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  • In Vitro Techniques  (22)
  • American Association for the Advancement of Science (AAAS)  (22)
  • American Institute of Physics (AIP)
  • Annual Reviews
  • 1985-1989  (22)
  • 1980-1984
  • 1975-1979
  • 1940-1944
  • 1986  (22)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (22)
  • American Institute of Physics (AIP)
  • Annual Reviews
Years
  • 1985-1989  (22)
  • 1980-1984
  • 1975-1979
  • 1940-1944
Year
  • 1
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    Associative induction of posttetanic and long-term potentiation in CA1 neurons of rat hippocampus (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-23
    Description: Electrical stimulation of fibers in the stratum radiatum causes an excitatory postsynaptic potential in CA1 neurons of the hippocampus. Other excitatory inputs to or direct depolarization of these CA1 neurons during stimulation of the stratum radiatum caused a subsequent increase in the excitatory postsynaptic potential. This enhancement was characterized as a brief potentiation (2 to 3 minutes, similar to posttetanic potentiation) and a long-term potentiation (presumed to be involved in learning and memory). These potentiations are probably induced by an interaction of the postsynaptic cell or other presynaptic terminals with the test presynaptic terminals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sastry, B R -- Goh, J W -- Auyeung, A -- New York, N.Y. -- Science. 1986 May 23;232(4753):988-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010459" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain Mapping ; Calcium/physiology ; Conditioning (Psychology)/physiology ; Electric Stimulation ; Hippocampus/*physiology ; In Vitro Techniques ; Learning/physiology ; Membrane Potentials ; Rats ; Synapses/physiology ; Synaptic Transmission
    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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    Three-dimensional structure of an antigen-antibody complex at 2.8 A resolution (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-15
    Description: The 2.8 A resolution three-dimensional structure of a complex between an antigen (lysozyme) and the Fab fragment from a monoclonal antibody against lysozyme has been determined and refined by x-ray crystallographic techniques. No conformational changes can be observed in the tertiary structure of lysozyme compared with that determined in native crystalline forms. The quaternary structure of Fab is that of an extended conformation. The antibody combining site is a rather flat surface with protuberances and depressions formed by its amino acid side chains. The antigen-antibody interface is tightly packed, with 16 lysozyme and 17 antibody residues making close contacts. The antigen contacting residues belong to two stretches of the lysozyme polypeptide chain: residues 18 to 27 and 116 to 129. All the complementarity-determining regions and two residues outside hypervariable positions of the antibody make contact with the antigen. Most of these contacts (10 residues out of 17) are made by the heavy chain, and in particular by its third complementarity-determining region. Antigen variability and antibody specificity and affinity are discussed on the basis of the determined structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amit, A G -- Mariuzza, R A -- Phillips, S E -- Poljak, R J -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):747-53.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2426778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies, Monoclonal ; *Antigen-Antibody Complex ; Chickens ; Egg White ; Epitopes ; *Immunoglobulin Fab Fragments ; Immunoglobulin Heavy Chains ; Immunoglobulin Light Chains ; In Vitro Techniques ; Kinetics ; Models, Molecular ; Muramidase/*immunology ; Protein Conformation ; X-Ray Diffraction
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  • 3
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    Dynamics of lymphocyte-endothelial interactions in vivo (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-01-24
    Description: The dynamics of the attachment of lymphocytes to the endothelium of high endothelial venules in murine Peyer's patches were studied in vivo. Lymphocytes adhered readily to the endothelium lining these vessels, but most of the adhering cells detached within a few seconds. Many lymphocytes, however, experienced multiple collisions with the high endothelial venules, and this substantially increased the efficiency of lymphocyte collection by these vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjerknes, M -- Cheng, H -- Ottaway, C A -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):402-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endothelium/physiology ; Female ; In Vitro Techniques ; Lymphocytes/*physiology ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Peyer's Patches/*physiology
    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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    Human beta-adrenoceptors: relation of myocardial and lymphocyte beta-adrenoceptor density (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-28
