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  • Cells, Cultured  (64)
  • American Association for the Advancement of Science (AAAS)  (64)
  • American Association for the Advancement of Science
  • American Institute of Physics (AIP)
  • 1985-1989  (64)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (64)
  • American Association for the Advancement of Science
  • American Institute of Physics (AIP)
Years
Year
  • 1
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    Cryopreservation, culture, and transplantation of human fetal mesencephalic tissue into monkeys (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-04
    Description: Studies in animals suggest that fetal neural grafts might restore lost neurological function in Parkinson's disease. In monkeys, such grafts survive for many months and reverse signs of parkinsonism, without attendant graft rejection. The successful and reliable application of a similar transplantation procedure to human patients, however, will require neural tissue obtained from human fetal cadavers, with demonstrated cellular identity, viability, and biological safety. In this report, human fetal neural tissue was successfully grafted into the brains of monkeys. Neural tissue was collected from human fetal cadavers after 9 to 12 weeks of gestation and cryopreserved in liquid nitrogen. Viability after up to 2 months of storage was demonstrated by cell culture and by transplantation into monkeys. Cryopreservation and storage of human fetal neural tissue would allow formation of a tissue bank. The stored cells could then be specifically tested to assure their cellular identity, viability, and bacteriological and virological safety before clinical use. The capacity to collect and maintain viable human fetal neural tissue would also facilitate research efforts to understand the development and function of the human brain and provide opportunities to study neurological diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Redmond, D E Jr -- Naftolin, F -- Collier, T J -- Leranth, C -- Robbins, R J -- Sladek, C D -- Roth, R H -- Sladek, J R Jr -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2903552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Cells, Cultured ; Cercopithecus ; Fetus ; Freezing ; Humans ; Male ; Mesencephalon/cytology/embryology/enzymology/*transplantation ; Preservation, Biological ; Transplantation, Heterologous ; Tyrosine 3-Monooxygenase/metabolism
    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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  • 2
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    Monocyte-derived human B-cell growth factor identified as interferon-beta 2 (BSF-2, IL-6) (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-29
    Description: Soluble products of either Epstein-Barr virus (EBV)-infected B cells or activated monocytes promote the proliferation of EBV-infected B cells and permit their growth at low cell densities. This suggests that growth factors are important for B-cell immortalization by EBV. In this study, a monocyte-derived factor that promotes the growth of EBV-infected b cells was purified and identified as interferon-beta 2 (IFN-beta 2), which is also known as 26-kilodalton protein, B-cell differentiation factor (BSF-2), and interleukin-6 (IL-6). The purified protein has a specific activity of approximately 4 X 10(7) units per milligram of protein in assays of B-cell growth. Thus, IFN-beta 2/BSF-2 is a B-cell growth factor that promotes the proliferation of human B cells infected with EBV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tosato, G -- Seamon, K B -- Goldman, N D -- Sehgal, P B -- May, L T -- Washington, G C -- Jones, K D -- Pike, S E -- AI-16262/AI/NIAID NIH HHS/ -- CA-44365/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):502-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biochemistry and Biophysics, Food and Drug Administration, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2829354" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/*cytology/microbiology ; Cell Count ; Cell Division ; Cells, Cultured ; Electrophoresis, Polyacrylamide Gel ; Herpesvirus 4, Human/*physiology ; Humans ; Immunoassay ; Interleukin-6 ; Interleukins/isolation & purification/*pharmacology ; Monocytes/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Endothelial interleukin-8: a novel inhibitor of leukocyte-endothelial interactions (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-12-22
    Description: Certain inflammatory stimuli render cultured human vascular endothelial cells hyperadhesive for neutrophils. This state is transient and reversible, in part because activated endothelial cells secrete a leukocyte adhesion inhibitor (LAI). LAI was identified as endothelial interleukin-8 (IL-8), the predominant species of which is an extended amino-terminal IL-8 variant. At nanomolar concentrations, purified endothelial IL-8 and recombinant human IL-8 inhibit neutrophil adhesion to cytokine-activated endothelial monolayers and protect these monolayers from neutrophil-mediated damage. These findings suggest that endothelial-derived IL-8 may function to attenuate inflammatory events at the interface between vessel wall and blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gimbrone, M A Jr -- Obin, M S -- Brock, A F -- Luis, E A -- Hass, P E -- Hebert, C A -- Yip, Y K -- Leung, D W -- Lowe, D G -- Kohr, W J -- P01-HL-36028/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1601-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2688092" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Biological Factors/pharmacology ; Cell Adhesion/drug effects ; Cells, Cultured ; Chemotactic Factors/*isolation & purification/pharmacology ; Culture Media/analysis ; Cytokines ; Endothelium, Vascular/cytology/drug effects/*physiology ; Humans ; Interleukin-1/*pharmacology ; Interleukin-8 ; Interleukins/*isolation & purification/pharmacology ; Molecular Sequence Data ; Neutrophils/cytology/drug effects/*physiology ; Recombinant Proteins/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Conserved repetitive epitope recognized by CD4+ clones from a malaria-immunized volunteer (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-12-22
