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Biomedical subjects

K Ziegler

Publications and source records attributed to K Ziegler.

At least 91 records · Page 5Linked to original sources
PubMed1988

Peculiarities of Mekong schistosomiasis with particular attention to the People's Democratic Republic of Laos.

The authors examined 10 children with clinical symptoms suggestive of intestinal or hepatolienal schistosomiasis. All the children were from the endemic focus in Laos. We found eggs of schistosomes that were smaller and rounder (60.95 X 51.55 microns) than those from a southern Chinese strain of S. japonicum (62.64 X 73.49 microns). There were no Oncomelania species found among the snails in this endemic area. These observations confirm those reports in the literature that assert a new species for S. mekongi based upon epidemiological, biological and morphological characteristics.

Animals↗
PubMed1987

Evidence for glycoprotein components of the hepatocellular bile acid transporter.

The hepatocellular transporter, responsible for the uptake of bile acids and some foreign substances, can be shown to contain carbohydrate moieties. The hepatocellular uptake of cholate and phallotoxin is immediately inhibited by addition of wheat-germ agglutinin. Concanavalin A and lentil lectin reduce the uptake in a time-dependent manner. Apparently sialic acids or N-acetylglucosamine residues are involved in the translocation process. Polypeptides (Mr 50,000, 54,000) of the above transport system, identified by affinity labeling with [3H]isothiocyanatobenzamido cholate and [3H2]diisothiocyano-1,2-diphenylethane-2,2'-disulfonic acid, are heterogenously glycosylated. Binding of 80-90% of the 54, 50 kDa polypeptides to all immobilized lectins tested suggests that both high-mannose and complex type oligosaccharides with fucose and terminal sialic acid residues occur as carbohydrate chains. A 67 kDa labeled polypeptide is not glycosylated. Pilot experiments for purification of the above glycosylated membrane proteins on concanavalin A, lentil lectin and wheat-germ lectin columns are described. However, lectin affinity chromatography is not suitable as a one-step purification procedure for the labeled polypeptides.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1987

[Current therapeutic aspects of echinococcosis].

It is reported on a 63-year-old female patient who fell ill 20 years after an echinococcus cyst of the liver with a multiple parasite-caused cyst-formation in the lung which was detected by chance and was already calcified at that time. On account of inoperability a conservative treatment with mebendazole (2,000 md/die, for 4 months). During a one-year follow-up period a drastic involution of the lung cysts with improvement of the general condition of the patient appeared. The affection of the liver, however, remained uninfluenced. The ELISA on echinococcus was unchanged strongly positive also after one year.

Drug Administration Schedule↗
PubMed1987

Dihydrotestosterone induces a sexual dimorphism in estrogen uptake by specific anterior pituitary cell types in vivo.

Castrated male and female rats pretreated with dihydrotestosterone (DHT) were injected i.v. with 3H-estradiol (E2). Nuclear uptake and retention of 3H-E2 was measured in each of five cell types of the anterior pituitary gland using a combined quantitative autoradiographic and immunocytochemical procedure. In non-pretreated groups, each cell type bound a characteristic amount of ligand but no sex differences were apparent. DHT pretreatment, however, caused a significant decrease in 3H-E2 retention by gonadotrophs in both males and females. The treatment also caused a decrease in binding by lactotrophs and somatotrophs, but only in the females. No other cell types were altered. Thus, androgen appears to modulate E2 binding and retention by pituitary cells in both a cell-type and sex-dependent manner. Our results also indicate that the inhibitory effects of androgens on E2 binding by the pituitary gland is more complex than can be explained by simple competition for the estrogen receptor.

Animals↗
PubMed1987

Synthesis of a cyclic retro analogue of somatostatin suitable for photoaffinity labelling.

Cyclic somatostatin analogues containing the modified retro sequence of the amino acids Phe7 to Phe11 of the natural compound have been found to exhibit high activity for cytoprotection of rat hepatocytes against cell poisons such as phallotoxins and galactosamine. Cyclo(-Phe(p-NH(1-14C)Ac)-Thr-Lys(CO(p-N3)C6H4)-Trp-Phe-D-Pro), a photoreactive and radioactive analogue of one of the most active cyclohexapeptides, was synthesized by a combination of solid phase technique and classical solution peptide synthesis. This peptide labels the same proteins in rat liver cell membrane that are modified by photolysable derivatives of bile acids, phalloidin and antamanide.

Affinity Labels↗
PubMed1987

Leptospirosis from the clinical viewpoint.

