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Biomedical subjects

B Wagner

Publications and source records attributed to B Wagner.

At least 163 records · Page 9Linked to original sources
PubMed1992

Structural equation modelling of some of the determinants of suicide risk.

Much of the psychological research with suicidal patients has examined, individually or in combination, correlates and predictors of the various measures in the suicide process. The present study investigated suicidal risk as an outcome measure. Several questionnaires were administered to a sample of 94 soldiers, 61 of whom had manifested some suicidal symptoms. Using LISREL analysis, the data showed that the best model had suicide risk as directly influenced by depression and indirectly by impulsivity.

Adult↗
PubMed1992

A continuous sequence of more than 70 amino acids is essential for antibody binding to the dominant antigenic site of glycoprotein gp58 of human cytomegalovirus.

Antigenic domain 1 (AD-1) on glycoprotein gp58 of human cytomegalovirus was characterized in detail, using mouse and human monoclonal antibodies as well as human convalescent sera. Series of procaryotically expressed fusion proteins and synthetic peptides of various lengths were used as sources of antigen. Binding of antibodies was found to depend on a continuous sequence of more than 70 amino acids between residues 552 and 635 of gp58. The fine specificities for sequences involved in antibody binding were (i) amino acids 557 to 635 for neutralizing as well as nonneutralizing mouse monoclonal antibodies, (ii) amino acids 552 to 630 for a neutralizing human monoclonal antibody, and (iii) amino acids 557 to 630 for antibodies present in human sera. Experiments involving fragments of AD-1, presented either as procaryotically expressed fusion protein or as synthetic peptides, indicated that the intact structure was required for recognition of AD-1 by antibodies.

Amino Acid Sequence↗
PubMed1992

Transplantation of human benign hyperplastic prostate tissue into nude mice: first results of systemic therapy.

Xenografts of human benign hyperplastic prostate tissue (BPH) have been established as a model for the investigation of the etiology of BPH. In this paper it is our aim to answer the question of whether this model is useful for the established therapy of the disease. Additionally we try to evaluate the value of a commonly used plant extract for the therapy of BPH. Is there any influence of the extract from Sabal serrulatum on the BPH tissue in our model? Human BPH tissue from 2 patients was transplanted into athymic nude mice and treated with three different regimens. Animals of group I did not receive any treatment and served as control, in groups II and III the tissue was stimulated by application of silicone tubes containing crystalline 5 alpha-dihydrotestosterone and estradiol. Animals of group II additionally were treated orally with the lipophilic extract of S. serrulatum (contained in Prostagutt N), which is commonly used for the treatment of BPH clinically. Significant inhibition of tissue growth was observed in group III when compared to group II. In group I (control) atrophy of the graft was observed as expected. However, histologically no differences were visible between groups II and III. Our experiment shows a significant growth-inhibiting effect of the plant extract for human BPH tissue in our model (p less than 0.05). We conclude that the nude mouse model can be useful for the evaluation of systemic therapy modalities of human BPH and that the plant extract may have a certain value for clinical treatment, which is not only due to subjective criteria.

Animals↗
PubMed1992

Sensitivity and specificity of five different mycoplasma detection assays.

The sensitivity and specificity of five different mycoplasma detection tests were evaluated in comparison with the classical microbiological culture assay on agar plates as the reference method: direct fluorochrome DNA staining (direct DAPI), DNA staining of an indicator cell line (indirect DAPI), RNA hybridization with a cDNA specific for ribosomal mycoplasmal RNA, an enzyme-linked immunosorbent assay (ELISA) with mycoplasma-specific antibodies, and a biochemical cytotoxicity assay (6-MPDR). A large panel of continuous cell lines (20 adherent and 233 suspension cell lines, most of the latter were human leukemia-lymphoma cell lines) were analyzed for infection with mycoplasma. The results of the comparative analysis for sensitivity and specificity of the various tests were as follows: 100% and 100% for the indirect DAPI, 100% and 98% for the RNA hybridization assay, 87% and 94% for the direct DAPI, 72% and 100% for the ELISA, 75% and 90% for the biochemical 6-MPDR assay. Each of these approaches has both advantages and disadvantages with regard to cost, time, reliability, specificity, and sensitivity. The best compromise for routine mycoplasma testing is a combination of several techniques (e.g. direct culture on agar, RNA hybridization, and direct or indirect DAPI).

Animals↗
PubMed1991

Expression and subcellular location of native and mutant hTNF alpha proteins in Escherichia coli.

