Kooperativer Bibliotheksverbund

Berlin Brandenburg

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  • 1
    In: Journal of the European Academy of Dermatology and Venereology, March 1996, Vol.6(2), pp.112-126
    Description: Since 1981, the standard therapy of herpes simplex virus infections has been based on acyclovir. Valaciclovir, the ‐valine ester of acyclovir and famciclovir, a pro‐drug of penciclovir with an improved oral bioavailability have been recently licensed. HPMPC, an acyclic nucleoside phosponate, is highly active and shows a broad range of activity against all the herpes viruses, and it is far more efficient than ganciclovir against cytomegalovirus. Ribonucleotidase inhibitors have so far been unsuccessful in the treatment of acyclovir‐resistant HSV infections. In the future, anti‐sense oligonucleotides may play a role in the therapy of herpes virus infections and many efforts continue to be made to develop vaccines which may prevent recurrences in already infected individuals. Resistance to anti‐HSV agents is almost exclusively encountered in immunocompromised patients. Failure of acyclovir therapy is mostly due to viral thymidine kinase (TK) deficiency as a result of mutation in the TK gene. Until now, the only alternatives for the treatment of acyclovir‐resistant infections have been the intravenous administration of foscarnet, frequently associated with relatively severe side effects, or the topical application of trifluridine either as single agent or in combination with interferon alpha. In vitro observations suggest that the failure of antiviral therapy is not directly due to the emergence of resistant virus isolates. Reduced uptake or activation of acyclovir may represent a selective pressure for resistant isolates in immunocompromised patients. New prodrugs with increased bioavailability, such as valaciclovir and famciclovir will perhaps prevent or delay the emergence of drug resistant isolates in immunocompromised patients since higher intracellular levels of the active compound can be achieved.
    Keywords: Acyclovir ; Famciclovir ; Valaciclovir ; Mechanism Of Action ; Antiviral Resistance
    ISSN: 0926-9959
    E-ISSN: 1468-3083
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  • 2
    Language: English
    In: International Journal of Cancer, 01/03/1996, Vol.65(1), pp.90-96
    Description: Human neuroblastoma cell line UKF-NB-4 persistently infected with human cytomegalovirus (HCMV) strain AD169 was established to study the effects of long-term HCMV infection on virus production and phenotypic characteristics of tumour cells. The cells designated UKF-NB-4 super(AD169) were subcultured (80 subcultures) over a period of more than 2 years after initiation of infection. UKF-NB-4 super(AD169) cells continued to produce infectious virus in successive passages, with a titre ranging from 9 x 10 super(3) to 1 x 10 super(5) and from 2 x 10 super(1) to 2 x 10 super(2) plaque-forming units per 10 super(6) cells and 1 ml culture medium, respectively; 10-20% of the cells produced HCMV-specific antigens, while 6-13% produced infectious virus progeny. The number of HCMV-specific DNA copies ranged from 9 x 10 super(4) to 9 x 10 super(6) per 10 super(6) cells. Transmission electron microscopy confirmed the productive nature of HCMV infection. UKF-NB-4 super(AD169) cultures proliferated, with population doubling time ranging from 24.5 to 26.6 hr (19.5 to 20.3 hr for UKF-NB-4) and cell viability from 79% to 85% (91-96% for UKF-NB-4). Significantly lower amounts of tyrosine hydroxylase and decreased activity for dopamine- beta -hydroxylase than in uninfected cells were observed in UKF-NB-4 super(AD169) cells. However, the expression of N-myc oncoprotein was significantly increased in persistently infected cultures. Our results show that long-term productive HCMV infection of UKF-NB-4 cell line is associated with the modulation of phenotypic properties, which may be related to the biological behaviour of neuroblastoma cells.
