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Biomedical subjects

H P Zimmermann

Publications and source records attributed to H P Zimmermann.

At least 19 recordsLinked to original sources
PubMed1992

Monoclonal antibodies distinguishing between two rat pancreatic carcinoma cell lines with different metastatic capacities.

Two new monoclonal antibodies, E5/E10 and E10/B4, were raised which reacted with surface antigens on the metastatic rat pancreatic adenocarcinoma cell line ASML, but not with antigens localized on the cell surface of the nonmetastatic rat pancreatic adenocarcinoma line AS. These two monoclonal antibodies are of the IgG1 subclass and recognize protein bands with molecular weight 28,000 and 35,000 D. E5/E10 and E10/B4 cross-reacted only with antigens on the human colon cancer cell line HT-29, as well as with normal rat kidney.

Adenocarcinoma↗
PubMed1989

[Mortality in influenza epidemics in Switzerland 1969-1985].

In Switzerland from 1969-1985, 9 out of 11 influenza epidemics were associated with a statistically significant increase in mortality. A total of 12,202 excess deaths from all causes was identified. Expected deaths were forecast for each epidemic period separately for 4 age groups using Fourier and Arima modeling. 75.7% of all-cause excess deaths occurred in age group 70 to 89 and 5.1% in age group 1-59. In the 70-89 years old group the excess mortality risk during influenza epidemics was 271.6 per 100,000, whereas in age group 1-59 it was only 1.7 per 100,000. Only 40% of all excess deaths had been ascribed to acute respiratory conditions. Influenza viruses A H3N2 were the most frequently identified agents. In some instances mortality increased before the morbidity reports of the Swiss practitioners indicated the occurrence of an epidemic. Also, morbidity reporting decreased over successive years. A decrease in mortality following the epidemics was not observed. A more complete vaccination of high risk patients in Switzerland is desirable.

Adolescent↗
PubMed1988

Fusion of lipid vesicles with ascites tumor cells and their lipid-depleted variants. Studies with radioactive- and fluorescent-labeled vesicles.

Cultured ascites tumor cells and their lipid-depleted variants, which contained 35-40% less membrane phospholipid and cholesterol, were used for fusion experiments with unilamellar lipid vesicles which were between 300 and 600 nm in diameter. Vesicle-cell interaction was followed by tracer studies using vesicles double-labeled in the lipid moiety, by vesicle-encapsulated [3H] dextran, and by measurements of energy transfer between N-(10-[1-pyrene]decanoyl)sphingomyelin-labeled vesicles and alpha-parinaric acid-labeled cells in the presence of poly(ethylene glycol) (PEG) as fusogen. The reaction rates measured with the radiolabeled vesicles were found to follow patterns similar to those obtained with the resonance energy transfer assay. This latter method revealed a vesicle-cell membrane fusion reaction, which was substantiated by radiolabeling the internal cellular compartment after treatment of the cells with [3H]dextran-encapsulated vesicles as shown by electron microscopic autoradiography on semi-thin sections. Endocytosis as a reaction mechanism can be excluded, since no energy transfer was observed at 25 degrees C in the absence of PEG. Investigations of vesicle bilayer order and fluidity on vesicle-cell interaction revealed optimal reactivity, with intermediate fluidity corresponding to cholesterol/phospholipid ratios between 0.7 and 1.0 and fluorescence depolarization (P) values of 0.18 and 0.21. Lipid depletion decreased the reaction velocity between cells and vesicles by about 20%, exhibiting V values of 33.2 mumol/min, as compared to the control of 41.4 mumol/min determined for 10(7) cells. The affinity constants for vesicle lipid were affected only slightly with Km values of 0.195 mM (0.210 mM). The activation energies for the reaction were calculated to give values of EA = 22.44 kJ/mol for the control and of EA = 20.4 kJ/mol for the modified cells. These data indicate that the decrease in membrane lipid content apparently has no major influence on the extent of the interaction.

Animals↗
PubMed1988

Identification of the phosphorylated beta-tubulin isotype in differentiated neuroblastoma cells.

The tubulin molecule consists of an alpha- and a beta-subunit, each of which exists in several isotypic forms. It has been previously shown that one of the isotypes of neuroblastoma beta-tubulin is phosphorylated at a serine residue in vivo [(1985) J. Cell Biol. 100, 764-774]. Here we identify the phosphorylated isotype as beta 2 (type III). Moreover, the large size of the phosphorylated tryptic peptide and sequence comparisons of vertebrate beta-tubulins suggest that one of the two serines in positions 444 and 446 is the phosphorylated residue. Our results raise the possibility that beta 2-tubulin differs functionally from the other beta-tubulin isotypes.

Cell Differentiation↗
PubMed1988

Microtubule rearrangements during mitosis in multinucleate cells.

