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P Reuter

Publications and source records attributed to P Reuter.

At least 19 recordsLinked to original sources
PubMed1992

[A prospective study to determine the recanalization time with a guide wire/recanalization catheter system in arterial occlusions].

The success rate and time taken for recanalization was determined in a prospective study of 82 consecutive unselected patients (53 men, 29 women; mean age 65.7 +/- 13, from 28 to 88 years). There were 106 complete occlusions of infrarenal arteries and a hydrophilic guide wire with a special 5-F recanalization catheter was used. Mean occlusion length was 12.97 +/- 10 cm (from 1 cm-45 cm). 79.3% of occlusions were in the femoro-popliteal territory, 6.6% were iliac and 14.1% tibial. 101 of the 106 occlusions were recanalized (95.3%). Mean recanalization time was 120.8 +/- 228.1 s (from 1 s-1440 s), mean recanalization velocity was 0.11 cm/s. The majority of obstructions could be recanalized in less than one minute. The five occlusions which could not be recanalized were distal lesions in the superficial femoral artery and which were longer than 10 cm; two were calcified. There were no complications resulting from the recanalization apart from three perforations which were clinically not apparent. Consequent angioplasty proved successful in 78.1% of these patients.

Adult↗
PubMed1992

Biocompatibility of synthetic oxygen carriers and fluorosurfactants.

A system for testing the biocompatibility of synthetic oxygen carriers is described including tests of hemolysis, complement activation and proliferation of cell lines or lymphocytes. Of 17 surfactants tested in this system, 6 were compatible in all tests while the other compounds showed individually differing patterns of incompatibility. We conclude that, in order to conduct a meaningful screening, a series of different assays has to be applied. In addition to our system, further assays, covering cytokine induction and phagocytosis should be attempted.

Blood Substitutes↗
PubMed1992

On the perfluorocarbon emulsions of second generation.

For formulation of perfluorocarbon-emulsions (PFC-emulsions) of second generation new perfluorocarbons (F-dimorpholines, F-dipiperidines and F-cyclohexylmorpholine) were synthesized, acting both as oxygen carriers and as interfacial active compounds (IFACs). The stabilizing effect of these IFACs is interpreted and a new theory is introduced. Also new classes of fluorosurfactants were synthesized and tested for biocompatibility. In PFC mixtures compounds of the type RFRH (RF = CmF2m + 1, RH = CnH2n + 1) are acting as IFACs but also as anchor-groups for lipophilic surfactants.

Biocompatible Materials↗
PubMed1992

Syntheses, interfacial active properties and toxicity of new perfluoroalkylated surfactants.

New surfactants have been synthesized with perfluorohexyl-groups as hydrophobic tail, a polyethyleneglycol-methylether as hydrophilic head and a prolongator between them. The prolongator units are -C4H8-, -C2H4OC5H10-, -C2H4OC3H6C(O)- and -CH2CH(OEt)CH2-. The surface tension, CMC and the interfacial tension water/perfluorocarbon were measured and the surface excess concentrations of the surfactant molecules were calculated. The influence of the surfactants on in vitro proliferation of human cell lines Hela and Molt 4 was investigated as a parameter for biocompatibility. The influence of the surfactants led to a reduction of cell proliferation depending on the concentration and chemical nature of the surfactant. Thus the prolongators changed the properties of the surfactants. They reduced the interfacial tension water/perfluorocarbon and improved the biocompatibility of surfactants.

Biocompatible Materials↗
PubMed1992

On the perfluorocarbon emulsions of second generation.

Perfluorocarbon-emulsions of second generation were prepared by means of new perfluorocarbons (F-dimorpholines, F-dipiperidines and F-cyclohexylmorpholine), acting both as oxygen carriers and as interfacial active compounds (IFACs). The stabilizing effect of these IFACs is interpreted and a new theory is introduced. Also new classes of fluorosurfactants were synthesized and tested for biocompatibility. In PFC mixtures compounds of the type RFRH (RF = CmF2m + 1, RH = CnH2n + 1) are acting as IFACs but also as anchor-groups for lipophilic surfactants.