    Keywords: Cytomegalovirus ; Cytomegalovirus ; Neuroblastoma Cells ; Man ; Tumor Cells ; Phenotyping ; Neuroblastoma Cells ; Man ; Tumor Cells ; Phenotyping ; Neurovirology ; Virus Behavior in Cell Culture ; Tyrosine 3-Monooxygenase ; Dopamine Beta -Monooxygenase ; N-Myc Protein ; Tyrosine 3-Monooxygenase ; Dopamine Beta -Monooxygenase ; N-Myc Protein ; N-Myc Protein ; Dopamine Beta -Monooxygenase ; Tyrosine 3-Monooxygenase;
    ISSN: 00207136
    E-ISSN: 10970215
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  • 3
    In: Transplantation, 1996, Vol.62(9), pp.1371-1374
    Description: In this study, we investigated the effects of the intracellular metal chelator desferrioxamine (DFO) and the extracellular metal chelator diethylenetriamine penta-acetic acid (DTPA), which were previously shown to have strong anticytomegalovirus potencies, on their ability to elicit immunomodulatory effects in vitro[fcn,3]. The results showed that nontoxic and in vivo attainable concentrations of both DFO and DTPA inhibited mitogen- and allogen-induced proliferation of peripheral blood lymphocytes. The immunomodulatory effects of DFO/DTPA seem to be due to the impaired expression of interleukin-2 receptor and the reduced secretion of interleukin-2. However, metal chelators were more effective than cyclosporine or tacrolimus (FK506) in our in vitro experiments. Moreover, cytotoxicity mediated by lymphokine-activated killer cells and natural killer cells and the expression of HLA and adhesion molecules on cytokine-stimulated endothelial cells were differentially impaired by DFO/DTPA. These results warrant further study of the immunological effects of metal chelators in vivo.
    Keywords: Immunopharmacology ; Immunoregulation ; Metal Chelators ; Desferrioxamine ; Diethylenetriamine Penta-Acetic Acid ; Desferrioxamine ; Diethylenetriamine Penta-Acetic Acid ; Immunoregulation ; Metal Chelators;
    ISSN: 0041-1337
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  • 4
    In: Transplantation, 1996, Vol.61(12), pp.1763-1770
    Description: Transplantation-related pathogenic factors such as ischemia or allograft-directed inflammation are associated with oxidative changes that might lead to cellular oxidative stress. The aim of this study was to investigate the impact of oxidative stress on: (1) CMV replication in cultured human endothelial cells and (2) the stimulation of endothelial cells by proinflammatory cytokines. Both pathomechanisms are known to contribute to graft rejection crises in vivo. Oxidative stress was induced in endothelial cell cultures with 10-200 μM buthionine sulfoximine. Western blotting showed a significant increase in the production of CMV-specific immediate early and late proteins in buthionine sulfoximine-treated cultures. Immunocytochemical staining suggested that this effect was caused by increased numbers of CMV antigen expressing cells (66% immediate early; 78%, late). Quantitative polymerase chain reaction for CMV-specific DNA and virus titration revealed that enhanced viral replication levels correlated with increased virion production. As a measure for the endothelial cell activation status, the surface expression of HLA-ABC and HLA-DR and adhesion molecules(ICAM-1, ELAM-1, VCAM-1) was quantified by fluorometric methods. Whereas oxidative stress alone did not modulate any surface molecule expression, the IFN-γ-mediated expression of HLA-ABC and HLA-DR and the IL-1-mediated expression of ICAM-1, but not of ELAM-1 and VCAM-1 (IL-1+TNF-α), was amplified. Interestingly, the amplification of HLA molecule expression was even higher in CMV-infected endothelial cells. This study provides evidence that oxidative stress contributes to the regulation of CMV replication, virus shedding, and the activation of endothelial cells by proinflammatory cytokines as it is observed in transplant recipients.
    Keywords: Human Cytomegalovirus ; Human Cytomegalovirus ; Endothelium ; Replication ; Oxidation ; Stress ; Man ; Endothelium ; Replication ; Oxidation ; Stress ; Man ; Viruses ; Immune Response & Immune Mechanisms ; Cytokines ; Cytokines ; Cytokines;
    ISSN: 0041-1337
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  • 5
    In: Anti-Cancer Drugs, 1996, Vol.7(7), pp.766-773
    Description: Valproic acid (VPA) is a simple branched-chain fatty acid that has anticonvulsant activity and is widely used in the treatment of epilepsy. VPA was found to effect growth and differentiation of human neuroblastoma (NB) cells in vitro at concentrations that have been achieved in humans with no significant adverse effects. Treatment of UKF-NB-2 and UKF-NB-3 NB cell lines with VPA at concentrations ranging from 0.5 to 2 mM resulted in neuronal morphological differentiation characterized by extension of cellular processes without significant effects on cell viability. Ultra-structural features of VPA-treated cells were consistent with the neuronal type of differentiation. VPA treatment of NB cells was associated with decreased expression of N-myc oncoprotein and increased expression of neural cell adhesion molecule in their membrane. Treatment of NB cells with 0.5 mM VPA increased their sensitivity to lymphokine-activated killer lysis. The results indicate that VPA, at non-toxic pharmacological concentrations, arrests the growth, induces differentiation and increases immunogenicity of NB cells through non-toxic mechanisms.