    Description: In human right atria obtained from 21 patients during open-heart surgery, beta-adrenoceptor density [assessed by iodine-125-labeled (-)-cyanopindolol binding] and responsiveness (positive inotropic responses to isoprenaline) were linearly related to the beta-adrenoceptor density in the corresponding circulating lymphocytes. This direct relation of human myocardial and lymphocyte beta-adrenoceptor alterations, therefore, makes it possible to monitor drug- or disease-induced beta-adrenoceptor changes in tissues not easily accessible in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brodde, O E -- Kretsch, R -- Ikezono, K -- Zerkowski, H R -- Reidemeister, J C -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1584-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006250" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Heart Atria ; Humans ; In Vitro Techniques ; Isoproterenol/pharmacology ; Lymphocytes/*metabolism ; Male ; Middle Aged ; Myocardial Contraction/drug effects ; Myocardium/*metabolism ; Receptors, Adrenergic, beta/*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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  • 5
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    A low threshold calcium spike mediates firing pattern alterations in pontine reticular neurons (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-11-07
    Description: Intracellular electrical recordings in an in vitro slice preparation of the brainstem medial pontine reticular formation, a region thought to be important in mediation of desynchronized sleep phenomena, demonstrate a population of neurons that have a calcium-dependent, low threshold spike. This low threshold spike was inactivated at relatively depolarized membrane potential levels and, when this spike was deinactivated, it induced a burst of action potentials. The membrane potential dependence of the spike may underlie changes in action potential firing patterns associated with behavioral state change because the baseline membrane potential in neurons of the medial pontine reticular population depolarizes during passage from waking and slow wave sleep to desynchronized sleep, which is characterized by the absence of burst firing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, R W -- Haas, H L -- McCarley, R W -- MH 39,683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):738-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775364" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/physiology ; Electric Stimulation ; In Vitro Techniques ; Membrane Potentials ; Pons/cytology/*physiology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Inhibition of endothelial regeneration by type-beta transforming growth factor from platelets (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-09-05
    Description: Damage to the vessel wall is a signal for endothelial migration and replication and for platelet release at the site of injury. Addition of transforming growth factor-beta (TGF-beta) purified from platelets to growing aortic endothelial cells inhibited [3H]thymidine incorporation in a concentration-dependent manner. A transient inhibition of DNA synthesis was also observed in response to wounding; cell migration and replication are inhibited during the first 24 hours after wounding. By 48 hours after wounding both TGF-beta-treated and -untreated cultures showed similar responses. Flow microfluorimetric analysis of cell cycle distribution indicated that after 24 hours of exposure to TGF-beta the cells were blocked from entering S phase, and the fraction of cells in G1 was increased. The inhibition of the initiation of regeneration by TGF-beta could allow time for recruitment of smooth muscle cells into the site of injury by other platelet components.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heimark, R L -- Twardzik, D R -- Schwartz, S M -- HL-18645/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1078-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3461562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/*physiology ; Cell Cycle/drug effects ; Cell Movement/drug effects ; Cells, Cultured ; Endothelium/cytology/*physiology ; Flow Cytometry ; *Growth Inhibitors ; Humans ; In Vitro Techniques ; Peptides/*pharmacology ; Rats ; Regeneration ; Transforming Growth Factors
    Print ISSN: 0036-8075
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  • 7
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    The role of chloride transport in postsynaptic inhibition of hippocampal neurons (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-06-13
    Description: Hippocampal inhibitory postsynaptic potentials are depolarizing in granule cells but hyperpolarizing in CA3 neurons because the reversal potentials and membrane potentials of these cells differ. Here the hippocampal slice preparation was used to investigate the role of chloride transport in these inhibitory responses. In both cell types, increasing the intracellular chloride concentration by injection shifted the reversal potential of these responses in a positive direction, and blocking the outward transport of chloride with furosemide slowed their recovery from the injection. In addition, hyperpolarizing and depolarizing inhibitory responses and the hyperpolarizing and depolarizing responses to the inhibitory neurotransmitter gamma-aminobutyric acid decreased in the presence of furosemide. These effects of furosemide suggest that the internal chloride activity of an individual hippocampal neuron is regulated by two transport processes, one that accumulates chloride and one that extrudes chloride.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Misgeld, U -- Deisz, R A -- Dodt, H U -- Lux, H D -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1413-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2424084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport/drug effects ; Cell Membrane Permeability/drug effects ; Chlorides/*physiology ; Furosemide/pharmacology ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Ion Channels/drug effects ; Membrane Potentials/drug effects ; *Neural Inhibition ; gamma-Aminobutyric Acid/*physiology
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  • 8
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    A macrophage-derived factor required by plasmacytomas for survival and proliferation in vitro (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-01