Blood Substitutes↗
PubMed1992

Biocompatibility of synthetic oxygen carriers and fluorosurfactants.

A system for testing the biocompatibility of synthetic oxygen carriers is described including tests of hemolysis, complement activation and proliferation of cell lines or lymphocytes. Of 17 surfactants tested in this system, 6 were compatible in all tests while the other compounds showed individually differing patterns of incompatibility. We conclude that, in order to conduct a meaningful screening, a series of different assays has to be applied. Addition to our system of further assays covering cytokine induction and phagocytosis should be attempted.

Biocompatible Materials↗
PubMed1990

Functional characterization of Tat protein from human immunodeficiency virus. Evidence that Tat links viral RNAs to nuclear matrix.

The processes of transcription and posttranscription are assumed to proceed in close association with the nuclear matrix. In this study we demonstrated that Tat, the trans-activating protein from human immunodeficiency virus type 1 (HIV-1), binds both to the TAR region of the nascent HIV mRNAs and the nuclear matrix with high affinity. Both North/Western blotting experiments and nitrocellulose binding studies revealed that Tat binds with an association constant (K alpha) of approximately 1 x 10(9) M-1 to the TAR segment of HIV RNA; binding of Tat to this sequence which is present between position 32 and 82 downstream from the TATA box was also confirmed by gel retardation assays. Binding of Tat to TAR only occurs if the loop segment in the proposed stem-loop secondary structure of HIV leader mRNA is present. Likewise, Tat binds to the nuclear matrix with a K alpha of 7.5 x 10(7) M-1. The number of binding sites has been estimated to be 2 x 10(8)/micrograms of matrix protein, corresponding to 4 x 10(3) sites/nucleus. Tat displays its bimodal function only in the presence of Zn2+ ions. In vitro transcription experiments, using HIV-1 infected nuclei, demonstrate that beyond the TAR-region HIV RNA synthesis occurs only in the presence of Tat. Present studies indicate that Tat may function as a linker by binding of nascent HIV RNAs to the nuclear matrix.

Cell Line↗
PubMed1990

Binding of Tat protein to TAR region of human immunodeficiency virus type 1 blocks TAR-mediated activation of (2'-5')oligoadenylate synthetase.

The TAR sequence of the 5' leader of HIV-1 long terminal repeat-directed mRNA was found to be able to bind to and to activate double-stranded RNA-dependent (2'-5')A synthetase. Binding of TAR to the purified synthetase in vitro was abolished by addition of HIV-1 Tat protein, which binds to this sequence with a high affinity. Inhibition of TAR-mediated activation of (2'-5')A synthetase by Tat was prevented in the presence of the Zn2+ and Cd2+ chelators o-phenanthroline and penicillamine, which did not impair TAR-synthetase interaction. Transient expression assays of bacterial chloramphenicol acetyltransferase (CAT) gene in HeLa cells revealed that the levels of both CAT mRNA and CAT protein decreased after treatment of the cells with interferon, if CAT gene was linked to HIV-1 TAR segment. Cotransfection of the cells with a tat sequence containing plasmid rendered CAT gene expression insensible to the action of interferon.

2',5'-Oligoadenylate Synthetase↗
PubMed1990

Polyclonal antibodies to mannan from yeast also recognize the carbohydrate structure of gp120 of the AIDS virus: an approach to raise neutralizing antibodies to HIV-1 infection in vitro.

This study initiates a new method of developing an antigen which might be useful in the prevention of HIV-1 infection. Using a mannan preparation from Saccharomyces cerevisiae neutralizing antiserum was raised in rabbits which prevents HIV-1 infection in vitro up to a titre of 1:128. The corresponding antibody preparation neutralized the in vitro infectivity down to a concentration of 5 micrograms/ml. Analytical studies suggest that the antibodies are directed against the mannose residues of the HIV-1 glycoprotein (gp) 120 and its precursor gp 160.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Effect of nonviable preparations from human immunodeficiency virus type 1 on nuclear matrix-associated DNA polymerase alpha and DNA topoisomerase II activities.