    Keywords: Antibiotics ; Miscellaneous, Reviews ; Sodium Valproate ; Neuroblastoma ; Neuroblastoma ; Sodium Valproate;
    ISSN: 0959-4973
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  • 6
    Language: English
    In: Cancer Letters, 1996, Vol.110(1), pp.63-70
    Description: The effect of reduced glutathione (GSH) and S-acetylglutathione (S-acglu) treatment on several tumor cell lines and normal cells in vitro was investigated. GSH and S-acglu applied at concentrations of 1 mM and 2 mM induced apoptosis in malignant cells as shown by DNA-fragmentation and staining of apoptotic cells with 7-amino-actinomycin D while viability and growth of normal cells were not significantly influenced by this treatment. The results demonstrated that GSH and S-acglu may be selective inducers of apoptosis in malignant cells.
    Keywords: Reduced Glutathione ; S-Acetylglutathione ; Apoptosis ; Flow-Cytometry ; DNA-Fragmentation ; Anti-Tumor Effect ; Medicine
    ISSN: 0304-3835
    E-ISSN: 1872-7980
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  • 7
    Language: English
    In: Intervirology, 1996, Vol.39(4), pp.259-269
    Description: Although there is no definitive evidence of the association of human cytomegalovirus (HCMV) infection with human cancers, the oncogenic potential of HCMV has been well established by in vitro studies demonstrating the ability of UV-irradiated or infectious virus to transform a variety of cells. After prolonged passaging the transformed cell type was maintained while HCMV DNA sequences were no more detectable. Three morphological transforming regions (mtr) of HCMV have been identified. The effects of HCMV on cellular functions which may be associated with the malignant phenotype include the expression of oncogenes and transcriptional activation of growth factors and interleukin synthesis. In infected cells, HCMV induces cytoskeletal alterations and changes in expression of cell surface receptors for extracellular matrix proteins which could result in increased motility and dissemination of cancer cells. Several human neuroblastoma cell lines undergo maturation in different neural crest derived cell types upon treatment with oncogenic potential agents, i. e. retinoic acid. The persistent HCMV infection of neuroblastoma cells (〉1 year) is accompanied by the increased expression of oncoproteins (i.e. N-myc) and decreased expression of tyrosine hydroxylase and dopamine-β-hydroxylase. The activation of the cellular metabolism is due to HCMV binding to cellular receptors (prior to virus gene expression) and to the activity of HCMV immediate early (IE) gene products. IE proteins act directly as transcriptional activators or their activity is mediated by a variety of cellular transcription factors. HCMV infection may result in activation of promoters of cellular genes coding for cytokines, replication enzymes, protooncogenes and viral promoters. Recently it has been demonstrated that HCMV IE proteins block apoptosis probably by suppressing the ability of the antioncogene p53 to activate a reporter gene. The interactions of HCMV with tumor suppressor proteins such as p53 or retinoblastoma (pRb) susceptibility protein are reminiscent of those mediated by the oncoproteins of DNA tumor viruses. The acquisition of a fully malignant phenotype by normal cells is thought to require several mutations in a number of cellular genes. In this connection, HCMV may play the role of a nonobligate either direct or indirect cofactor for tumor genesis, e.g. by blocking apoptosis, which may be an essential requirement for tumor progression. Due to the stimulation of growth factors and/or inhibition of antioncogenes by its gene products, HCMV may modulate the malignant potential of tumor cells.
    Keywords: Original Paper ; Cytomegalovirus, Human ; Neuroblastoma ; Oncogenic Potential ; Differentiation ; Biology
    ISSN: 0300-5526
    E-ISSN: 1423-0100
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