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Biomedical subjects

U Schwedes

Publications and source records attributed to U Schwedes.

At least 19 recordsLinked to original sources
PubMed1990

Evidence for a role of anti-idiotypic antibodies in the induction of remission in Graves' disease.

Serum and Ig samples obtained from a patient with Graves' disease during exacerbation and remission were evaluated in the nu/nu bioassay. Blocking of the exacerbation serum's biological activity was demonstrated by several biological assay parameters after it was mixed with the remission serum. Since this blocking effect can be ascribed to immunoglobulins, anti-idiotypic antibodies in the remission serum and immunoglobulin samples are the most likely cause of this blocking effect. Therefore a role of anti-idiotypic antibodies in the induction of remission in Graves' disease is postulated.

Animals↗
PubMed1989

[Results of clinical trials with the gluconeogenesis inhibitor 2-(3-methylcinnamylhydrazono)-propionate (MCHP)].

Many compounds which directly or indirectly inhibit gluconeogenesis have been described. Some of them showed hypoglycemic action in animal experiments. 2-(3-Methylcinnamylhydrazono)-Propionat (MCHP) a derivative of hydrazine demonstrated marked hypoglycemic action in animal experiments. Nontheless the administration of MCHP to type II diabetic patients showed no hypoglycemic action. Clinical or biochemical sideeffects could not be observed.

Aged↗
PubMed1989

The role of gastric and duodenal pH in the cysteamine-induced duodenal ulcer in the rat.

Many secretory studies reported an increase in gastric acid secretion by the duodenal ulcerogen cysteamine. A detailed analysis of these experiments, especially the results from rats with chronic gastric fistula suggest that direct stimulation of gastric acid secretion may not be the primary mechanism of the duodenal ulcerogenic action of cysteamine. We used a different approach and measured the pH at the site of ulceration in the proximal duodenum. A duodenal ulcerogenic dose of cysteamine did not change the pH at the anterior or posterior wall of the duodenum during 4 hr. In the same dose and by the same route of administration, cysteamine nevertheless induced duodenal ulcers in 24 hr. These experiments demonstrate that in addition to the effect on gastric acid secretion, other factors are needed to the effect on gastric acid secretion, other factors are needed to explain the early duodenal ulcerogenic action of cysteamine.

Animals↗
PubMed1987

[The hypothalamo-hypophyseal thyroid axis, plasma protein concentrations and the hypophyseo-gonadal axis in low T3 syndrome following acute myocardial infarct].

In patients with severely acute diseases, a special relationship of thyroidal hormones with decreased T3 and increased rT3 levels is known, the so-called low T3 syndrome. The aim of this study was to elucidate the involvement of the hypothalamo-pituitary thyroid axis, the pituitary-gonadal axis, the altered hepatic function, the plasma proteins in the low T3 syndrome, and the evaluation of these parameters for prognosis in patients with acute myocardial infarction. Thirty-one patients (29 male, 2 female) with AMI entered the study for the determination of hypothalamo-pituitary thyroid axis and the plasma proteins. Besides routine laboratory determinations, TRH, TSH, T4, T3, rT3, CHE, albumin, total protein, TBG, and estradiol concentrations in plasma were measured daily for 5 days after AMI using immunological and other methods. Twelve male patients with AMI entered the study for the determination of pituitary-gonadal axis; the T3, rT3, estradiol, testosterone, FSH, and LH concentrations in serum were determined using immunological methods. We found that T3 and T4 decreased significantly to a minimum on the first and the second day, respectively, after admission and increased in the course of the observation period. In contrast, rT3 was elevated significantly within the first 2 days and decreased later. TSH and TRH decreased in the first 2 days and increased in the following days. CHE, albumin, and total protein levels significantly showed a minimum on day 4 and TBG significantly showed a minimum on the second day after AMI and increased to day 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Proteins↗
PubMed1987

Plasma levels of thyrotropin-releasing-hormone in various splanchnic, renal, suprarenal, and cerebral veins.

Endogenous TRH levels were determined in plasma obtained selectively via percutaneous transhepatic and femoral catheterization. TRH was measured using a very sensitive RIA method. In the pancreatic veins, internal jugular vein, left testicular vein, and other described veins, normal peripheral levels were found. An involvement of the TRH degrading enzyme (TDE) or a rapid intravasal dilution leading to normal peripheral TRH levels in the veins leaving the brain or pancreas, respectively, is discussed.

Adenoma↗
PubMed1987

Is remission of Graves' disease regulated by anti-idiotypic antibodies?

Our results show evidence for regulation of Graves' disease remission by anti-idiotypic antibodies in a biologic assay. The polyclonality and functional heterogeneity of thyroid receptor antibodies is most likely the reason why evidence for idiotypic-anti-idiotypic regulation can be demonstrated in the autologous but not consistently in the homologous system.

Animals↗
PubMed1987

Transplantation of human endocrine tissues to nude mice: a suitable in vivo model for the study of pathomechanisms involved in autoimmune thyroid diseases.

After transplantation of human tissue to nu/nu mice the human lymphocytes disappear. In this context, interestingly, the DR-expression is not detectable anymore after transplantation of the tissues from patients with autoimmune thyrotoxicosis and cancer. Neopterin release was only demonstrable when T-lymphocytes from patients with autoimmune thyrotoxicosis or PHA-stimulated lymphocytes were added, independently of the presence of DR-expression in the used culture tissues. These results seem to exclude a functional role of DR-expression as a trigger mechanism of autoimmunity. It is supposed that DR-priming on epithelial cells is mediated by kinine production of activated T-lymphocytes or macrophages.

