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  • 1
    Digitale Medien
    Digitale Medien
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 660 (1992), S. 0 
    ISSN: 1749-6632
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Allgemeine Naturwissenschaft
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 494 (1987), S. 0 
    ISSN: 1749-6632
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Allgemeine Naturwissenschaft
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 349 (1980), S. 0 
    ISSN: 1749-6632
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Allgemeine Naturwissenschaft
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 39 (1989), S. 477-487 
    ISSN: 0730-2312
    Schlagwort(e): TGFβ gene ; hepatic regeneration ; hepatomas ; carcinogens ; growth inhibitor ; Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Notizen: TGFβ is a potent, nontoxic inhibitor of mitogen-induced DNA synthesis in primary cultures of adult rat hepatocytes. Using a cDNA probe, we investigated TGFβ gene expression in quiescent, regenerating, and neoplastic liver, and several hepatoma lines by Northern gel analysis. We found that regenerating liver had increased TGFβ gene transcripts beginning at about 8 h, with a broad peak of 48-120 h and return to normal after 9 days. Separation of the regenerating liver into its constituent cell types, followed by RNA extraction and reprobing, revealed that increased TGFβ gene transcripts were confined to the enriched endothelial-cell population and not the hepatocytes. Increased hepatic TGFβ expression was also found in fetal liver and in rats immediately after birth. Elevated TGFβ mRNA levels were also found in primary cultures of oval cells and an established bile ductular cell line, as well as in carcinogen-altered liver epithelial cell lines. Transcripts were undetectable in normal human liver but were abundant in the human hepatoma lines Hep G2, Hep 3B, PLC/PRF/5, and SK-Hep-1. Elevated levels were also found in the normal rat liver-derived lines BRL-3A and clone 9 and the H4IIE rat hepatoma, but not in the HTC, MH1C1, and MH7777 rat hepatomas. The hepatocarcinogen diethylnitrosamine induced high transcript levels after single injections in a time- and dose-dependent manner. These results suggest that the liver may be a paracrine organ with respect to TGFβ gene expression, which can be induced by carcinogens and by growth stimulation.
    Zusätzliches Material: 5 Ill.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 125 (1985), S. 82-90 
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: Primary monolyer cultures of adult rat hepatocytes can be induced to undergo DNA synthesis in serum-free medium in the presence of insulin, glucagon, and epidermal growth factor (three factors). We have found that hepatocyte DNA synthesis is affected not only by an endogenous stimulant produced by the hepatocytes and released into the culture medium. Serum has a strong inhibitory effect on hepatocyte DNA synthesis. Partially purified human platelet extract (“platelet inhibitor”) inhibits the three-factor-induced DNA synthesis in a concenration-dependent manner. Pure βTGF at 0.5 ng/ml as well as HPLC-purified PDGF at 10 ng/ml completely inhibit the three-factor-induced DNA synthesis. Determination of the time required for the presence of the three factors and the platelet inhibitor to exert their effects indicated that the inhibition of DNA synthesis is caused not by competition of the platelet inhibitor with any of the three factors but through an independent pathway. Hepatocyte DNA synthesis is density-dependent and is greater if medium is not changed during the course of an experiment than if medium is changed daily. Hepatocyte-conditioned medium is also affective in stimulating DNA synthesis beyond the level induced by the three factors. These results suggest that an endogenous stimulant for hepatocyte DNA synthesis is produced by the hepatocytes themselves. Our studies demonstrate that hepatocyte DNA synthesis is subject to both stimulatory and inhibitory controls. Unlike the three factors, the endogenous stimulant can overcome the inhibition by the platelet inhibitor, suggesting the importance of these factors in the physiological control of hepatocyte DNA synthesis.
    Zusätzliches Material: 11 Ill.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 129 (1986), S. 59-63 
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: Male Fischer F344 rats (180-220 g) were fed either a basal diet, a diet supplemented with 2-acetylaminofluorene (AAF) 0.02% (w/w) for up to 3 months or dietary tumor promoters. Normal or AAF-altered hepatic microsomes were compared with respect to drug-induced lipid peroxidation. A three-fold decrease was found in the ability of adriamycin to induce lipid peroxidation on AAF-altered and promoter-altered microsomes, compared to normal microsomes. A similar decrease was found when using a direct acting organic peroxidant. The microsomal hepatic lipid was extracted, and AAF-altered lipid was found to be a poorer substrate for adriamycin-mediated lipid peroxidation compared to normal microsomal lipid. Similar results were obtained with purified phosphatidylcholine from AAF-altered compared to normal microsomes. It was concluded that carcinogen treatment causes alterations in the microsomal phospholipids that render them less susceptible to lipid peroxidation, which is probably due to a carcinogen-induced decrease in the level of fatty acid saturation.