Several mutant hTNF alpha genes were constructed by deletion and stepwise reconstitution of regions coding for C-terminal sequences. The mutant hTNF alpha proteins behaved differently from native hTNF alpha when expressed in Escherichia coli. They were either sensitive to proteolytic degradation or formed insoluble aggregates depending on the strains and conditions used for expression. By contrast, native hTNF alpha was always present in a soluble form and had a tendency to associate with the cytoplasmic membrane. It was even transported to the periplasmic space in E. coli as shown by both cell fractionation and immunoelectron microscopy. The different behaviour of mutant hTNF alpha proteins probably results from a disturbance of protein folding.

Amino Acid Sequence↗
PubMed1991

Priming effect of glucagon-like peptide-1 (7-36) amide, glucose-dependent insulinotropic polypeptide and cholecystokinin-8 at the isolated perfused rat pancreas.

The priming effect of glucagon-like peptide-1 (7-36) amide (GLP-1 (7-36) amide), glucose-dependent insulin-releasing polypeptide (GIP) and cholecystokinin-8 (CCK-8) on glucose-induced insulin secretion from rat pancreas was investigated. The isolated pancreas was perfused in vitro with Krebs-Ringer bicarbonate buffer containing 2.8 mmol/l glucose. After 10 min this medium was supplemented with GLP-1 (7-36) amide, GIP or CCK-8 (10, 100, 1000 pmol/l) for 10 min. After an additional 10 min period with 2.8 mmol/l glucose alone, insulin secretion was stimulated with buffer containing 10 mmol/l glucose for 44 min. In control experiments the typical biphasic insulin response to 10 mmol/l glucose occurred. Pretreatment of the pancreas with GIP augmented insulin secretion: 10 pmol/l GIP enhanced only the first phase of the secretory response to 10 mmol/l glucose; 100 and 1000 pmol/l GIP stimulated both phases of hormone secretion. After exposure to CCK-8, enhanced insulin release during the first (at 10 and 1000 pmol/l CCK-8) and the second phase (at 1000 pmol/l) was observed. Priming with 100 pmol/l GLP-1 (7-36) amide significantly amplified the first and 1000 pmol/l GLP-1 (7-36) amide both secretion periods, 10 pmol/l GLP-1 (7-36) amide had no significant effect. All three peptide hormones influenced the first, quickly arising secretory response more than the second phase. Priming with forskolin (30 mM) enhanced the secretory response to 10 mM glucose plus 0.5 nM GLP-1 (7-36) amide 4-fold. With a glucose-responsive B-cell line (HIT cells), we investigated the hypothesis that the priming effect of GLP-1 (7-36) amide is mediated by the adenylate cyclase system. Priming with either IBMX (0.1 mM) or forskolin (2.5 microM) enhanced the insulin release after a consecutive glucose stimulation (5 mM). This effect was pronounced when GLP-1 (7-36) amide (100 pM) was added during glucose stimulation. Priming capacities of intestinal peptide hormones may be involved in the regulation of postprandial insulin release. The incretin action of these hormones can probably, at least in part, be explained by these effects. The priming effect of GLP-1 (7-36) amide is most likely mediated by the adenylate cyclase system.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Immunogold labelling of human IFN alpha 2 and an IFN alpha 1/ alpha 2 hybrid produced by recombinant Escherichia coli.

In recombinant Escherichia coli strains the subcellular location of human interferon (IFN) alpha 2 and a hybrid IFN alpha 1/alpha 2 was investigated by immunogold labelling techniques. The gold label was scattered throughout the cytoplasm in cells containing the gene for mature IFN alpha 2 under the control of heterologous staphylokinase sak42D transcription and translation initiation signals. In contrast, in cells containing in addition the sak42D signal peptide coding region in front of the IFN gene, the gold label was found mainly near the cell membrane and in the periplasmic space. Inclusion bodies were identified in cells accumulating IFN in the cytoplasm.

Blotting, Western↗
PubMed1991

Assessing the validity of the Plutchik Suicide Risk Scale.

One of the newer scales of suicide risk devised by Plutchik and colleagues was tested to see if it could discriminate between levels of suicide ideation and suicide attempts. A sample of 80 subjects were placed into various categories of suicide risk on the basis of a psychiatric examination. Results showed that the full scale did not adequately discriminate among groups. An explantation of the results has been proposed and a design to test this suggestion described.

Adult↗
PubMed1991

Chromosomal hyperdiploidy in a feline sarcoma.

An eight-year-old male cat developed a sarcoma. The cytogenetic evaluation of the tumour cells showed the presence of hyperdiploidy (range 40 to 46 chromosomes). This hyperdiploidy was encountered in all the cells examined. Extra-chromosomes numbers C1, C2, B4, D4 and E3 were mainly responsible for the hyperdiploid chromosomal complements. There was a high incidence of monosomy E3.

