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  • Cells, Cultured  (7)
  • American Association for the Advancement of Science (AAAS)  (7)
  • Periodicals Archive Online (PAO)
  • 1980-1984  (7)
  • 1955-1959
  • 1940-1944
  • 1981  (7)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (7)
  • Periodicals Archive Online (PAO)
Years
  • 1980-1984  (7)
  • 1955-1959
  • 1940-1944
Year
  • 1
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    Malignant potential of murine stromal cells after transplantation of human tumors into nude mice (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-04-03
    Description: Human malignant cancer tumors grafted into nude mice produce tumors containing both human cancer cells and the host's stromal cells. After short-term propagation of these tumors in vitro, the murine mesenchymal cells appear transformed and are tumorigenic in nude mice. However, established human cancer cell lines fail to similarly after adjacent murine stromal cells when used to produce tumors in nude mice. These experiments suggest that cancer cells may recruit normal cells to become malignant, qualifying the view of the clonal (unicellular) origin of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldenberg, D M -- Pavia, R A -- 1R01 CA17198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209521" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/pathology ; Animals ; Cell Line ; Cells, Cultured ; Colonic Neoplasms/pathology ; Fibrosarcoma/*etiology ; Humans ; Karyotyping ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Transplantation ; Neoplasms, Experimental/*etiology ; Transplantation, Heterologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Calcium spike electrogenesis and other electrical activity in continuously cultured small cell carcinoma of the lung (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-06-05
    Description: Spike electrogenesis, local depolarizing and hyperpolarizing responses, spontaneous rhythmic firing, and alternating resting potentials were measured in cells from a continuously cultured small cell carcinoma of the lung. Spike generation was blocked by MnCl2. In view of this evidence for calcium-spike electrogenesis and previous evidence of secretory activity in these cells, this cell line (DMS 53) can provide a model for the study of excitation-secretion behavior in human neoplastic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCann, F V -- Pettengill, O S -- Cole, J J -- Russell, J A -- Sorenson, G D -- CA 25845/CA/NCI NIH HHS/ -- DA 23108/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 5;212(4499):1155-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6262914" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Calcium/pharmacology ; Carcinoma, Small Cell/*physiopathology ; Cells, Cultured ; Electric Conductivity ; Humans ; Lung Neoplasms/*physiopathology ; Manganese/pharmacology ; Membrane Potentials/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Fc and C3b receptors on pulmonary endothelial cells: induction by injury (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-30
    Description: Receptors for the activated third component of complement and for the Fc portion of immunoglobulin G are not expressed by apparently normal bovine pulmonary endothelial cells, but are expressed when the cells are exposed to white cell lysates or are infected with influenza or cytomegalovirus. The unmasking of these latent receptors may contribute to the pulmonary inflammatory response characteristic of, for example, anaphylaxis and to those lung diseases characterized by the deposition of immune complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, U S -- Schultz, D R -- Ruan, J W -- HL 21568/HL/NHLBI NIH HHS/ -- HL 22087/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1981 Oct 30;214(4520):557-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6270789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Complement C3b/metabolism ; Cytomegalovirus Infections/physiopathology ; Endothelium/metabolism ; Orthomyxoviridae Infections/physiopathology ; Pulmonary Artery/*cytology ; Receptors, Complement/*metabolism ; Receptors, Fc/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Interferon-resistant cell line lacks fatty acid cyclooxygenase activity (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-04-17
    Description: A clone of L1210 mouse leukemia cells selected for resistance to both the antiviral and anticellular properties of mouse interferon were essentially devoid of fatty acid cyclooxygenase activity. Experiments in which broken cell preparations were mixed or the two cell types were cultivated together failed to indicate the presence of a diffusible enzyme inhibitor. Fatty acid lipoxygenase activity of similar magnitude was detectable in both cell types. A selective impairment of fatty acid cyclooxygenase in interferon-resistant cells is consistent with recently described data suggesting that this enzyme may play a crucial role in mediating the antiviral and anticellular effects of interferon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandrabose, K A -- Cuatrecasas, P -- Pottathil, R -- Lang, D J -- New York, N.Y. -- Science. 1981 Apr 17;212(4492):329-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6163214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids/metabolism ; Cells, Cultured ; Clone Cells/drug effects/enzymology ; Cyclooxygenase Inhibitors ; Interferons/*pharmacology ; Leukemia L1210 ; Lipoxygenase/metabolism ; Lipoxygenase Inhibitors ; Mice ; Prostaglandin-Endoperoxide Synthases/*deficiency ; Prostaglandins/biosynthesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Lectins mimic insulin in the induction of tyrosine aminotransferase (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-11-13