    Description: Plasmacytoma (PCT) cell lines dependent for proliferation and survival on a factor elaborated by the murine macrophage cell line, P388D1, were established in vitro. Adherent peritoneal cells induced by pristane produced 50-fold greater amounts of this activity in vitro than did resident cells. The molecules responsible for plasmacytoma growth were distinct from a number of characterized factors including interleukin-1, -2, and -3, macrophage colony-stimulating factor, B-cell stimulatory factor-1, B-cell growth factor II, epidermal growth factor, transforming growth factor-beta, and gamma- and beta-interferon, none of which were able to support the growth of the factor-dependent PCT cell lines. These results suggest that PCT growth factor may be a novel factor that has not been previously characterized and, further, that its production is associated with the pristane-induced, chronic peritoneal inflammatory response that precedes plasmacytoma formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nordan, R P -- Potter, M -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):566-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726549" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Division/drug effects ; Cell Line ; *Cell Survival/drug effects ; Growth Substances/*isolation & purification/pharmacology/physiology ; Humans ; In Vitro Techniques ; Macrophages/*physiology ; Mice ; Plasmacytoma/*physiopathology
    Print ISSN: 0036-8075
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  • 9
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    Effect of antibodies to recombinant and synthetic peptides on P. falciparum sporozoites in vitro (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-01-10
    Description: Antibodies were raised in mice immunized with several recombinant and synthetic peptides of the circumsporozoite protein of Plasmodium falciparum. The antibodies were evaluated for protective activity in a human hepatocyte culture system. They exerted their protective effect against the parasite at three points: sporozoite attachment to the hepatocyte surface, entry, and subsequent intracellular development. Inhibition of attachment and entry were found to be related to the antibody titer against the authentic circumsporozoite protein on the sporozoite surface, especially when peptides were administered with alum or complete Freund's adjuvant. Even when invasion was not totally inhibited, the presence of abnormal trophozoites and a frequent inhibition of schizont development in long-term cultures suggested continued activity of antibodies at the intracellular level after sporozoite penetration had been completed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mazier, D -- Mellouk, S -- Beaudoin, R L -- Texier, B -- Druilhe, P -- Hockmeyer, W -- Trosper, J -- Paul, C -- Charoenvit, Y -- Young, J -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):156-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3510455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*immunology ; Antigens, Protozoan/*immunology ; Fluorescent Antibody Technique ; Humans ; In Vitro Techniques ; Liver/cytology/parasitology ; Mice ; Peptides/immunology ; Plasmodium falciparum/*immunology ; Recombinant Proteins/immunology
    Print ISSN: 0036-8075
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  • 10
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    Calcium channels in planar lipid bilayers: insights into mechanisms of ion permeation and gating (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-28
    Description: Electrophysiological recordings were used to analyze single calcium channels in planar lipid bilayers after membranes from bovine cardiac sarcolemmal vesicles had been incorporated into the bilayer. In these cell-free conditions, channels in the bilayer showed unitary barium or calcium conductances, gating kinetics, and pharmacological responses that were similar to dihydropyridine-sensitive calcium channels in intact cells. The open channel current varied in a nonlinear manner with voltage under asymmetric (that is, physiological) ionic conditions. However, with identical solutions on both sides of the bilayer, the current-voltage relation was linear. In matched experiments, calcium channels from skeletal muscle T-tubules differed significantly from cardiac calcium channels in their conductance properties and gating kinetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, R L -- Hess, P -- Reeves, J P -- Smilowitz, H -- Tsien, R W -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1564-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2420007" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Pyridinecarboxylic acid, ; 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Animals ; Calcium/*physiology ; Cattle ; Electric Conductivity ; Heart/physiology ; In Vitro Techniques ; Ion Channels/*physiology ; Lipid Bilayers ; Nicotinic Acids/pharmacology ; Nifedipine/analogs & derivatives/pharmacology ; Nimodipine ; Potassium/physiology ; Sarcolemma ; Sodium/physiology
    Print ISSN: 0036-8075
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  • 11
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    Direct polyclonal activation of human B lymphocytes by the acquired immune deficiency syndrome virus (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-09-05
