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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 199 (1963), S. 513-514 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The large effect of combined treatment suggested, however, that it was not solely due to inhibition of mutants exhibiting limited cross-resistance, but that, in addition, HBB and guanidine acted synergistically. The following experiment was carried out to test this possibility. Coxsackie A9 virus ...
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 197 (1963), S. 1327-1328 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The virus-cell system used consisted of Coxsackie A9 virus and primary monolayer cultures of rhesus monkey kidney cells3. A coverslip technique5 was used, and RNA synthesis was measured by incorporation of tritiated uridine, as follows: at intervals, cells were exposed to 1*0 AC. of tritiated ...
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 201 (1964), S. 639-640 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The hydrochlorides of D-( )- and L( + )-2-(a-hydroxybenzyl)-benzimidazole were synthesized by the method of Phillips12 in which the D-() and L-( + ) forms of mandelic acid were allowed to condense with o-phenylenediamine in acidic medium. The isomeric benzimidazoles were isolated and purified as ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Medical microbiology and immunology 147 (1961), S. 588-594 
    ISSN: 1432-1831
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 19 (1991), S. 99-108 
    ISSN: 0886-1544
    Keywords: inhibition of cell motility and proliferation by interferon-β ; interferon-β increases stationary time in fibroblasts ; interferon-β decreases translocation rate in fibroblasts ; fibroblast motility in culture ; cell motility: translocation rate and stationary time ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The rate of translocation and the percent of the time that cells are stationary have been measured by computer-assisted time-lapse cinemicrography in over 1,000 freshly planted human foreskin fibroblasts (FS-4 cell strain) for periods of up to a week and the effects of interferon-β (IFN-β) on these parameters have been determined. Cells were planted at 2.5 × 103 cells/cm2 in Eagle's minimal essential-medium (MEM) with 10% fetal bovine serum (FBS). Frames were taken every 2 or 4 minutes and data were collected on both cell location and cell division as a function of time. After planting FS-4 cells require ∼48 hr to reach maximum motility both with respect to the translocation rate when moving and percent time cells are moving. Recombinant human IFN-β (800 μ/ml) caused a marked increase in the fraction of time cells were stationary and a decrease of lesser magnitude in the translocation rate, as quantitated during the period during which the stationary fraction for control cells was at a minimum. IFN-β also decreased the rate of cell proliferation, without any evidence of degeneration or death of cells. Our results contribute new evidence that the fraction of time cells spend moving directionally is an important determinant of their locomotory behavior and that this determinant is responsive to modulation by cytokines.
    Additional Material: 12 Ill.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 45 (1991), S. 327-334 
    ISSN: 0730-2312
    Keywords: multiple-cytokine responsive enhancer (MRE) ; glucocorticoid repression ; promoter occlusion ; keratinocytes ; breast carcinoma cell lines ; cell proliferation ; cell motility ; cell-cell association ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Epithelial cells both produce and are affected by interleukin-6 (IL-6). Experiments with an adenocarcinoma-derived cell line (HeLa) reveal that activation of the transfected human IL-6 promoter occurs largely through two partially overlapping second messenger (cAMP, phorbol ester)- and cytokine (IL-1, TNF, serum)-responsive enhancer elements (MRE I, -173 to -151 and MRE II, -158 to -145). MRE I contains the typical GACGTCA cAMP and phorbol ester-responsive (CRE/TRE) motif, whereas MRE II defines a new CRE/TRE motif that contains an imperfect dyad repeat. The mechanism of dexamethasone-mediated repression of IL-6 gene expression in epithelial cells involves occlusion of the entire MRE enhancer region and of the core-promoter elements (TATA-box and RNA start site) by ligand-activated glucocorticoid receptor. Enhanced levels of IL-6 expression are observed in many solid tumors and in the hyperprolifer active (and glucocorticoid-suppressible)lesions of psoriasis. In cell culture, IL-6 enhances, inhibits, or has no effect on the proliferation of epithelial cells depending upon the cell-type examined IL-6 enhances proliferation of keratinocytes but inhibits that of breast carcinoma cell lines ZR-75-1 and T-47D. In these breast carcinoma cells, IL-6 elicits a major change in cell phenotype which is characterized by a fibroblastoid morphology, enhanced motility, increased cell-cell separation, and decreased adherens type junctions (desmosomes and focal adhesions). The new data identify IL-6 as a regulator of epithelial cell growth and of cell-cell association.