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  • Rats  (84)
  • Cell Line  (46)
  • American Association for the Advancement of Science (AAAS)  (123)
  • American Association for the Advancement of Science
  • Oxford University Press
  • 1985-1989  (123)
  • 1986  (123)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (123)
  • American Association for the Advancement of Science
  • Oxford University Press
Years
  • 1985-1989  (123)
Year
  • 1
    Publication Date: 1986-10-17
    Description: The regulation of nerve growth factor (NGF) protein and NGF messenger RNA (mRNA) in the developing rat brain has been studied to assess the hypothesis that NGF supports the differentiation of cholinergic neurons in the basal forebrain. In the adult, the major targets of these neurons, the hippocampus and neocortex, contain the highest concentrations of NGF mRNA, but comparatively low ratios of NGF protein to its mRNA. In contrast, a high concentration of NGF protein and a low concentration of NGF mRNA were seen in the basal forebrain, consistent with retrograde transport of NGF protein into this region from the neocortex and hippocampus. In these two target regions NGF and NGF mRNA were barely detectable at birth, their concentrations increased to a peak at day 21, and then NGF mRNA, but not NGF protein, declined threefold by day 35. NGF accumulation in the basal forebrain paralleled that in the target regions and preceded an increase in choline acetyltransferase, suggesting that the differentiation of cholinergic projection neurons is indeed regulated by retrogradely transported NGF. In addition, high ratios of NGF protein to NGF mRNA, comparable to that in the basal forebrain, were seen in the olfactory bulb and cerebellum, suggesting that NGF may be transported into these regions by unidentified neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Large, T H -- Bodary, S C -- Clegg, D O -- Weskamp, G -- Otten, U -- Reichardt, L F -- NS21824/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 17;234(4774):352-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764415" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*growth & development/metabolism ; Brain Chemistry ; Cerebellum/analysis ; Cerebral Cortex/analysis ; Hippocampus/analysis ; Nerve Growth Factors/analysis/*biosynthesis/genetics ; RNA, Messenger/analysis ; Rats ; Rats, Inbred Strains
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  • 2
    Publication Date: 1986-02-28
    Description: Transgenic mice expressing a metallothionein-somatostatin fusion gene contain high concentrations of somatostatin in the anterior pituitary gland, a tissue that does not normally produce somatostatin. Immunoreactive somatostatin within the anterior pituitaries was found exclusively within gonadotrophs. Similarly, a metallothionein-human growth-hormone fusion gene was also expressed selectively in gonadotrophs. It is proposed that sequences common to the two fusion genes are responsible for the gonadotroph-specific expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Low, M J -- Lechan, R M -- Hammer, R E -- Brinster, R L -- Habener, J F -- Mandel, G -- Goodman, R H -- AM 01313/AM/NIADDK NIH HHS/ -- AM 30457/AM/NIADDK NIH HHS/ -- AM 31400/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):1002-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2868526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Recombinant/metabolism ; Genes ; Genetic Engineering ; Humans ; Immunoenzyme Techniques ; Luteinizing Hormone/metabolism ; Metallothionein/*genetics ; Mice ; Pituitary Gland, Anterior/*metabolism ; Rats ; Somatostatin/*genetics/metabolism
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  • 3
    Publication Date: 1986-05-02
    Description: The development of simultaneous resistance to multiple structurally unrelated drugs is a major impediment to cancer chemotherapy. Multidrug resistance in human KB carcinoma cells selected in colchicine, vinblastine, or Adriamycin is associated with amplification of specific DNA sequences (the multidrug resistance locus, mdr1). During colchicine selection resistance is initially accompanied by elevated expression of a 4.5-kilobase mdr1 messenger RNA (mRNA) without amplification of the corresponding genomic sequences. During selection for increased levels of resistance, expression of this mRNA is increased simultaneously with amplification of mdr1 DNA. Increased expression and amplification of mdr1 sequences were also found in multidrug-resistant sublines of human leukemia and ovarian carcinoma cells. These results suggest that increased expression of mdr1 mRNA is a common mechanism for multidrug resistance in human cells. Activation of the mdr1 gene by mutations or epigenetic changes may precede its amplification during the development of resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, D W -- Fojo, A -- Chin, J E -- Roninson, I B -- Richert, N -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1986 May 2;232(4750):643-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA, Neoplasm/genetics ; Doxorubicin/pharmacology ; *Drug Resistance ; Female ; *Gene Amplification ; Humans ; Leukemia, Lymphoid/drug therapy ; Neoplasms/*drug therapy/genetics ; Nucleic Acid Hybridization ; Ovarian Neoplasms/drug therapy ; RNA, Messenger/genetics ; Vinblastine/pharmacology
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  • 4
    Publication Date: 1986-08-22