In a previous paper, we determined that treatment of lymphocytes with nonviable preparations of human immunodeficiency virus type 1 (HIV-1) results in an impairment of the phosphatidylinositol/protein kinase C pathway, most likely due to an inhibition of the cleavage of phosphatidylinositol bisphosphate into inositol trisphosphate and diacylglycerol, mediated by phospholipase C. Here we show that one consequence of these changes is a reduced phosphorylation of nuclear matrix-associated DNA topoisomerase II, resulting in an inhibition of the activity of this enzyme. Antibodies to the viral proteins suppressed the inhibitory effects caused by the HIV-1 preparation. Furthermore, the phytohemagglutinin A-caused augmentation of nuclear matrix-associated DNA polymerase alpha and beta activities was found to be abolished by coincubation with the HIV preparation or with the HIV-1 gp120. The phytohemagglutinin A-enhanced matrix association and processivity of DNA polymerase alpha was determined to be reduced if the lymphocytes were in contact with HIV-1 preparation. These results suggest that the reduced proliferative response of lymphocytes to phytohemagglutinin A in the presence of disrupted HIV-1 preparation is due to inhibition of at least two, perhaps separate, pathways, one involving protein kinase C resulting in a reduced phosphorylation of DNA topoisomerase II and the other changing the state of matrix association of DNA polymerase alpha and beta.

DNA Polymerase II↗
PubMed1989

Inhibitory effect of nonviable preparations from human immunodeficiency virus 1 on inositol phospholipid metabolism.

Previously it was established [Pahwa, S., Pahwa, R., Saxinger, C., Gallo, R. C. & Good, R. A. (1985) Proc. Natl. Acad. Sci. USA 82, 8198] that nonviable preparations of human immunodeficiency virus 1 (HIV-1) abolish the proliferative response of human lymphocytes to phytohemagglutinin A. Now we describe that this effect might be, at least partially, due to an impairment of the function of phospholipase C. It was found that addition of HIV-1 preparation to lymphocytes diminished the stimulation of phosphatidylinositol phosphorylation caused by phytohemagglutinin A. Moreover, this preparation completely abolished the phytohemagglutinin-A-stimulated release of inositol trisphosphate and prevented a translocation of protein kinase C from cytosol to membranes. From this data we conclude that nonviable HIV-1 preparations inhibit the intracellular signalling pathway, leading to a reduced mitogenic response to phytohemagglutinin A, at the level of protein kinase C.

Biological Transport↗
PubMed1989

Association of Tat protein and viral mRNA with nuclear matrix from HIV-1-infected H9 cells.

The transactivating protein from human immunodeficiency virus type 1 (HIV-1), Tat, was found to bind to the nuclear matrix from uninfected and HIV-1-infected H9 cells. Addition of the Zn2+, Cd2+ and Cu2+ chelator o-phenanthroline destroyed the matrix fibrils and the binding affinity of Tat to the matrix. A sequential treatment of the matrix, first with o-phenanthroline and then with ZnCl2, partially restored the fibrillar-like matrix structure. Infection of H9 cells with HIV-1 resulted in a displacement of cellular mRNA by viral mRNA from the nuclear matrix. Both the matrix-bound host cell and HIV-1 mRNA were found to dissociate from the matrix in the presence of o-phenanthroline. This could be prevented by coincubation with Zn2+ or Cu2+ (but not Mg2+), which stabilize the mRNA containing nuclear matrix structure.

Cell Nucleus↗
PubMed1989

Suppression of the modulatory effects of the antileukemic and anti-human immunodeficiency virus compound avarol on gene expression by tryptophan.

The amino acid L-tryptophan is known to be a modulator of many processes of cell metabolism. In this contribution we show that L-tryptophan interferes with some biological effects of the antileukemic and anti-human immunodeficiency virus agent avarol, possibly by different mechanisms. Avarol has been shown to be able to modulate posttranscriptional events of mRNA synthesis, resulting in an increase of the base-sequence complexities of the nonabundant and rare mRNA classes. Here it is demonstrated that this change in mRNA abundancy distribution is accompanied by an increase in the level of some specific, low abundant mRNAs (ras and c-myc). Addition of L-tryptophan was found to abolish avarol-caused gene relaxation in L1210 mouse leukemia cells. In addition, L-tryptophan suppressed the induction of gamma-interferon mRNA production in human peripheral blood lymphocytes. At the level of DNA, L-tryptophan inhibited the production of strand breaks by cytotoxic avarol concentrations in Friend erythroleukemia cells in vitro. Moreover, it competed with avarol for binding to the nuclear envelope binding site; this effect was not shown by other amino acids.