The peroxidase-antiperoxidase (PAP) method for the detection of polymerized tubulin has been used to study the microtubule rearrangements during mitosis in PtK1 and HeLa multinucleate cells obtained by polyethyleneglycol (PEG)-mediated fusion. We demonstrate here that the transition of the microtubular cytoskeleton from interphase to mitosis is an inducible event and independent of the factor(s) responsible for chromatin condensation and nuclear envelope breakdown. However, for the induction of the microtubule rearrangements nuclear envelope breakdown is required. At midprophase, cytoskeletal microtubule rearrangements start for multinucleate PtK1 cells, whereas in HeLa cells such changes are delayed, and a more abrupt transition is observed here. After complete nuclear envelope breakdown (prometaphase) mitotic asters and spindles but no cytoplasmic (interphase) microtubuli can be observed in both systems. Metaphase is characterized by an interaction between the different mitotic poles which show the form of bipolar spindles, but individual separated mitotic poles far removed from the chromatin can also be seen.

Animals↗
PubMed1988

The interaction of triethyl lead with tubulin and microtubules.

The impact of triethyl lead chloride was studied on: (i) the in vitro assembly and disassembly of microtubules from porcine brain by turbidometry and electron microscopy, (ii) the microtubule system of living mammalian cells using immunofluorescence microscopy, (iii) cell motility and chemotaxis employing the methods of phagokinetic track formation and the Boyden chamber assay, respectively, and (iv) thiol groups of the protein tubulin by their titration in the presence and absence of the organic lead compound. Triethyl lead chloride inhibited microtubule assembly and depolymerized preformed microtubules in vitro and in living cells. Random motility of cells was not markedly inhibited by triethyl lead chloride, whereas chemotaxis (directed cellular movement) was strongly inhibited. Triethyl lead chloride was found to interact with 2 thiol groups of the tubulin dimer. The interaction of triethyl lead chloride with the tubulin/microtubule system in vivo likely causes aneuploidy and is at least partly responsible for the cytotoxicity of the drug.

Animals↗
PubMed1987

Influence of triethyl lead on neurofilaments in vivo and in vitro.

The influence of triethyl lead chloride (TriEL) on the organization of neurofilaments in vivo was studied by indirect immunofluorescence microscopy employing mouse neuroblastoma cells (Neuro-2a). TriEL induces perinuclear coil formation of neurofilaments in those cells. The rearrangements observed are not correlated with significant changes of the microtubular system. Cells in which the microtubular network was stabilized by Taxol treatment prior to incubation with TriEL even show the rearrangement of the neurofilaments. The effect of TriEL is reversible. In vitro, the effect of TriEL on isolated neurofilaments and on filament formation as well as on the structure of preformed filaments was investigated by electron microscopy. If isolated neurofilaments from porcine spinal cord are incubated in the presence of TriEL, they show constrictions and bulges. Additionally, many fragments are seen. If preformed filaments are treated with TriEL, unraveling of fibers into protofilamentous strands is observed. The assembly of neurofilaments in vitro is disturbed in the presence of TriEL. The interaction of TriEL with neurofilaments in vivo is likely to be at least partly responsible for the neurotoxicity of TriEL.

Animals↗
PubMed1986

Radiation induced formation of giant cells in Saccharomyces uvarum. III: Effect of X-rays on nuclear division.

Spindle formation and nuclear division of budding and irradiated yeast cells (Saccharomyces uvarum) was investigated by fluorescence microscopy of protoplasted cells. Protoplasts were treated with antitubulin antibodies and DAPI, a fluorescent dye staining DNA. In budding yeast cells, duplication of spindle pole bodies as well as formation of complete 1-micron spindles and elongated 8-micron spindles were documented. In X-irradiated cells, spindle pole bodies were duplicated as well, forming the complete 1-micron spindle. Nuclei of giant cells have lost the elongation ability and remain in a "normal" G2-phase state, thus preventing nuclear as well as cellular division.

Cell Cycle↗
PubMed1986

[Morbidity detection in general practice].

A system of morbidity registration in the domain of primary health care is presented on the basis of experiences made abroad. A pilot project (Sentinella) functions in the environments of Berne since November 1984. Its extension to the whole of Switzerland is scheduled for the middle of 1986.

Air Pollution↗
PubMed1986

Changes in the organization of non-epithelial intermediate filaments induced by triethyl lead chloride.

The in vivo effect of triethyl lead chloride (TriEL) (10(-6)-10(-8) M) on the organization of non-epithelial intermediate filaments (vimentin and desmin filaments) was studied by indirect immunofluorescence microscopy employing different mammalian cell lines. The in vitro effect of TriEL on filament formation as well as on the structure of preformed filaments was investigated by electron microscopy. TriEL induces perinuclear coil formation of intermediate filaments in SV40-transformed human fibroblasts and baby hamster kidney (BHK21) cells. The rearrangements observed are not correlated with significant changes in the microtubular system as tested by double labelling of both filament systems. The effect of TriEL is reversible. Assembly of intermediate filaments in vitro is disturbed in the presence of TriEL such that only short filaments and various kinds of fragments are formed. When preformed filaments are incubated in the presence of TriEL, unravelling of fibres into protofilamentous strands is observed. Possible mechanisms of TriEL-filament interaction are discussed.