    Description: When B lymphocytes from normal human peripheral blood were incubated for 1 hour with the retrovirus that causes the acquired immune deficiency syndrome (AIDS), the B cells showed marked proliferation and differentiation. Proliferative responses to the virus peaked on day 4 and appeared to be independent of accessory cells. This finding was repeated with three separate viral isolates, one of which was from a patient from Zaire. The magnitude of the observed responses was comparable to that seen with standard polyclonal B-cell activators. This phenomenon may be at least partially responsible for the polyclonal B-cell activation seen in patients with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schnittman, S M -- Lane, H C -- Higgins, S E -- Folks, T -- Fauci, A S -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1084-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016902" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology ; B-Lymphocytes/*immunology ; Cell Differentiation ; Deltaretrovirus/*immunology ; Humans ; Immunoglobulins/metabolism ; In Vitro Techniques ; Lymphocyte Activation ; Receptors, Virus/physiology
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  • 12
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    Direct cloning and sequence analysis of enzymatically amplified genomic sequences (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-09-05
    Description: A method is described for directly cloning enzymatically amplified segments of genomic DNA into an M13 vector for sequence analysis. A 110-base pair fragment of the human beta-globin gene and a 242-base pair fragment of the human leukocyte antigen DQ alpha locus were amplified by the polymerase chain reaction method, a procedure based on repeated cycles of denaturation, primer annealing, and extension by DNA polymerase I. Oligonucleotide primers with restriction endonuclease sites added to their 5' ends were used to facilitate the cloning of the amplified DNA. The analysis of cloned products allowed the quantitative evaluation of the amplification method's specificity and fidelity. Given the low frequency of sequence errors observed, this approach promises to be a rapid method for obtaining reliable genomic sequences from nanogram amounts of DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scharf, S J -- Horn, G T -- Erlich, H A -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1076-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3461561" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cloning, Molecular/*methods ; Coliphages/*genetics ; DNA Polymerase I/metabolism ; Gene Amplification ; *Genetic Vectors ; Globins/*genetics ; HLA-DQ Antigens ; Histocompatibility Antigens Class II/*genetics ; Humans ; In Vitro Techniques ; Polymorphism, Genetic
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  • 13
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    Solid phase synthesis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merrifield, B -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):341-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3961484" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Chemical Phenomena ; Chemistry ; In Vitro Techniques ; Methods ; Nucleotides/*chemical synthesis ; Peptide Fragments/metabolism ; Peptides/*chemical synthesis ; Ribonuclease, Pancreatic/chemical synthesis/metabolism ; Structure-Activity Relationship
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  • 14
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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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  • 15
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    Heterogeneous nuclear ribonucleoproteins: role in RNA splicing (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-28
    Description: Splicing in vitro of a messenger RNA (mRNA) precursor (pre-mRNA) is inhibited by a monoclonal antibody to the C proteins (anti-C) of the heterogeneous nuclear RNA (hnRNA)-ribonucleoprotein (hnRNP) particles. This antibody, 4F4, inhibits an early step of the reaction: cleavage at the 3' end of the upstream exon and the formation of the intron lariat. In contrast, boiled 4F4, or a different monoclonal antibody (designated 2B12) to the C proteins, or antibodies to other hnRNP proteins (120 and 68 kilodaltons) and nonimmune mouse antibodies have no inhibitory effect. The 4F4 antibody does not prevent the adenosine triphosphate-dependent formation of a 60S splicing complex (spliceosome). Furthermore, the 60S splicing complex contains C proteins, and it can be immunoprecipitated with 4F4. Depletion of C proteins from the splicing extract by immunoadsorption with either of the two monoclonal antibodies to the C proteins (4F4 or 2B12) results in the loss of splicing activity, whereas mock-depletion with nonimmune mouse antibodies bodies has no effect. A 60S splicing complex does not form in a C protein-depleted nuclear extract. These results indicate an essential role for proteins of the hnRNP complex in the splicing of mRNA precursors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Y D -- Grabowski, P J -- Sharp, P A -- Dreyfuss, G -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1534-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952495" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Antibodies, Monoclonal/*immunology ; HeLa Cells ; Heterogeneous-Nuclear Ribonucleoproteins ; Humans ; In Vitro Techniques ; Macromolecular Substances ; *RNA Splicing ; RNA, Heterogeneous Nuclear/metabolism ; Ribonucleoproteins/immunology/*physiology
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  • 16
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    Role of platelet-activating factor-acether in mediating guinea pig anaphylaxis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-04
