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Biomedical subjects

M Hermann

Publications and source records attributed to M Hermann.

At least 181 records · Page 10Linked to original sources
PubMed1989

[Prostaglandin interaction in the human liver].

The binding of prostaglandin (PG) E1 and Iloprost, a chemically stable PGI2-analogue, to purified plasma cell membranes (LPZM) from liver tissue samples obtained at surgery revealed heterogeneity of the binding sites identifying high and low affinity subpopulations. In contrast to these findings only high affinity binding sites were characterized for PGE2. Displacement studies exhibited the highest competition for the PGE1-sites by PGE1 and subsequently by PGE2, Iloprost, PGD2 and PGF2 alpha. The binding of PGE2 to the hepatic receptor could be best displaced by PGE2 and subsequently by PGE1 and Iloprost, PGD2 and PGF2 alpha. In addition, PGE1, PGE2 and Iloprost enhanced cAMP-production dose-dependently over baseline. Clinical studies revealed a remarkably lower binding capacity for PGE1 in hepatocellular cancer tissue than in normal liver parenchyma. The different binding behaviour of PGE1 (Iloprost) and PGE2 for the first time provides evidence that PGE1 and PGI2 like at platelet membranes occupate the same receptor also at human LPZM. Since a reasonable number of binding sites for these substances and an enhanced cAMP-production were shown in the liver, the study indicates a regulatory role of PGs in hepatic function.

Alprostadil↗
PubMed1989

Haematological and biochemical findings in cattle with dilatation and torsion of the caecum.

A biochemical examination was made of the blood and rumen fluid of 111 heifers and cows suffering from caecal dilatation, with or without torsion. Haematological values were normal in the majority of cattle. Concentrations of chloride were normal in the rumen fluid of 83 per cent of the animals and higher in the remainder. Nine cows that had to be slaughtered had higher bile concentrations than those which recovered. Twenty-eight per cent had increased blood urea concentrations probably due to dehydration.

Animals↗
PubMed1989

Binding of globin mRNA, beta-globin mRNA segments and RNA homopolymers by immobilized protein of polysomal globin messenger ribonucleoprotein.

The binding of rabbit globin mRNA, in-vitro-generated beta-globin mRNA segments, and RNA homopolymers by proteins of rabbit reticulocyte polysomal messenger ribonucleoproteins (mRNP) after SDS gel electrophoresis and electroblotting was examined. The polysomal mRNP proteins have a higher affinity for mRNA than for rRNA and tRNA while having a higher affinity for polypurine than polypyrimidine homopolymers. Binding experiments with synthetic poly(A) and with segments of beta-globin mRNA transcribed from a cDNA in vitro revealed a set of polysomal mRNP proteins which preferentially bind the poly(A)-free beta-globin mRNA. A protein of Mr 90,000 binds specifically the 3'-nontranslated trailer of the poly(A)-free beta-globin mRNA and not the poly(A)-containing globin mRNA. Another set of proteins preferentially binds poly(A). The latter group of proteins contains a prominent species of Mr 72,000, which is most likely the rabbit poly(A)-binding protein. Three polysomal mRNP proteins which bound rabbit globin mRNA did not bind preferentially any of the other RNA probes used.

Animals↗
PubMed1989

Differential effect of hemin-controlled eIF-2 alpha kinases from mouse erythroleukemia cells on protein synthesis.

Cultured mouse erythroleukemia (MEL) cells can be induced to erythroid differentiation by a variety of chemical agents. This differentiation process is marked by the onset of globin mRNA and hemoglobin synthesis. In rabbit reticulocytes, globin synthesis is regulated by a hemin-controlled translational inhibitor (HCI) which acts via phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF-2). From both uninduced and induced MEL cells, hemin-controlled eIF-2 alpha kinases have been partially purified. They resemble HCI with respect to their chromatographic behaviour and their sensitivity towards physiological concentrations of hemin (5-10 microM). Further purification on phosphocellulose, however, reveals that the eIF-2 alpha kinase from uninduced MEL cells is chromatographically distinct from HCI, whilst the eIF-2 alpha kinase activity from induced MEL cells represents a mixture of the former and the HCI-type eIF-2 alpha kinase. The latter inhibits protein synthesis in a fractionated system from rabbit reticulocytes which is free of, but sensitive to, HCI, whereas the eIF-2 alpha kinase from uninduced MEL cells does not show any inhibitory activity. This observation is supported by the finding that induced MEL cells respond in vivo to iron depletion with a shut-off of protein synthesis (as do rabbit reticulocytes), whilst uninduced MEL cells do not.

Animals↗
PubMed1989

Decrease of the prostaglandin I2 binding capacity in thyroids from patients with Graves' disease.