    Description: Various lectins were found to induce tyrosine aminotransferase in H-35 rat hepatoma cells grown in monolayer culture. Wheat germ agglutinin gave a maximal induction of tyrosine aminotransferase 6 hours after its addition. The induction time course was similar to that elicited by insulin. Fourteen micrograms of wheat germ agglutinin per milliliter gave half-maximal enzyme induction and 50 micrograms per milliliter gave the maximal response. The induction of tyrosine aminotransferase by wheat germ agglutinin was additive with the induction by either dexamethasone or dibutyryl adenosine 3',5'-monophosphate, but was not additive with the tyrosine amino transferase induction by insulin. Wheat germ agglutinin also mimicked insulin in the inhibition of cellular protein degradation in the absence of serum. The insulin-like effects of lectins should be considered in lectin-mediated manipulations such as agglutination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, J D -- Liu, A Y -- AM20274/AM/NIADDK NIH HHS/ -- GM 07258/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1981 Nov 13;214(4522):799-800.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6117128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bucladesine/pharmacology ; Cells, Cultured ; Dexamethasone/pharmacology ; Enzyme Induction/drug effects ; Insulin/*pharmacology ; Lectins/*pharmacology ; Liver/*enzymology ; Liver Neoplasms, Experimental/enzymology ; Peptide Hydrolases/metabolism ; Rats ; Receptor, Insulin/drug effects ; Tyrosine Transaminase/*biosynthesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Activation of the transforming potential of a normal cell sequence: a molecular model for oncogenesis (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-22
    Description: The molecularly cloned, long terminal repeat (LTR) of the Moloney sarcoma virus (M-MSV) provirus has been covalently linked to c-mos, the cellular homolog of the M-MSV-specific sequence, v-mos. These newly constructed clones lack any M-MSV-derived sequences other than the LTR, but in DNA transfection assays they transform cells as efficiently as cloned subgenomic M-MSV fragments containing both v-mos and LTR. Cells transformed by LTR:c-mos hybrid molecules contain additional copies of mos DNA, and several size classes of polyadenylated RNA's with sequence homology to mos. The activation of the transforming potential of c-mos by the proviral LTR suggests a model whereby LTR-like elements could activate other normal cell sequences with oncogenic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blair, D G -- Oskarsson, M -- Wood, T G -- McClements, W L -- Fischinger, P J -- Vande Woude, G G -- New York, N.Y. -- Science. 1981 May 22;212(4497):941-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Viral ; Cells, Cultured ; DNA, Recombinant ; Defective Viruses/genetics ; Gene Expression Regulation ; *Genes, Viral ; Mice ; Moloney murine leukemia virus/*genetics ; Nucleic Acid Hybridization ; Operon ; Plasmids
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Regulation of muscle differentiation: stimulation of myoblast fusion in vitro by catecholamines (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-18
    Description: Epinephrine and isoproterenol provoke primary chick myoblasts to initiate precocious cell fusion. Both the rise in intracellular adenosine 3' ,5-monophosphate (cyclic AMP) and cell fusion generated by these effectors are prevented by propranolol, which is a specific blocker of the beta-adrenergic receptor. Propranolol has no effect either on the precocious cell fusion provoked by prostaglandin E or on cell fusion in control cultures. The results support the idea that a rise in cyclic AMP is the critical intracellular change responsible for initiating events that culminate in myoblast differentiation 4 to 5 hours later. They also indicate that the culminate in myoblast differentiation 4 to 5 hours later. They also indicate that the hormone responsible for the positive regulation of myoblast differentiation in vitro is not acting through the beta-adrenergic receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtis, D H -- Zalin, R J -- New York, N.Y. -- Science. 1981 Dec 18;214(4527):1355-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6274017" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catecholamines/*pharmacology ; Cell Differentiation/drug effects ; Cell Fusion/*drug effects ; Cells, Cultured ; Chick Embryo ; Cyclic AMP/metabolism ; Epinephrine/pharmacology ; Isoproterenol/pharmacology ; Muscles/*cytology ; Propranolol/pharmacology ; Prostaglandins E/pharmacology ; Receptors, Adrenergic, beta/drug effects ; Stimulation, Chemical
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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