Epidemiological, clinical and microbiological data of 27 patients suffering from leptospirosis are presented. Because of the sporadic occurrence of the disease, diagnosis on admission was correct in only 18% of the patients. As proved by the agglutination test, most of the infections were due to serotype icterohaemorrhagiae, but in only one case could the leptospires be detected directly in the blood culture. In most of the cases the course of the disease was moderately severe with one fatality. Symptomatology and treatment are discussed.

Adolescent↗
PubMed1986

[Kinetics of the antibody level in schistosomiasis under chemotherapy].

The antibody level (ELISA) in schistosomiasis much increased one month after therapy. The sanation of the parasitosis within 6 months led to the reduction of the values to the initial level without any further later decrease. The antibody kinetics was the same after successful Niridazol and Praziquantel treatment. When Niridazol failed a second treatment with Praziquantel led to a repeated significant increase. The decrease after the second peak was much steeper and obtained the initial level already 3 months after sanation. Patients with falsely negative ELISA before the treatment reacted partly positive one month after this. One third of all patients examined reacted negatively also at this time. Falsely positive findings in patients from endemic areas (specificity 0.74) seem to be no cross reaction to another affection with helminths, but seem to be traced back to an earlier inapparent schistosomiasis.

Adolescent↗
PubMed1986

Cyclosporin A and a diaziridine derivative inhibit the hepatocellular uptake of cholate, phalloidin and rifampicin.

Cyclosporin A inhibits the uptake of cholate into isolated hepatocytes in a non-competitive manner (Ki = 3.6 microM). It protects liver cells against phalloidin injury by a mixed competitive/non-competitive inhibition of phalloidin uptake (Ki = 0.08 microM). Rifampicin, a well-known substrate of the bilirubin transporter is also incorporated in a decreased quantity in the presence of cyclosporin A (IC50 = 80 microM). A photolabile diaziridine derivative of cyclosporin A was used for the identification of binding sites. In comparison with the original cyclosporin A the photoaffinity label exhibits a 2-3-fold lower affinity to the cholate (and phalloidin) transporter in the liver cell membrane. In the dark the label inhibits the uptake of both cholate and of phalloidin reversibly; after treatment with ultraviolet light flashes the inhibition becomes irreversible. The degree of inhibition is concentration dependent. Our results suggest binding of cyclosporin A to protein components of the cholate (and phalloidin) transporter of liver cells without uptake by this system. The inhibition of cholate (and phalloidin) uptake by cyclosporin A is non-competitive and may be due to nonspecific hydrophobic binding to compounds of the cholate transporter.

Aminoisobutyric Acids↗
PubMed1986

Photoaffinity labeling of whole cells by flashed light: a simple apparatus for high-energy ultraviolet flashes.

A simple apparatus for the photolysis of affinity labels is described. A commercial quartz tube produces high-energy flashes (wavelength from 200 to 1000 nm). A single flash is normally sufficient to activate photoaffinity labels in the presence of cells. Flash photolysis has several advantages over continuous irradiation, e.g. there is no need for cooling and photolabeling may be performed after different preincubation periods. The above apparatus is therefore suitable for investigations on time-dependent uptake of substrates by intact cells. Examples are demonstrated by photoaffinity labeling of rat liver cells by [3H]cyclosporin-diaziridine.

Affinity Labels↗
PubMed1986

Identification of cyclosporin binding sites in rat liver plasma membranes, isolated hepatocytes, and hepatoma cells by photoaffinity labeling using [3H]cyclosporin-diaziridine.

[3H]Cyclosporin diaziridine, a new photoaffinity label, enters rat liver cells in the dark. Photoaffinity labeling of isolated rat liver-cell plasma membranes with this probe modifies several polypeptides with molecular mass of 200, 85, 54, 50, 34 kDa. The major labeled protein of 85 kDa represents 2% of the total plasma membrane protein. A 50 kDa protein is heavily labeled in freshly isolated rat hepatocytes at low temperature and after short incubation in the dark. The 85 kDa protein becomes substituted after longer preincubation periods at temperatures above 10 degrees C. This suggests a localisation at the cytoplasmic side of the membrane. Several controls point to a specific interaction with the above mentioned proteins. Comparison of [3H]cyclosporin-diaziridine- and isothiocyanatobenzamido[3H] cholic acid-labeled membrane proteins reveals identity of binding proteins with the exception of the 85 kDa protein. However, the interaction of bile acids with the 85 kDa protein became apparent at higher concentrations as demonstrated by the differential photoaffinity labeling experiments. In the cytosol of rat liver cells, further [3H]cyclosporin-diaziridine binding proteins could be identified. In particular, a 17 kDa polypeptide was found which appears similar to cyclophilin, a protein known to be present in T-lymphocytes (R. Handschumacher et al. (1984) Science 226, 544-547: Cyclophilin. A specific cytosolic binding protein for cyclosporin A). Proteins with molecular mass of 90, 56, 30, 24, 20 kDa are labeled in AS-30D ascites hepatoma cells and those with molecular mass of 200, 150, 80, 70, 42, 25 kDa in Ehrlich ascites tumor cells.

