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Biomedical subjects

H Kather

Publications and source records attributed to H Kather.

At least 55 records · Page 3Linked to original sources
PubMed1984

Autoimmune hemolytic anemia by coexisting anti-I and anti-Fl cold agglutinins.

In association with atypical pneumonia, a patient developed acute severe autoimmune hemolytic anemia. Hemoglobin temporarily was only 7.0 g/100 ml, so that the patient needed red blood cell (RBC) transfusion. Hemolysis was found to be caused by high titer cold agglutinins (CA), which occurred transiently during the acute period of the disease. CA of two different specificities, anti-I and anti-Fl, were demonstrated in the patient's serum. Antibodies of the two specificities were clearly separated by absorption/elution experiments using neuraminidase (RDE)-treated RBC. They were distinguished by serologic means: Both anti-I and anti-Fl react more strongly with adult RBC than with newborn and i adult RBC; in contrast to anti-I, anti-Fl does not agglutinate RDE-treated cells. Inhibition experiments showed that I-active substances prepared from papainized RBC exhibited both I and Fl antigenic activity. By RDE-treatment of I-active substances, Fl-activity was markedly reduced, while I-activity was increased.

Adult↗
PubMed1983

[The cAMP system and bacterial toxins].

The effects of cytotoxic proteinaceous bacterial toxins on the adenylate cyclase cyclic adenosine monophosphate (cAMP) system of host cells are reviewed. Bacterial exotoxins affecting intracellular cAMP levels of host cells can be classified into two subgroups: (1) adenosine diphosphate (ADP)-ribosyl-transferases and, (2) invasive adenylate cyclases. Among the ADP-ribosylating toxins are the enterotoxins of Vibrio cholerae, of Escherichia coli and one of the pertussis toxins termed "islet-activating protein". Toxins within this class share several structural and functional features. The three toxins consist of two functionally distinct parts: an A-component that is active enzymatically and a B-component that binds to surface receptors on cells or, if added in isolation blocks, the action of the complete toxin. The complete toxin shows little or no activity in broken cell preparations. When these toxins act on whole cells the contact is made initially through component B and then component A, but not B enters the cell and catalyzes the ADP-ribosylation of nucleotide regulatory components within the adenylate cyclase complex. The activities of the A-subunits of cholera toxin and heat-labile coli enterotoxin are directed against the stimulatory nucleotide-binding protein of adenylate cyclase whereas islet-activating protein probably alters the inhibitory coupling protein of host-cells. Only recently two bacterial adenylate cyclases from Bacillus anthracis and Bordetella pertussis were described which are capable of invading mammalian cells. These invasive adenylate cyclases, like ADP-ribosylating toxins, require the presence of specific proteins for binding and are activated by calmodulin which is not present in bacteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylate Cyclase Toxin↗
PubMed1983

Islet-activating protein discriminates the antilipolytic mechanism of insulin from that of other antilipolytic compounds.

In vivo administration of islet-activating protein to rats resulted in an increase in fat cell lipolysis in vitro, which was associated with almost complete resistance of adipocytes towards the antilipolytic effects of N6-phenylisopropyladenosine, prostaglandin E2 and nicotinic acid. Concomitantly, the inhibitory effects of these compounds on adenylate cyclase activity in membranes were impaired. In contrast, the antilipolytic action of insulin was not only preserved, but even augmented in cells from rats treated with islet-activating protein. The data suggest that insulin exerts its antilipolytic effects via mechanisms which are different from those involved in the effects of prostaglandin E2, N6-phenylisopropyladenosine and nicotinic acid.

Adenosine Deaminase↗
PubMed1982

Microdetermination of glycerol using bacterial NADH-linked luciferase.