    Zusätzliches Material: 4 Ill.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 165 (1995), S. 459-467 
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: The growth characteristics of a newly established cell line, Hep40, derived from a human hepatoma are described. An absolute requirement was found for serum to mediate cell growth. Neither EGF, TGF-α, nor HGF altered cell growth in the presence or absence of serum. A partial suppression of cell growth was achieved by several TGF-β family proteins. Affinity crosslinking gels using 125I-labeled TGF-β showed a significant decrease in the TGF-β cell-surface type II receptor in Hep40 cells, compared to the TGF-β-sensitive Hep3B cell line. However, growth could be completely suppressed by addition of vitamins K to the culture medium in both Hep40 and several other hepatoma cell lines. Growth suppression by vitamins K was accompanied by an increased level of transcripts for c-myc, c-jun, and prothrombin genes, in contrast to the actions of TGF-β1 protein, which caused a decrease in the level of c-myc transcripts. These data show that this new human hepatoma cell line has partial resistance to growth inhibition by TGF-β with a unique TGF-β receptor defect. However, growth was completely suppressed by vitamins K. The differing gene expression patterns in response to TGF-β as compared to vitamin K suggest that these two growth inhibitors act through differing pathways. © 1995 Wiley-Liss Inc.
    Zusätzliches Material: 11 Ill.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 158 (1994), S. 215-222 
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: Epidermal growth factor and transforming growth factor alpha stimulated DNA synthesis in primary cultures of adult rat hepatocytes. Neurotensin amplified epidermal growth factor-stimulated or transforming growth factor alpha-stimulated DNA synthesis by three- to eightfold. Neurotensin by itself did not stimulate DNA synthesis. Amplification of DNA synthesis by neurotensin was observed as low as 10-10 M, and it was increased in a dose-dependent manner with maximal effects at 10-8 M. These results were obtained when hepatocytes were cultured in Williams' medium E, but not in Leibovitz L-15 medium, suggesting that a minor component(s) in the medium is required for hepatocytes to fully respond to neurotensin. Neurotensin effect on DNA synthesis was observed not only in normal rat hepatocytes but also in partially hepatectomized rat hepatocytes, although its effect was stronger in normal hepatocytes. Amplified DNA synthesis was inhibited by transforming growth factor β. Secondary mitogens (co-mitogens) such as insulin, vasopressin, or angiotensin II interacted additively with low concentrations of epidermal growth factor as well as with neurotensin. Neurotensin-related peptides such as kinetensin or neuromedin-N, which was released from blood plasma by pepsin digestion, did not have this amplifying effect on DNA synthesis at any concentrations tested. Neurotensin mRNA was found in several organs including brain and intestine, but not liver. These results suggest that neurotensin can be regarded as a new secondary mitogen and that it may be involved in cell proliferation, including regenerating liver as a gastrointestinal hormone and/or a neurotransmitter. © 1994 Wiley-Liss, Inc.
    Zusätzliches Material: 8 Ill.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 158 (1994), S. 365-373 
    ISSN: 0021-9541
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: Adult rat hepatocytes in primary culture responded to epidermal growth factor (EGF) by increased DNA synthesis. When hepatocytes were cultured in Leibovitz L-15 medium, their response to EGF was low compared with that in Williams' medium E or Koga's medium L. Furthermore, female rat hepatocytes showed almost no response to the mitogenic action of EGF compared with male rat hepatocytes in L-15 medium. Addition of glutamic acid (1-20 μM) to EGF-containing L-15 medium not only enhanced DNA synthesis 〉 tenfold in both male and female hepatocytes, but eliminated the sex differences in DNA synthesis. Aspartic acid, glutamine, or ornithine at 20 mM did not replace the glutamic acid effect on DNA synthesis. Proline also enhanced EGF-induced DNA synthesis, although it was less effective than glutamic acid. Therefore, this effect may be specific to a high concentrations of glutamic acid. Glutamic acid by itself did not stimulate DNA synthesis at any concentrations tested. In the presence of glutamic acid, EGF showed a dose-dependent (0.5-20 ng/ml) stimulation of DNA synthesis with a maximal effect at 10 ng/ml. Almost the same effect was obtained with transforming growth factor alpha (0.5-20 ng/ml). Glutamic acid also induced an expansion of the mitogenic action of angiotensin II. Since glutamic acid did not affect [125I]EGF binding to hepatocytes or its processing, the effect may occur internal to the receptor. These results suggest that glutamic acid modulates the sensitivity of the hepatocyte response to mitogens © 1994 Wiley-Liss, Inc.
    Zusätzliches Material: 12 Ill.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    Publikationsdatum: 2005-06-01
    Print ISSN: 0167-6997
    Digitale ISSN: 1573-0646
    Thema: Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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