Animals↗
PubMed1988

Inhibition of expression of natural UAG suppressor glutamine tRNA in HIV-infected human H9 cells in vitro by Avarol.

HTLV-IIIB-infected H9 cells are shown to contain a high level of the natural UAG suppressor glutamine tRNA(UmUG Gln); this tRNA has been demonstrated to be required for the synthesis of Moloney murine leukemia virus (Mo-MuLV)-encoded protease. After cultivation of HTLV-IIIB-infected H9 cells with Avarol at a concentration (1 microgram/ml), previously found to protect the cells against the cytopathic effects of HTLV-III, an almost complete inhibition of the synthesis of the tRNA(UmUG Gln) was observed. Moreover, we obtained some evidence that the processing of the HTLV-III precursor protein p53 to p24 is inhibited by Avarol in infected cells, suggesting that the compound interferes with the expression of the viral protease gene.

Animals↗
PubMed1988

Induction of gamma-interferon by avarol in human peripheral blood lymphocytes.

Avarol is a cytostatic and anti-human immunodeficiency virus (HIV) agent. In this study, the avarol caused induction of gamma-interferon (IFN-gamma) in buffy coat cells (human peripheral blood lymphocytes) is demonstrated by immunological and molecular biological techniques. IFN-gamma production was detected after a 24-hr incubation period with avarol; maximal production was obtained after 5 days in the presence of the optimal avarol concentration of 0.75 microgram/ml. Blotting experiments using human IFN-gamma cDNA and beta-actin cDNA containing plasmids showed that in the absence of avarol no IFN-gamma transcripts were present in lymphocytes. Already after a 24-hr incubation with avarol, IFN-gamma gene induction was detected, and maximal induction was found after a 5-day incubation period. The enhanced IFN-gamma production seems to be caused by a change at the transcriptional and/or post-transcriptional level, but not during subsequent nucleocytoplasmic transport of mRNA. This molecular event is specific, at least in relation to the expression of the beta-actin gene. Our studies demonstrate that avarol displays, besides its potential anti-tumor and anti-HIV activity, a potential immunomodulating effect.

Gene Expression Regulation↗
PubMed1987

Contrasuppression and tumor rejection.

The growth of a highly progressive MCA-induced tumor 3152-PRO is dependent on the activity of suppressor T cells (Ts). Injection of syngeneic mice with antibodies specific for Ts leads to enhanced tumor transplantation resistance of the 3152-PRO tumor. In addition, injection of recipient mice with highly immunogenic regressor tumors conjugated with trinitrophenyl (TNP) activates a T cell population which also mediates protection to transplantation of TNP-conjugated 3152-PRO tumor cells. One such tumor, 1591-RE, was investigated in detail to determine the phenotype and biologic activity of this T cell population in overcoming Ts cell activity. Induction of transplantation resistance requires the presence of TNP hapten on both the highly regressive immunizing tumor (and not its progressor variant 1591-PRO4), and on the challenge tumor 3152-PRO. The cell population from TNP-1591-RE immunized animals which mediates protection against the transplantation of TNP-3152-PRO is Thy-1+, CD4+, 8-, Lyt1+, I-J+, and Vicia villosa lectin adherent, the identical phenotype to antigen-specific contrasuppressor T cells in the contact sensitivity (CS) response to TNP in vivo. A T cell population of identical phenotype from TNP-1591-RE immunized mice can overcome the effects of antigen-specific Ts cells on PCl-immune cells in the adoptive transfer of CS in vivo. These results suggest that immunoregulatory cells that mediate protection against progressive tumors may be identical in function to antigen-specific contrasuppressor T cells.

Animals↗