A bioluminescent assay for determination of glycerol using bacterial NADH-linked luciferase was developed and successfully applied to measurement of glycerol release from human fat cells. The procedure is based on enzymic conversion of glycerol to 3-phosphoglycerate, which is irreversible in the presence of arsenate, and subsequent determination of NADH formed in the glycerol-phosphate- and glyceraldehyde-3-phosphate dehydrogenase reactions respectively. Bioluminescent determination of glycerol is about 100 times more sensitive than conventional spectrophotometry, thus permitting more than 100 determinations to be carried out on needle biopsy specimens.

Adipose Tissue↗
PubMed1982

[Inhibition of acid secretion with substituted benzimidazole. A new principle in ulcer therapy?].

Substituted benzimidazoles inhibit gastric acid secretion stimulated by histamine, pentagastrin and vagal innervation. In contrast to anticholinergic agents and H2-receptor antagonists these compounds also block secretion induced by exogenous cyclic AMP suggesting a more peripheral site of action. Recent data show that these substances inhibit a H+/K+-ATPase which is localized at the secretory surface of the parietal cells and is generally regarded as the proton pump within the gastric mucosa. Because of the unique distribution of H+/K+-ATPase the inhibitory action of substituted benzimidazoles may offer a new therapeutic approach in hypersecretory states.

Adenosine Triphosphatases↗
PubMed1982

Sodium ions discriminate between stimulatory and inhibitory effects of prostaglandin E2 on human fat cell adenylate cyclase.

Prostaglandin E2 (PG E2) has biphasic effects on human fat cell adenylate cyclase with inhibition occurring in the nanomolar concentration range and stimulation at PG E2-concentrations above 1 mumol/l. Sodium ions stimulate the human fat cell adenylate cyclase in a hormone-like manner. The inhibitory component of PG E2-action is markedly augmented by sodium ions. In addition, the monovalent cation, by interfering with the stimulatory component of PG E2 discriminates between the opposing effects of PG E2 suggesting that the antagonistic effects of the E-type prostaglandins are mediated through distinct processes.

Adenylyl Cyclases↗
PubMed1982

Adrenergic regulation of fat-cell lipolysis in multiple symmetric lipomatosis.

The responsiveness towards catecholamines of normal and lipomatous fat cells of two male subjects suffering from multiple symmetric lipomatosis has been studied by means of a newly developed bioluminescent method for microdetermination of glycerol. In contrast to previous findings, lipomatous fat cells displayed normal alpha 2-and beta-adrenergic responsiveness in both subjects studied. The apparent discrepancies between the results of the present study and those reported by others therefore support the contention that multiple symmetric lipomatosis is a symptom with various underlying causes rather than a nosological entity.

Adipose Tissue↗
PubMed1982

Effects of prazosin on human fat-cell lipolysis and adenylate cyclase activity in vitro.

The effects of prazosin on adrenergic-stimulated fat-cell lipolysis and adenylate cyclase activity were investigated. The results revealed that the antilipolytic alpha-adrenergic catecholamine effects on human fat-cell metabolism are mediated via alpha 2-receptor sites displaying extremely low affinity to prazosin, which is alpha 1-site selective. The data provide an explantation for the lack of effect of prazosin on lipid mobilization in vivo. The molecular sites mediating the lipid-lowering action of the drug, however, remain to be elucidated.

Adenylyl Cyclase Inhibitors↗
PubMed1982

Inhibition of hormone-stimulated human fat cell-lipolysis by prostaglandin E2 and its synthetic analogue sulprostrone.

The effects of prostaglandin E2 (PG E2) and of its synthetic analogue Sulprostrone on isoproterenol-stimulated human fat cell-lipolysis and adenylate cyclase activity were compared. Glycerol release and adenylate cyclase activity were depressed to a similar maximal extent by both compounds (30%-35%) with Sulprostrone being 3 - 10-times more potent than the parent compound PG E2. The results strengthen the concept of prostaglandins exerting their antilipolytic effects via inhibition of human fat cell adenylate cyclase and demonstrate that Sulprostrone is not tissue-specific in vitro.

Adenylyl Cyclase Inhibitors↗