrenaline infused to healthy dogs in doses imitating spontaneous secretion after coronary occlusion.

We have previously shown that acute coronary occlusion in the dog is often accompanied by increased adrenaline release into the blood. In the present study the consequences of this humoral reaction were studied in anaesthetised healthy mongrel dogs subjected to adrenaline infusion administered at a rate relevant to spontaneous release of this amine in coronary occlusion. Adrenaline was infused in a dose of 1.2 microgram.kg-1.min-1 for 4 h. Dogs receiving saline served as the control. Adrenaline administration led to the decrease in insulin/glucose ratio, to a significant fall in serum triiodothyronine and in blood pH. Free fatty acid levels doubled. Histochemically, a diminution in succinic dehydrogenase and ATPase activity in adrenaline-treated hearts was found. A significant fall in the activity of mitochondrial hexokinase in these hearts was detected spectrophotometrically. Electron microscopic study revealed alterations in the mitochondrial structure. These findings indicate that an excess of adrenaline in ammounts similar to that seen in experimental infarction leads to profound metabolic and hormonal disturbances and exerts a detrimental effect upon myocardium.

Animals↗