Animals↗
PubMed1986

The role of adrenal medulla in endogenous dopaminergic inhibition of aldosterone secretion.

Evidence has accumulated that aldosterone secretion is under endogenous dopaminergic inhibition. To examine potential sources of the dopamine thus inhibitorily acting in the adrenal zona glomerulosa, the responsiveness of aldosterone, plasma renin activity, prolactin, and plasma catecholamines to haloperidol, a dopaminergic antagonist, was studied in rats 6 weeks after unilateral adrenalectomy (Group B), 6 weeks after unilateral adrenal demedullation followed by contralateral adrenalectomy 5 days later (Group C), and in controls without any pretreatment (Group A). In Group C, there were increases in basal levels of norepinephrine (P less than 0.01), prolactin (P less than 0.02), and aldosterone (P less than 0.01). Basal plasma renin activity was also increased (P less than 0.05), epinephrine concentrations were decreased. Two hours after haloperidol 1 mg/kg b.wt. i.p., aldosterone levels were increased in Groups A + B (P less than 0.01) but unresponsive in Group C. Haloperidol-induced stimulation of prolactin and norepinephrine was not impaired by the surgical procedures. Epinephrine levels were increased by haloperidol only in groups A + B (P less than 0.002). In none of the groups were plasma renin activity or dopamine levels influenced by haloperidol. It is concluded that dopaminergic inhibition of aldosterone production is brought about neither by circulating dopamine nor by potential dopaminergic nerves accompanying arterial blood supply of the adrenal cortex but by dopamine originating directly in adrenal medulla.

Adrenal Medulla↗
PubMed1986

Endogenous dopaminergic inhibition of aldosterone and prolactin secretion is apparently not increased in primary aldosteronism.

To examine the previous suggestion that the endogenous dopaminergic activity would be increased in patients with primary aldosteronism, dose-response curves of aldosterone and prolactin stimulation by the dopamine antagonist metoclopramide were established in a pilot study by injecting metoclopramide 1, 2.5, and 10 mg i.v. consecutively at hourly intervals to 6 patients with primary aldosteronism and 14 healthy volunteers. All three metoclopramide doses induced clear-cut rises in aldosterone levels both in patients with primary aldosteronism and healthy controls. Basal aldosterone concentration was higher in range in the patients but the dose-response curves were nearly parallel one with the other. Prolactin responsiveness was also very similar. Thus, the present findings do not support the hypothesis of an increase in endogenous dopaminergic activity in primary aldosteronism.

Adult↗
PubMed1986

Evidence for increased endogenous dopaminergic inhibition of aldosterone secretion in prolactinoma.

Aldosterone responsiveness to consecutive i.v. injections of metoclopramide 1 mg, 2.5 mg and 10 mg was studied in 8 patients with prolactinoma and normally preserved adrenal function and in 14 healthy volunteers. In the patients, aldosterone response to metoclopramide 1 mg was blunted. After metoclopramide 10 mg, aldosterone rose to the same levels in patients and volunteers. In the patients, however, percentage rise of aldosterone was enhanced, since the appropriate base line concentration of aldosterone was decreased. Thus, there is evidence for increased endogenous dopaminergic inhibition of aldosterone secretion in prolactinoma.

Adult↗
PubMed1986

Clinical effect of dopamine on incidence of peptic ulceration.

Dopamine and its agonists diminish gastric acid secretion and exert a protective effect on experimentally induced peptic ulcers in rats. For treatment of peptic ulcer disease in man, dopamine and dopamine antagonists have been recommended, but clear evidence is not yet available. To answer the question of whether dopamine has any protective effect regarding peptic ulcer formation in man, autopsy reports were evaluated for the incidence of acute peptic ulcerations before and after the introduction of dopamine as a common drug in intensive care units. The analysis showed no change in ulcer incidence, i.e., our retrospective study demonstrated no ulceroprotective action of dopamine in critically ill patients.

Dopamine↗
PubMed1986

Cytoprotective properties of somatostatins.

Secretion of many hormones is inhibited by regular cyclic somatostatin-14. Since additional cytoprotective properties of this hormone have been described, the question arises of whether analogs of somatostatin with increased endocrine activity may also exert increased cytoprotective activity. It could be shown that the endocrine and the cytoprotective property of somatostatin-14 must have different modes of action. In analogs of somatostatin with increased endocrine activity the cytoprotective effect is also increased. A maximal increase in the cytoprotective effect of certain analogs of somatostatin is accompanied by a loss of endocrine activity.

Amino Acid Sequence↗
PubMed1986

Protection against duodenal ulceration by somatostatins.

The purpose of our investigation was to study the effect of two somatostatin analogs (SMS 201-995 and 008) on duodenal ulcer disease induced by cysteamine in rats. Male Wistar rats were given cysteamine (28 mg/100 g body wt.) by rubber stomach tube three times in a single day. All animals of the test group were injected subcutaneously either with SMS 201-995 in different doses or with 008. On the 3rd day stomach, duodenum, and adrenal glands were macroscopically examined for lesions (duodenal ulceration, gastrointestinal bleeding, adrenal hemorrhage). Our results showed a dose-dependent effect of SMS 201-995 on the mortality, incidence, and intensity of cysteamine-induced duodenal lesions in rats. The incidence and the intensity of gastrointestinal bleeding and adrenal hemorrhage were also dose-dependently reduced by SMS 201-995. There was no definite effect of 008 on the mortality, incidence, or intensity of cysteamine-induced duodenal ulceration.

Adrenal Glands↗