    Description: The pathophysiology of anaphylaxis is very complex, and the sequelae of events are not fully explained in terms of the effects of histamine and peptide leukotrienes alone. Platelet-activating factor (1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine, PAF-acether) has been detected in animals undergoing anaphylaxis. Injection of synthetic PAF-acether induces similar effects, including bronchoconstriction, respiratory arrest, systemic hypotension, neutropenia, and thrombocytopenia. The results reported here demonstrate that the histamine- and leukotriene-independent component of guinea pig anaphylaxis in vivo and in isolated lung parenchymal strips in vitro is mediated by PAF-acether. However, PAF-acether is not responsible for the anaphylaxis-induced thrombocytopenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darius, H -- Lefer, D J -- Smith, J B -- Lefer, A M -- HL-25575/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):58-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3082008" target="_blank"〉PubMed〈/a〉
    Keywords: 4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyrazol-3-amine ; Alprazolam ; *Anaphylaxis ; Animals ; Anti-Inflammatory Agents/pharmacology ; Benzodiazepines/pharmacology ; Blood Pressure ; Diphenhydramine/pharmacology ; Guinea Pigs ; In Vitro Techniques ; Kinetics ; Lung/drug effects/*immunology ; Male ; Ovalbumin ; Platelet Activating Factor/*immunology ; Platelet Count/drug effects ; Pyrazoles/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Vasoconstriction: a new activity for platelet-derived growth factor (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-04-04
    Description: Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells that has been implicated in the pathogenesis of atherosclerosis. The potential role of PDGF in the altered vasoreactivity of atherosclerotic vessels has been studied through an examination of its effects on contractility in the rat aorta. PDGF caused a concentration-dependent contraction of aortic strips and was significantly more potent on a molar basis than the classic vasoconstrictor peptide angiotensin II. Furthermore, PDGF increased the cytosolic free calcium concentration in cultured rat aortic smooth muscle cells. These observations suggest a new biological activity for PDGF that may contribute to the enhanced vasoreactivity of certain atherosclerotic vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berk, B C -- Alexander, R W -- Brock, T A -- Gimbrone, M A Jr -- Webb, R C -- HL20054/HL/NHLBI NIH HHS/ -- HL22602/HL/NHLBI NIH HHS/ -- HL35013/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):87-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3485309" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Angiotensin II/pharmacology ; Animals ; Aorta/*drug effects/metabolism/physiology ; Calcium/metabolism ; Cytosol/metabolism ; Dose-Response Relationship, Drug ; Epidermal Growth Factor/pharmacology ; Fluorescent Dyes ; Homeostasis/drug effects ; Humans ; In Vitro Techniques ; Kinetics ; Platelet-Derived Growth Factor/*pharmacology ; Rats ; Vasoconstriction/*drug effects
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  • 18
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    Inhibition of vasopressin action by atrial natriuretic factor (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-03-28
    Description: Atrial natriuretic factor results in diuresis in animals and humans, perhaps because atrial natriuretic factor increases renal blood flow. The possibility that this diuresis is due to direct inhibition of renal tubular epithelial water transport was examined in rabbit collecting tubules perfused in vitro. Atriopeptin III inhibition of the hydraulic conductivity response to the hormone arginine vasopressin but not to either 3'5'-cyclic adenosine monophosphate or forskolin was found. These results suggest that atriopeptin III acts proximal to cyclic adenosine monophosphate formation to directly affect vasopressin-stimulated water transport in the mammalian nephron. They also suggest a potential role for inhibition by atrial natriuretic factor of the renal response to arginine vasopressin as a contributor to a diuretic state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dillingham, M A -- Anderson, R J -- 1K08 AM-01245/AM/NIADDK NIH HHS/ -- AM-26111/AM/NIADDK NIH HHS/ -- AM-30448/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1572-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006248" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*antagonists & inhibitors ; Atrial Natriuretic Factor/*pharmacology ; Colforsin/pharmacology ; Cyclic AMP/physiology ; Cyclic GMP/physiology ; Diuresis/drug effects ; In Vitro Techniques ; Kidney Tubules/*drug effects ; Kidney Tubules, Collecting/*drug effects/physiology ; Rabbits
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Activation of smooth muscle contraction: relation between myosin phosphorylation and stiffness (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-04
    Description: Contraction and myosin light-chain phosphorylation were measured in electrically stimulated tracheal smooth muscle. Latencies for the onset of force, stiffness, and light-chain phosphorylation were 500 milliseconds. Myosin light chain was phosphorylated from 0.04 to 0.80 mole of phosphate per mole of light chain with a pseudo-first-order rate of 1.1 per second with no evidence of an ordered or negatively cooperative process. Following the period of latency, stiffness increased with phosphorylation and both increased more rapidly than isometric force. The linear relation between stiffness and phosphorylation during activation suggests independent attachment of each myosin head upon phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamm, K E -- Stull, J T -- HL 26043/HL/NHLBI NIH HHS/ -- HL 32607/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):80-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754063" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbachol/pharmacology ; Electric Stimulation ; In Vitro Techniques ; Kinetics ; *Muscle Contraction/drug effects ; Muscle, Smooth/*physiology ; Myosin-Light-Chain Kinase ; Myosins/*metabolism ; Phosphorylation ; Protein Kinases/metabolism ; Trachea/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Differential conditioning of associative synaptic enhancement in hippocampal brain slices (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-04-04