Animals↗
PubMed1991

Fluorescent probes as tools to assess the receptor for the urokinase-type plasminogen activator on tumor cells.

Flow cytofluorometric protocols (FACScan) are described for the rapid and quantitative real-time analysis of binding of FITC-pro-u-PA to cell surface receptors (u-PAR) on living, resting, and also on PMA-stimulated human monocytic U937 cells. Binding of pro-u-PA was visualized by CLSM. This fairly new technique is superior over conventional fluorescence microscopy and is an alternative to electron microscopic approaches. Both flow cytofluorometry and confocal laser scanning microscopy allow the analysis quantitatively and with high-sensitivity binding of FITC-pro-u-PA to single suspended or adherent cells. By CLSM u-PA/u-PAR were found to be located in heterogeneously distributed discrete patches at the cell surface on U937 and not inside the cell. This is in agreement with previous studies by Hansen et al, who applied radioiodinated u-PA and electron microscopy to locate u-PAR on microvilli of fixed U937 cells. By flow cytofluorometry, it was possible to quantify the time-dependent and temperature-dependent binding of FITC-pro-u-PA to living single U937. Apparent saturation of u-PAR was achieved at 5 nM FITC-pro-u-PA for both nonstimulated and PMA-stimulated U937 cells. Half saturation of u-PAR was also determined. Nonstimulated U937 was 0.7 nM, and PMA-stimulated U937 was 1.1 nM of FITC-pro-u-PA. This increase in half-saturation concentration in PMA-stimulated cells is paralleled by a steep increase in binding sites (3.6-fold). The use of fluoresceinated reference beads is recommended to verify changes in affinity and binding sites. Using CLSM or flow cytofluorometry, it is also possible to study the structure relationship of u-PA/u-PAR in the presence of competitive binding analogues or inhibitors. Fluorescence techniques will also permit the identification of u-PAR-positive cells in blood, ascitic fluid, or biopsies obtained from cancer patients.

Amino Acid Sequence↗
PubMed1991

Red tattoo reactions: X-ray microanalysis and patch-test studies.

Eighteen patients who developed cutaneous reactions to red tattoos were studied to identify the chemicals responsible for the reactions to modern red tattoo pigments. Biopsies from the tattoos were examined histologically and the chemical composition of the red pigments was analysed by X-ray microanalysis. A variety of metallic elements including aluminium, iron, calcium, titanium, silicon, mercury and cadmium were detected. Patch tests were performed to the relevant chemicals in nine cases, and only one patient reacted to mercury. This study demonstrates that although reactions to mercury still occur, other red dyes containing a variety of inorganic pigments may provoke a cutaneous inflammatory response.

Adult↗
PubMed1991

Degradation of 2,4,6-trichlorophenol by Azotobacter sp. strain GP1.

A bacterium which utilizes 2,4,6-trichlorophenol (TCP) as a sole source of carbon and energy was isolated from soil. The bacterium, designated strain GP1, was identified as an Azotobacter sp. TCP was the only chlorinated phenol which supported the growth of the bacterium. Resting cells transformed monochlorophenols, 2,6-dichlorophenol, and 2,3,6-trichlorophenol. Phenol and a number of phenolic compounds, including 4-methylphenol, all of the monohydroxybenzoates, and several dihydroxybenzoates, were very good carbon sources for Azotobacter sp. strain GP1. The organism utilized up to 800 mg of TCP per liter; the lag phase and time for degradation, however, were severely prolonged at TCP concentrations above 500 mg/liter. Repeated additions of 200 mg of TCP per liter led to accelerated degradation, with an optimum value of 100 mg of TCP per liter per h. TCP degradation was significantly faster in shaken than in nonshaken cultures. The optimum temperature for degradation was 25 to 30 degrees C. Induction studies, including treatment of the cells with chloramphenicol prior to TCP or phenol addition, revealed that TCP induced TCP degradation but not phenol degradation and that phenol induced only its own utilization. Per mol of TCP, 3 mol of Cl- was released. 2,6-Dichloro-p-benzoquinone was detected in the resting-cell medium of Azotobacter sp. strain GP1. By chemical mutagenesis, mutants blocked in either TCP degradation or phenol degradation were obtained. No mutant defective in the degradation of both phenols was found, indicating separate pathways for the dissimilation of the compounds. In some of the phenol-deficient mutants, pyrocatechol was found to accumulate, and in some of the TCP-deficient mutants, 2,6-dichlorohydroquinone was found to accumulate.

Azotobacter↗