Animals↗
PubMed1985

Interaction of triethyl lead chloride with microtubules in vitro and in mammalian cells.

The effects of triethyl lead chloride (TriEL) on the in vitro assembly and disassembly of microtubules (MTs) from porcine brain were studied by turbidometry at 350 nm and by electron microscopy. TriEL inhibited MT assembly at 50 microM concentration and caused an almost complete disassembly of preformed MTs. The drug depolymerized MTs more effectively than colchicine. Concentrations higher than 50 microM TriEL caused an aberrant assembly process. Fibers about 10 nm width were formed in addition to aggregates of amorphous material. In vivo TriEL also caused MT depolymerization in interphase and mitotic PtK-1 and Ehrlich ascites tumor (EAT) cells as monitored by indirect immuno-fluorescent staining of tubulin and electron microscopy. The extent of MT depolymerization was concentration- and time-dependent. Recovery occurred as early as 5 min after removal of the drug. The fluorescent actin pattern in PtK-1 cells typical of stress fibers and subcortical filaments seemed not to be altered by the presence of TriEL. The vimentin intermediate filament system was, however, rearranged as a juxtanuclear complex after TriEL treatment. Furthermore, TriEL effected the inhibition of cellular growth (100% inhibition at about 10(-5) M). Cytokinesis is prevented to a great extent, resulting in the formation of binucleate cells which can additionally possess some micronuclei.

Animals↗
PubMed1984

The molecular mechanism of interaction of Et3Pb+ with tubulin.

Triethyllead ion (Et3Pb+) was found to interact with 2 out of 18 thiol groups present in tubulin dimers. Specificity of the interaction was shown by the high affinity of Et3Pb+ to tubulin, by the fact that the 16 residual thiol groups in tubulin remained unaffected, and by the observation that other proteins with exposed thiol groups, e.g., actin, did not react with Et3Pb+. After complexation of the two thiol groups, tubulin in vitro had lost its capability for microtubule assembly. Likewise, polymerized tubulin disassembled on addition of the lead compound.

Actins↗
PubMed1984

High cytotoxicity and membrane permeability of Et3Pb+ in mammalian and plant cells.

Cells of mammalian origin as well as those of higher plants appear to be very sensitive to triethyllead ion (Et3Pb+). Neuroblastoma cells kept in the presence of 1 microM Et3Pb+ lost their viability within 6 h. Growth of suspension culture cells of soybean (G. max(L.)Merr.) was inhibited by 1 microM Et3Pb+, and finally the cells died. Morphologically, Et3Pb+ caused the complete breakdown of microtubular structures in neuroblastoma cells; thus microtubules appeared to be the main target for the toxin. While in a previous study the effect of Et3Pb+ on microtubules has been well documented at concentrations of 50-200 microM 1, the present study demonstrates that the formation of microtubules from pig brain tubulin is disturbed at concentrations of Et3Pb+ as low as 0.5 to 1 microM. We conclude from these data that Et3Pb+ freely permeates the plasma membranes of mammalian as well as plant cells.

Animals↗
PubMed1984

Influence of triethyl lead on the activity of enzymes of the ascites tumor cell plasma membrane and its microviscosity.

The influence of triethyl lead (TriEL) on the activity of plasma membrane-bound enzymes of Ehrlich ascites tumor cells and on membrane fluidity has been investigated. TriEL completely inhibits the (Na+-K+)-ATPase in its membrane-bound and even more pronounced in its solubilized form between 5 and about 20 microM. It also alters the microviscosity of the isolated plasma membrane up to a temperature of about 30 degrees C, but it does not have any influence on the fluidity of the membrane-derived liposomes. From these data it is concluded that the inhibitor may interact directly with the catalytic subunit of the (Na+ + K+)-ATPase, and may not exert its influence by interfering with the membrane lipids.

5'-Nucleotidase↗
PubMed1984

Monitoring yeast spindles in the fluorescence microscope.

Formation of the complete spindles during the budding process of Saccharomyces uvarum was investigated by fluorescence microscopy of protoplasted cells. Protoplasts were treated with anti-tubulin antibodies and DAPI, a fluorescent dye staining DNA. Thus, both chromatin and spindles could be visualized. Duplication as well as formation of separated spindle pole bodies during the different stages of budding are documented, demonstrating the occurrence and behaviour of microtubules during yeast cell cycle.

Antibodies↗