    Description: An electrophysiological stimulation paradigm similar to one that produces Pavlovian conditioning was applied to synaptic inputs to pyramidal neurons of hippocampal brain slices. Persistent synaptic enhancement was induced in one of two weak synaptic inputs by pairing high-frequency electrical stimulation of the weak input with stimulation of a third, stronger input to the same region. Forward (temporally overlapping) but not backward (temporally separate) pairings caused this enhancement. Thus hippocampal synapses in vitro can undergo the conditional and selective type of associative modification that could provide the substrate for some of the mnemonic functions in which the hippocampus is thought to participate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelso, S R -- Brown, T H -- NS07408/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):85-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conditioning, Classical ; Electric Stimulation ; Hippocampus/*physiology ; In Vitro Techniques ; Models, Neurological ; Models, Psychological ; Neurons/physiology ; Pyramidal Tracts/physiology ; Rats ; Synapses/*physiology ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Induction of synaptic potentiation in hippocampus by patterned stimulation involves two events (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-05-23
    Description: Electrical stimulation of axons in the hippocampus with short high-frequency bursts that resemble in vivo activity patterns produces stable potentiation of postsynaptic responses when the bursts occur at intervals of 200 milliseconds but not 2 seconds. When a burst was applied to one input and a second burst applied to a different input to the same target neuron 200 milliseconds later, only the synapses activated by the second burst showed stable potentiation. This effect was observed even when the two inputs innervated completely different regions of the postsynaptic cells; but did not occur when the inputs were stimulated simultaneously or when the second burst was delayed by 2 seconds. Intracellular recordings indicated that the first burst extended the decay phase of excitatory postsynaptic potentials evoked 200 milliseconds later. These results suggest that a single burst of axonal stimulation produces a transient, spatially diffuse "priming" effect that prolongs responses to subsequent bursts, and that these altered responses trigger spatially restricted synaptic modifications. The similarity of the temporal parameters of the priming effect and the theta rhythm that dominates the hippocampal electroencephalogram (EEG) during learning episodes suggests that this priming may be involved in behaviorally induced synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Larson, J -- Lynch, G -- New York, N.Y. -- Science. 1986 May 23;232(4753):985-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3704635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Hippocampus/*physiology ; In Vitro Techniques ; Learning/physiology ; Membrane Potentials ; Neuronal Plasticity ; Periodicity ; Rats ; Synapses/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Control of cachectin (tumor necrosis factor) synthesis: mechanisms of endotoxin resistance (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-23
    Description: Cachectin (tumor necrosis factor) is a macrophage hormone strongly implicated in the pathogenesis of endotoxin-induced shock. The availability of a DNA probe complementary to the cachectin messenger RNA (mRNA), as well as a specific antibody capable of recognizing the cachectin gene product, has made it possible to analyze the regulation of cachectin gene expression under a variety of conditions. Thioglycollate-elicited peritoneal macrophages obtained from mice contain a pool of cachectin mRNA that is not expressed as protein. When the cells are stimulated with endotoxin, large quantity of additional cachectin mRNA is produced, and immunoreactive cachectin is secreted. Macrophages from mice of the C3H/HeJ strain do not produce cachectin in response to endotoxin. A dual defect appears to prevent cachectin expression. First, a diminished quantity of cachectin mRNA is expressed in response to low concentrations of endotoxin. Second, a post-transcriptional defect prevents the production of cachectin protein. Macrophages from endotoxin-sensitive mice do not produce cachectin if they are first treated with dexamethasone, apparently for similar reasons. These findings give new insight into the nature of the C3H/HeJ mutation and suggest an important mechanism by which glucocorticoids may act to suppress inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, B -- Krochin, N -- Milsark, I W -- Luedke, C -- Cerami, A -- AI21359/AI/NIAID NIH HHS/ -- AM01314/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):977-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dexamethasone/pharmacology ; Drug Resistance ; Endotoxins/*pharmacology ; Gene Expression Regulation/drug effects ; In Vitro Techniques ; Macrophages/drug effects/*metabolism ; Mice ; Mice, Inbred C3H/physiology ; *Protein Biosynthesis ; Proteins/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic/drug effects ; Tumor Necrosis Factor-alpha
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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