Properties of prostaglandin (PG) I2-binding sites in human thyroids from euthyroid and thyrotoxic patients were investigated. The specific binding of 3H-iloprost (ZK 36374, a chemically stable PGI2-analogue) to normal thyroids approached saturation at a concentration of more than 150 nmoles/L and could be displaced most effectively by unlabeled iloprost (concentration causing the half maximal inhibition, IC-50 = 5.9 +/- 2.9 mumoles/L) and PGI2 (IC-50 = 9.8 +/- 3.1 mumoles/L) and less effectively by unlabeled PGF2 alpha (IC-50 = 847.9 +/- 123.8 mumoles/L) at 4 degrees C. The Scatchard analysis clearly indicated heterogeneity revealing the presence of 0.65 +/- 0.18 pmoles/mg protein at the high-affinity binding sites (equilibrium dissociation constant, Kd = 18.2 +/- 9.1 nmoles/L) and 5.35 +/- 1.6 pmoles/mg protein at the low-affinity binding sites (Kd = 151.3 +/- 43.1 nmoles/L). In contrast, in diffuse colloid struma derived from patients with Graves' disease a single class of binding sites with an apparent binding capacity of 0.18 +/- 0.05 pmoles/mg protein (Kd = 70.4 +/- 27.3 nmoles/L) was indicated. However, in diffuse colloid struma derived from euthyroid patients no difference in the number of binding sites and binding affinity of 3H-iloprost was noted compared to normal thyroids. The data provide evidence for the presence of specific PGI2-binding sites in the human thyroid gland and demonstrate a significant decrease of the receptor density in patients with Graves' disease. It is suggested, that PGI2 has an important role in the regulation of human thyroid function.

Binding Sites↗
PubMed1989

Human hepatocellular cancers show decreased prostaglandin E1 binding capacity.

Specific binding of 3H-PGE1 to plasma membranes prepared from normal human hepatic tissue in the presence of Mg2+ reached saturation at concentrations greater than 50 nM, and could be displaced in the rank-order PGE1 greater than PGE2 greater than PGI2 greater than PGD2 greater than PGF2 alpha at 4 degrees C. Plasma membranes prepared from normal human hepatic tissue showed a high-affinity 3H-PGE1-binding capacity of 51.3 +/- 19.2 fmol mg-1 plasma membrane protein with an equilibrium dissociation constant of 3.8 +/- 1.9 nM, and a low-affinity 3H-PGE1-binding capacity of 104.2 +/- 17.3 fmol mg-1 protein with an equilibrium dissociation constant of 13.9 +/- 2.7 nM. Plasma membranes prepared from hepatocellular cancer tissue revealed a single class of binding sites with an apparent binding capacity of 38.4 +/- 17.3 fmol mg-1 plasma membrane protein (P less than 0.05) and an equilibrium dissociation constant of 12.1 +/- 2.8 nM. Competition studies on plasma membranes prepared from hepatocellular cancer tissue indicated no significant difference in the affinity of various prostaglandins to the receptor proteins as compared to normal hepatic tissue. It is assumed that the decreased 3H-PGE1-binding capacity found in human hepatocellular cancer tissue may reflect an alteration of the receptor protein content of the hepatocytes during carcinogenesis.

Adult↗
PubMed1989

Comparison of respiratory secretion cytology and pulmonary histology in horses.

Equine respiratory secretions (RS) collected before (33 horses) and after (76 horses) slaughter were evaluated cytologically and grouped according to the histological diagnosis of the lungs from which they were obtained. The histological categories included normal lungs (control; 17 horses), chronic small airway disease with mild (23 horses), moderate (13 horses) and severe lesions (25 horses), interstitial pneumonia (13 horses), pulmonary eosinophilic infiltration (13 horses) and pulmonary haemorrhage (5 horses). On a group basis there were significantly more neutrophils in RS of horses with mild, moderate and severe chronic small airway disease and interstitial pneumonia than in control horses. Horses with severe chronic small airway disease had significantly more lymphocytes and significantly fewer ciliated columnar epithelial cells in RS than control horses. Significantly more eosinophils were seen in RS of horses with pulmonary eosinophilic infiltration than in control horses. On an individual horse basis all horses with moderate and severe chronic small airway disease and with pulmonary haemorrhage had a RS cytology which differed from that of control horses; however, some horses with mild chronic small airway disease (11 horses), pulmonary eosinophilic infiltration (4 horses) and interstitial pneumonia (3 horses) did not have an RS cytology that differed from control horses.

Animals↗
PubMed1989

Similarities between the effects of pinacidil and diazoxide on ionic and secretory events in rat pancreatic islets.