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 143 (1990), S. 494-500 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The great majority of murine Balb/c-3T3 fibroblasts in density-inhibited, quiescent cultures disintegrate and die rapidly when cells are deprived of serum in the medium. Platelet-derived growth factor (PDGF, 5 ng/ml) used alone and insulin-like growth factor (IGF-1, 40 ng/ml) + epidermal growth factor (EGF, 10 ng/ml) prevent most of this cell death and all three factors used together protect close to all cells in the confluent monolayer as determined by counting trypsinized cell suspensions in a Coulter counter. IGF-1 used alone affords a high level of protection during the first 5 hours of incubation in serum-free medium but the protective effect declines subsequently unless EGF is also present. EGF alone has little protective activity. The survival-promoting activity of PDGF used alone or of PDGF + EGF + IGF-1 is not significantly decreased by selective inhibition of messenger precursor RNA transcription with 5,6-dichloro-1-β-D-ribofuranosylbenzimidazole (DRB,20 or 40 μM), which prevents G1 traverse of the cells mediated by the combination of the three growth factors. DRB also does not interfere with the early protective effect of IGF-1 + EGF, but decreases the late protective effect of this growth factor combination. DRB by itself decreases cell viability in the absence of growth factors or serum. In these experiments viability was assayed by neutral red uptake by using an automated microplate reader. Inhibition of protein synthesis with cycloheximide (CHX, 1 or 5 μg/ml) over a 20-hour period was associated with decreased survival of cells protected by IGF-1 + EGF or PDGF + EGF + IGF, but also with decreased survival of cells incubated in the absence of growth factors or serum. The decrease in survival was somewhat more marked when IGF + EGF was present than when PDGF + EGF + IGF-1 was present. Insulin (1,500 ng/ml) mimics the action of IGF-1 (40 ng/ml). The cell survival-enhancing activities of growth factors are concentration dependent. The evidence presented indicates that PDGF, EGF, and IGF-1 (or insulin) act through distinctive mechanisms in affording protection of cells against death. The short-term protective effects of the growth factors are independent of gene expression and may be mediated via metabolic events. Long-term protection may be dependent on gene expression, especially in the case of IGF-1 + EGF.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 148 (1991), S. 85-95 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), and insulin protect density-inhibited murine Balb/c-3T3 fibroblasts against death by distinctive mechanisms. Determination of the cell survival-enhancing activity of growth factors by cell enumeration and neutral red uptake measurement gives equivalent results. PDGF displays a steep doseresponse relationship in the 1-5 ng/ml range. The other factors display shallow log-linear relationships in the following ranges: EGF: 0.2-5 ng/ml; IGF-1: 2-80 ng/ml; and insulin: 57-4,500 ng/ml. Agonists that lead to the activation of protein kinase A, including forskolin, 8-bromoadenosine 3′:5′-cyclic monophosphate (Br-cAMP) and N6,2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate (db-cAMP), markedly increase both short-term (5-h) and long-term (20-h) survival of cells. 2-lsobutyl-1-methylxanthine (IBMX) markedly enhances short-term survival, but its effect decays with time. The protein kinase C agonist 12-O-tetradecanoyl phorbol-13-acetate (TPA) has a moderate protective effect at concentrations of 16-32 nM, and 64 nM TPA is highly effective. The synthetic diacylglycerols 1,2-dioctanoylglycerol (DiC8) and 1-oleoyl-2-acetylglycerol (OAG) and the calcium ionophore ionomycin show low activity. Supplemation of EGF with a protein kinase A or C agonist results in a varying additive increase in short-term (5-h) cell survival and supplementation of EGF+insulin or PDGF+EGF+insulin increases further the already high level of protection given by the growth factor combinations. Combining a protein kinase A and a protein kinase C agonist in the absence of growth factors gives an approximately additive increase in cell survival. Results obtained with kinase, RNA, and protein synthesis inhibitors suggest that: (1) activated protein kinase C catalyzes one or more phosphorylation events in quiescent Balb/c-3T3 cells that lead to gene expression with the protein product(s) mediating protection of quiescent cells against death, and (2) phosphorylation events Catalyzed by protein kinase A largely serve to protect cells by a mechanism not requiring de novo RNA and protein biosynthesis.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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