Affinity Labels↗
PubMed1986

Iodipamide uptake by rat liver plasma membrane vesicles enriched in the sinusoidal fraction: evidence for a carrier-mediated transport dependent on membrane potential.

Iodipamide, a cholecystographic agent, is known to be taken up by isolated hepatocytes by a mechanism similar or identical with the inward transport of bile salts (Petzinger, E., Joppen, C. and Frimmer, M. (1983) Naunyn-Schmiedeberg's Arch. Pharmacol. 322, 174-179). To elucidate its mode of transport, uptake of iodipamide was studied by rapid-filtration techniques on plasma membrane vesicles enriched in the sinusoidal fraction. Uptake was found to be dependent upon the temperature, the intravesicular volume, a gradient of monovalent cations (Na+, K+ or Li+) and the substrate concentration (saturation kinetics with respect to iodipamide: apparent Km = 70 microM, Vmax = 0.31 nmol per mg protein per min at 100 mM NaCl and 25 degrees C). Countertransport and transstimulation in tracer exchange experiments indicate that in vesicles, iodipamide uptake rather than binding occurs. Na+ could be replaced by K+ or Li+ in our system without any effect. However, in the presence of choline chloride a slight, but distinct reduction occurred. Iodipamide uptake was inhibited by cholate, phalloidin, 4,4'-diisothiocyanato-1,2-diphenylethane-2,2'-disulfonic acid and by bromosulfophthalein with inhibition being competitive in the case of cholate and non-competitive in the case of bromosulfophthalein. Alteration of the membrane potential by addition of NO3-, SCN- or SO4(2-) modified the uptake rate for iodipamide. The above results support our earlier hypothesis that the hepatocellular uptake of iodipamide is due to a carrier-mediated transport, probably similar to that of bile acids. However, translocation of iodipamide is assumed to be driven by the membrane potential only and not by Na+ contransport.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1986

Intraepithelial lymphocyte mitosis in a jejunal biopsy correlates with intraepithelial lymphocyte count, irrespective of diagnosis.

When there is villus atrophy in a jejunal biopsy, intraepithelial lymphocyte (IEL) mitosis correlates with a diagnosis of coeliac disease. We have examined the significance of IEL mitosis in jejunal biopsies with normal villi. Counts of IEL per 100 villus enterocytes, and IEL mitosis per 1000 IEL, were carried out in 81 jejunal biopsies. Thirty one were from patients with coeliac disease or dermatitis herpetiformis, and many of these, from treated patients, were histologically normal; 40 were from patients with other diagnoses, selected to include biopsies with a high IEL count (greater than 40 IEL per 100 enterocytes) but normal villi. Three coeliacs and 10 dermatitis herpetiformis patients had an IEL count of less than 40, and no IEL mitoses were found in these biopsies. Two dermatitis herpetiformis patients had IEL counts of 43.7% and 43.9%, with no IEL mitoses, but in all other coeliac and dermatitis herpetiformis biopsies high IEL counts were associated with IEL mitotic indices between 0.05% and 1.77%. In the non-coeliac, non-dermatitis herpetiformis group, no IEL mitoses were found in the 22 biopsies with IEL count less than 43%. In the others, IEL counts ranged from 44.8% to 127.0%, and IEL mitoses were present, with mitotic indices ranging from 0.06% to 0.49%. This work shows that IEL mitosis in a jejunal biopsy is not specific for coeliac disease, but occurs whenever there is an increased density of IEL within the villus epithelium.

Biopsy↗
PubMed1986

Molecular aspects of cytoprotection by modified somatostatins.

Somatostatin and cyclic modifications of this molecule inhibit the development of protrusions on the surface of isolated hepatocytes in presence of phalloidin. This prevention of phalloidin injury is caused by competitive inhibition of the phallotoxin uptake. Transport inhibition is not a hormonal effect of somatostatin. The concentrations needed are in the micromolar range. The most protective somatostatin modifications lack hormonal activity (GH release). Somatostatin and its analogs are substrates of a hepatocellular transporter which also translocates other cyclopeptides, among them phalloidin, antamanide, and several organic anions, such as iodipamide and fusidic acid. Physiological substrates of this multispecific transport system are bile acids. The protection of phallotoxin injury by somatostatin is a specific mechanism only representative for liver cells. No other cell contains the above multispecific transporter.

Affinity Labels↗