The present study aimed at comparing the effects of pinacidil, a putative K+ channel opener, and diazoxide on ionic and secretory events in rat pancreatic islets. Pinacidil and diazoxide provoked a dose-dependent increase in 86Rb outflow from pancreatic islets perifused in the presence of glucose. Both drugs inhibited the glucose- and tolbutamide-induced increase in 45Ca outflow and insulin release whereas failing to affect the ionic and secretory responses to K+ depolarization. Pinacidil and diazoxide, in contrast to quinine, failed to affect 86Rb outflow from pancreatic islets stimulated by the Ca++-ionophore A23187. Pinacidil as well as diazoxide abolished the glucose-induced increase in [Ca++]i but did not modify the rise in [Ca++]i provoked by KCl. Lastly, both drugs were shown to stimulate an ouabain-resistant modality of 86Rb inflow into the islet cells. The close similarities between the ionic and secretory events mediated by pinacidil and diazoxide suggest that pinacidil could interfere with the same target site as diazoxide; namely the beta-cell ATP-sensitive K+ channel.

Animals↗
PubMed1989

[Loss of high-affinity prostacyclin binding sites in patients with Basedow's disease].

Prostacyclin (PGI2) mediates like TSH its cellular effects through the interaction with specific binding sites associated with the adenylate cyclase-cAMP-system. Binding of PGI2 and the generation of cAMP induced by PGI2 was evaluated in thyroid tissue obtained intraoperatively from euthyroid and hyperthyroid patients with diffuse normofollicular colloid struma. Transformation of the binding data according to Scatchard revealed heterogeneity of the PGI2 binding sites in the tissue of euthyroid patients: the high-affinity binding sites were calculated to be 0.68 +/- 0.18 pmol/mg protein (Ka = 16.2 +/- 9.1 nM) and the low-affinity binding sites to be 5.4 +/- 1.6 pmol/mg protein (Ka = 151 +/- 43.1 nM). In contrast, in the hyperthyroid patients the low-affinity binding sites were not demonstrable and the high-affinity sites were significantly (p less than 0.001) reduced (0.17 +/- 0.05 pmol/mg protein, Ka = 83.5 +/- 19.6 nM). The competition of the agonist for the PGI2 sites in hyperthyroid patients was significantly (p less than 0.005) diminished (IC-50-values: 0.98 +/- 3.1 vs 46.9 +/- 12.1 microM). PGI2 stimulated cAMP-production in a dose-dependent manner. However, the basal value was significantly lower also in the hyperthyroid patients (p less than 0.001). The evidence of reduced PGI2 sites as well as reduced PGI2-induced cAMP production in the thyroid gland of patients with Graves' disease may indicate an important role for PGI2 to play in the modulation of thyroid cell function.

Adult↗
PubMed1989

["Secondary surgery" in the oncologic concept of malignant struma].

Between 1978-1987 a reoperation had to be performed on 115 patients with carcinoma of the thyroid gland due to oncologically inadequate initial surgery. In papillary carcinomas, the high percentage of T1-tumors (43.1%) were the reason for lack of prae- or intraop. diagnostic evaluation, with the follicular carcinomas the high percentage of borderline frozen section. With invasive carcinomas, residues of the tumor were found either in the remaining thyroid tissue or in the lymph nodes (20.8%) while no further tumor has been found in encapsulated carcinomas. The rate of recurrent nerve paralysis document right after reportation was 18%, and its frequency depended on the time interval between initial surgery and reoperation. With encapsulated carcinomas of the type T1 we would suggest not to consider a reoperation, because we do not expect intrathyreoidal metastasation nor tumor involved lymph nodes and the risk of causing a recurrent nerve paralysis by a reoperation is not justifiable.

Adenocarcinoma↗
PubMed1988

Pinacidil inhibits insulin release by increasing K+ outflow from pancreatic B-cells.

Pinacidil, a putative K+ channel opener, increased 86Rb outflow from rat pancreatic islets perifused in the presence of glucose, 2-ketoisocaproate or tolbutamide. Furthermore, the drug markedly inhibited 45Ca outflow and insulin release from glucose-stimulated islets. These results represent the first indication of an effect of pinacidil on ionic and secretory events in endocrine cells. Indirect findings suggest that, in pancreatic islet cells, pinacidil could affect ATP-sensitive K+ channels.

Adenosine Triphosphate↗
PubMed1988

Failure of Leiurus quinquestriatus venom to affect potassium movements in pancreatic islets.

The venom from the Israeli scorpion Leiurus quinquestriatus failed to affect 86Rb and 45Ca outflow from rat pancreatic islets perifused in the presence of tetrodotoxin and stimulated by the Ca2+-ionophore A23187 or the hypoglycaemic sulfonylurea tolbutamide. In non-stimulated islets, the venom components whose effects are insensitive to tetrodotoxin did not affect 45Ca and 86Rb outflow. Last, the venom did not alter 86Rb inflow. These findings suggest that 86Rb, 45Ca fluxes and more specifically the Ca2+-activated K+ permeability in the pancreatic B-cell are insensitive to the venom.