    Description: T cell clones obtained from a human volunteer immunized with Plasmodium falciparum sporozoites specifically recognized the native circumsporozoite (CS) antigen expressed on P. falciparum sporozoites, as well as bacteria- and yeast-derived recombinant falciparum CS proteins. The response of these CD4+ CD8- cells was species-specific, since the clones did not proliferate or secrete gamma interferon when challenged with sporozoites or recombinant CS proteins of other human, simian, or rodent malarias. The epitope recognized by the sporozoite-specific human T cell clones mapped to the 5' repeat region of the CS protein and was contained in the NANPNVDPNANP sequence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nardin, E H -- Herrington, D A -- Davis, J -- Levine, M -- Stuber, D -- Takacs, B -- Caspers, P -- Barr, P -- Altszuler, R -- Clavijo, P -- AI25085/AI/NIAID NIH HHS/ -- AI62533/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1603-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Molecular Parasitology, New York University, NY 10010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2480642" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*immunology ; Antigens, Protozoan/*immunology ; Cells, Cultured ; Clone Cells ; Epitopes/*analysis ; Humans ; Interferon-gamma/biosynthesis ; Lymphocyte Activation ; Malaria/*immunology ; Molecular Sequence Data ; Plasmodium falciparum/*immunology ; *Protozoan Proteins ; Recombinant Proteins/immunology ; T-Lymphocytes/*immunology
    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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    Genetically transformed maize plants from protoplasts (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-08
    Description: Genetically transformed maize plants were obtained from protoplasts treated with recombinant DNA. Protoplasts that were digested from embryogenic cell suspension cultures of maize inbred A188 were combined with plasmid DNA containing a gene coding for neomycin phosphotransferase (NPT II) next to the 35S promoter region of cauliflower mosaic virus. A high voltage electrical pulse was applied to the protoplasts, which were then grown on filters placed over feeder layers of maize suspension cells (Black Mexican Sweet) and selected for growth in the presence of kanamycin. Selected cell lines showed NPT II activity. Plants were regenerated from transformed cell lines and grown to maturity. Southern analysis of DNA extracted from callus and plants indicated the presence of the NPT II gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhodes, C A -- Pierce, D A -- Mettler, I J -- Mascarenhas, D -- Detmer, J J -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):204-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sandoz Crop Protection Corporation, Palo Alto, CA 94304-1104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832947" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Membrane Permeability ; Cells, Cultured ; DNA/analysis ; DNA, Recombinant ; Electricity ; Genetic Engineering/*methods ; Kanamycin Kinase ; Phosphotransferases/metabolism ; Plasmids ; Transformation, Genetic ; Zea mays/*genetics
    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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    A cell-cycle constraint on the regulation of gene expression by platelet-derived growth factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-27
    Description: In density-arrested monolayer cultures of Balb/c 3T3 cells, platelet-derived growth factor (PDGF) stimulates expression of the c-myc and c-fos proto-oncogenes, as well as the functionally uncharacterized genes, JE, KC, and JB. These genes are not coordinately regulated. Under ordinary conditions, c-fos, JE, KC, and JB respond to PDGF only when the cells are in a state of G0 growth arrest at the time of PDGF addition. The c-myc gene is regulated in opposition to the other genes, responding best to PDGF in cycling cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rollins, B J -- Morrison, E D -- Stiles, C D -- CA 20042-09/CA/NCI NIH HHS/ -- GM 31489-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medicine, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Interphase ; Mice ; Mice, Inbred BALB C ; Platelet-Derived Growth Factor/*pharmacology ; Proto-Oncogenes/*drug effects ; Transcription, Genetic/*drug effects
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Nicotinic antagonists enhance process outgrowth by rat retinal ganglion cells in culture (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: Functional nicotinic cholinergic receptors are found on mammalian retinal ganglion cell neurons in culture. The neurotransmitter acetylcholine (ACh) can be detected in the medium of many of these retinal cultures, after release presumably from the choline acetyltransferase-positive amacrine cells. The postsynaptic effect of endogenous or applied ACh on the ganglion cells can be blocked with specific nicotinic antagonists. Here it is shown that within 24 hours of producing such a pharmacologic blockade, the retinal ganglion cells begin to sprout or regenerate neuronal processes. Thus, the growth-enhancing effect of nicotinic antagonists may be due to the removal of inhibition to growth by tonic levels of ACh present in the culture medium. Since there is a spontaneous leak of ACh in the intact retina, the effects of nicotinic cholinergic drugs on process outgrowth in culture may reflect a normal control mechanism for growth or regeneration of retinal ganglion cell processes that is exerted by ACh in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipton, S A -- Frosch, M P -- Phillips, M D -- Tauck, D L -- Aizenman, E -- EY05477/EY/NEI NIH HHS/ -- EY06087/EY/NEI NIH HHS/ -- NS00879/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1293-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/*pharmacology ; Cells, Cultured ; Mecamylamine/*pharmacology ; Picrotoxin/pharmacology ; Rats ; Receptors, Nicotinic/drug effects/*physiology ; Retina/*cytology ; Retinal Ganglion Cells/*cytology/drug effects ; Tubocurarine/*pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Retroviral vector-mediated gene transfer into human hematopoietic progenitor cells (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-29
    Description: The transfer of the human gene for hypoxanthine phosphoribosyltransferase (HPRT) into human bone marrow cells was accomplished by use of a retroviral vector. The cells were infected in vitro with a replication-incompetent murine retroviral vector that carried and expressed a mutant HPRT complementary DNA. The infected cells were superinfected with a helper virus and maintained in long-term culture. The production of progeny HPRT virus by the bone marrow cells was demonstrated with a colony formation assay on cultured HPRT-deficient, ouabain-resistant murine fibroblasts. Hematopoietic progenitor cells able to form colonies of granulocytes or macrophages (or both) in semisolid medium in the presence of colony stimulating factor were present in the nonadherent cell population. Colony forming units cloned in agar and subsequently cultured in liquid medium produced progeny HPRT virus, indicating infection of this class of hematopoietic progenitor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, H E -- Finley, K D -- Hershberg, R M -- Katzman, S S -- Laikind, P K -- Seegmiller, J E -- Friedmann, T -- Yee, J K -- Jolly, D J -- AM 13622/AM/NIADDK NIH HHS/ -- GM 28223/GM/NIGMS NIH HHS/ -- HD20034/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Nov 29;230(4729):1057-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3864246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Gene Expression Regulation ; *Genetic Engineering ; Genetic Vectors ; Hematopoietic Stem Cells/*physiology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Mice ; Retroviridae/*genetics ; Transfection
    Print ISSN: 0036-8075
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  • 9
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    Steroid hormone metabolites are barbiturate-like modulators of the GABA receptor (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-23
    Description: Two metabolites of the steroid hormones progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydrodeoxycorticosterone, are potent barbiturate-like ligands of the gamma-aminobutyric acid (GABA) receptor-chloride ion channel complex. At concentrations between 10(-7) and 10(-5)M both steroids inhibited binding of the convulsant t-butylbicyclophosphorothionate to the GABA-receptor complex and increased the binding of the benzodiazepine flunitrazepam; they also stimulated chloride uptake (as measured by uptake of 36Cl-) into isolated brain vesicles, and potentiated the inhibitory actions of GABA in cultured rat hippocampal and spinal cord neurons. These data may explain the ability of certain steroid hormones to rapidly alter neuronal excitability and may provide a mechanism for the anesthetic and hypnotic actions of naturally occurring and synthetic anesthetic steroids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Majewska, M D -- Harrison, N L -- Schwartz, R D -- Barker, J L -- Paul, S M -- New York, N.Y. -- Science. 1986 May 23;232(4753):1004-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422758" target="_blank"〉PubMed〈/a〉
    Keywords: 20-alpha-Dihydroprogesterone/*analogs & derivatives/metabolism/pharmacology ; Animals ; Bicyclo Compounds/metabolism ; *Bicyclo Compounds, Heterocyclic ; Binding, Competitive ; Brain/metabolism ; Cells, Cultured ; Chlorides/metabolism ; Desoxycorticosterone/*analogs & derivatives/metabolism/pharmacology ; Drug Synergism ; Flunitrazepam/metabolism ; Hippocampus/metabolism ; In Vitro Techniques ; Ion Channels/metabolism ; Progesterone/*analogs & derivatives/metabolism/pharmacology ; Rats ; Receptors, GABA-A/*drug effects/metabolism ; Spinal Cord/metabolism
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  • 10
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    CD8+ lymphocytes can control HIV infection in vitro by suppressing virus replication (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-19
    Description: Lymphocytes bearing the CD8 marker were shown to suppress replication of human immunodeficiency virus (HIV) in peripheral blood mononuclear cells. The effect was dose-dependent and most apparent with autologous lymphocytes; it did not appear to be mediated by a cytotoxic response. This suppression of HIV replication could be demonstrated by the addition of CD8+ cells at the initiation of virus production as well as after several weeks of virus replication by cultured cells. The observations suggest a potential approach to therapy in which autologous CD8 lymphocytes could be administered to individuals to inhibit HIV replication and perhaps progression of disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, C M -- Moody, D J -- Stites, D P -- Levy, J A -- New York, N.Y. -- Science. 1986 Dec 19;234(4783):1563-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2431484" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology/therapy ; Antigens, Surface ; Cells, Cultured ; HIV/immunology/*physiology ; Humans ; Male ; RNA-Directed DNA Polymerase/metabolism ; T-Lymphocytes/*immunology ; *Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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