Animals↗
PubMed1988

Evaluation of prostaglandin-receptors in human and rat liver: interspecies differences at the prostaglandin receptor-level.

The properties of PGE1-, PGE2- and iloprost (stable PGI2-analogue)-binding sites on normal human and rat liver surface cell membranes were investigated. The specific binding of [3H]PGE1 to human (rat) liver surface cell membranes could be displaced most effectively by unlabeled PGE1 (IC-50:2.5 +/- 1.7, (6.1 +/- 2.1) microM) and the specific binding of [3H]PGE2 by unlabeled PGE2 (IC-50: 1.9 +/- 0.9 (2.0 +/- 0.8) microM. The Scatchard analysis on [3H]PGE1- as well as on [3H]iloprost-binding was curvilinear whereas it was clearly linear on [3H]PGE2-binding in both the species. The high-affinity [3H]PGE1-sites showed a Bmax of 36.3 +/- 5.2 (21.3 +/- 4.3) fmol/mg protein and a Kd of 2.1 +/- 1.8 (1.9 +/- 0.7) nM, the low-affinity [3H]PGE1-sites a Bmax of 93.4 +/- 18.2 (86.1 +/- 13.2) fmol/mg protein and a Kd of 10.5 +/- 2.9 (15.1 +/- 3.2) nM. The high-affinity [3H]iloprost-sites exhibited a Bmax of 71.4 +/- 13.9 (35.9 +/- 8.2) fmol/mg protein and a Kd of 4.1 +/- 1.2 (1.7 +/- 1.8) nM, the low-affinity [3H]iloprost-sites a Bmax of 217.3 +/- 42.1 (142.9 +/- 17.8) fmol/mg protein and a Kd of 16.3 +/- 4.9 (9.2 +/- 7.2) nM. The [3H]PGE2-sites showed a Bmax of 135.4 +/- 51.9 (38.8 +/- 7.4) fmol/mg protein and a Kd of 16.2 +/- 3.2 (2.5 +/- 1.2) nM. It is assumed that prostaglandins of the E-series are promising substances in the regulation of human and rat liver function since liver cells are able to bind reasonable amounts of these substances in a high affinity manner. However, interspecies differences in the affinity of the prostaglandins to their receptor-sites make it strange to assume that the same biological findings claimed several times for the rat liver are relevant for human too.

Animals↗
PubMed1988

Decrease of prostaglandin I2 binding sites in thyroid cancer.

The properties of specific prostaglandin I2 (prostacyclin, PGI2) binding sites in normal thyroid tissue have been characterised. Tissue samples obtained intraoperatively from patients with 'cold' solitary thyroid nodules (as preoperatively selected by thyroid gland scintigraphy, thyroid gland ultrasonography and Papanicolaou cytology following fine needle aspiration of the nodule area) have been used for thyroid membrane preparation. Employing [3H]iloprost, a chemically stable PGI2-analogue as a radioligand, saturation experiments for comparative binding studies have been attempted. Scatchard analysis of the binding data obtained for normal thyroid parenchyma distant to the nodule area revealed heterogeneity of the [3H]iloprost sites exhibiting a high-affinity binding capacity (Bmax) of 613.2 +/- 130.4 fmol mg-1 membrane protein and a low-affinity binding capacity of 5.1 +/- 1.6 pmol mg-1 membrane protein. The equilibrium dissociation constant (Kd) amounted to 18.9 +/- 8.9 nM and to 131.5 +/- 39.2 nM, respectively. Scatchard analysis of the binding data obtained for benign thyroid adenoma indicated significant lower binding capacities exhibiting a Bmax of 325.8 +/- 110.0 fmol mg-1 membrane protein (Kd: 31.0 +/- 7.5 nM) for the high-affinity sites and of 3.9 +/- 2.5 pmol mg-1 membrane protein (Kd: 364.9 +/- 183.6) for the low affinity sites. In cancer tissue a selective loss of the low affinity sites and a significant diminution of the high-affinity sites was observed: in well differentiated cancer the high-affinity sites showed a Bmax of 299.7 +/- 46.0 fmol mg-1 membrane protein (Kd: 38.9 +/- 7.3 nM), in anaplastic cancer, less differentiated papillar and follicular cancers of 180.6 +/- 25.1 fmol mg-1 membrane protein (Kd: 54.6 +/- 16.7 nM). Well differentiated papillar and follicular cancers did not differ from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