    Description: Continuous measurement and imaging of the intracellular free calcium ion concentration ([Ca2+]i) of mitotic and interphase PtK1 cells was accomplished with the new fluorescent Ca2+ indicator fura-2. No statistically significant difference between basal [Ca2+]i of interphase and mitotic cells was detected. However, mitotic cells showed a rapid elevation of [Ca2+]i from basal levels of 130 nM to 500 to 800 nM at the metaphase-anaphase transition. The [Ca2+]i transient was brief, lasting approximately 20 seconds and the elevated [Ca2+]i appeared uniformly distributed over the entire spindle and central region of the cell. The close temporal association of the [Ca2+]i transient with the onset of anaphase suggests that calcium may have a signaling role in this event.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poenie, M -- Alderton, J -- Steinhardt, R -- Tsien, R -- EY04372/EY/NEI NIH HHS/ -- GM31004/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 22;233(4766):886-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3755550" target="_blank"〉PubMed〈/a〉
    Keywords: *Anaphase ; Animals ; Benzofurans ; Calcium/*metabolism ; Cell Line ; Fluorescent Dyes ; Fura-2 ; Mitosis
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  • 5
    Publication Date: 1986-03-28
    Description: The genome of the human T-lymphotropic virus type III (HTLV-III/LAV) has the potential to encode at least three polypeptides in addition to those encoded by the gag, pol, and env genes. In this study, the product of the sor (short open reading frame) region, which overlaps the 3' end of the pol gene, was found to be a protein with a molecular weight of 23,000. An assay was developed for testing the ability of cloned HTLV-III proviruses to produce viruses cytopathic for T4+ lymphocytes. In the cell line used, C8166, neither the HTLV-III sor gene product nor the complete 3'-orf gene product were necessary for the replication or cytopathic effects of the HTLV-III.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sodroski, J -- Goh, W C -- Rosen, C -- Tartar, A -- Portetelle, D -- Burny, A -- Haseltine, W -- CA07580/CA/NCI NIH HHS/ -- CA40658/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1549-53.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006244" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cytopathogenic Effect, Viral ; Deltaretrovirus/*genetics/pathogenicity ; *Genes, Viral ; Humans ; Retroviridae Proteins/genetics ; T-Lymphocytes/microbiology ; *Virus Replication
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  • 6
    Publication Date: 1986-04-04
    Description: Experiments were conducted to isolate and characterize the gene and gene product of a human hematopoietic colony-stimulating factor with pluripotent biological activities. This factor has the ability to induce differentiation of a murine myelomonocytic leukemia cell line WEHI-3B(D+) and cells from patients with newly diagnosed acute nonlymphocytic leukemia (ANLL). A complementary DNA copy of the gene encoding a pluripotent human granulocyte colony-stimulating factor (hG-CSF) was cloned and expressed in Escherichia coli. The recombinant form of hG-CSF is capable of supporting neutrophil proliferation in a CFU-GM assay. In addition, recombinant hG-CSF can support early erythroid colonies and mixed colony formation. Competitive binding studies done with 125I-labeled hG-CSF and cell samples from two patients with newly diagnosed human leukemias as well as WEHI-3B(D+) cells showed that one of the human leukemias (ANLL, classified as M4) and the WEHI-3B(D+) cells have receptors for hG-CSF. Furthermore, the murine WEHI-3B(D+) cells and human leukemic cells classified as M2, M3, and M4 were induced by recombinant hG-CSF to undergo terminal differentiation to macrophages and granulocytes. The secreted form of the protein produced by the bladder carcinoma cell line 5637 was found to be O-glycosylated and to have a molecular weight of 19,600.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Souza, L M -- Boone, T C -- Gabrilove, J -- Lai, P H -- Zsebo, K M -- Murdock, D C -- Chazin, V R -- Bruszewski, J -- Lu, H -- Chen, K K -- CA00966/CA/NCI NIH HHS/ -- CA20194/CA/NCI NIH HHS/ -- CA32516/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):61-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2420009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Line ; Colony-Forming Units Assay ; Colony-Stimulating Factors/genetics/*pharmacology ; DNA/metabolism ; Escherichia coli/genetics ; Genes ; Granulocyte Colony-Stimulating Factor ; Granulocytes/*physiology ; Humans ; Leukemia/*pathology ; Leukemia, Myeloid/pathology ; Mice ; Plasmids ; Recombinant Proteins/*pharmacology
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  • 7
    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
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  • 8
    Publication Date: 1986-10-24
    Description: The protein product of oncogene c-myc is believed to be important in regulation of the cell cycle. However, its direct role in DNA synthesis has not been explored. Experiments presented here show that the addition of affinity-purified antibodies against the human c-myc protein to nuclei isolated from several types of human cells reversibly inhibited DNA synthesis and DNA polymerase activity of these nuclei. This suggests that c-myc encodes a protein that is functionally involved in DNA synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Studzinski, G P -- Brelvi, Z S -- Feldman, S C -- Watt, R A -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):467-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3532322" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Nucleus/physiology ; Cell-Free System ; DNA/biosynthesis ; *DNA Replication ; Humans ; Immunologic Techniques ; Nucleic Acid Synthesis Inhibitors ; Proto-Oncogene Proteins/*physiology ; *Proto-Oncogenes
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-18
    Description: The historical background of studies in Japan on chemical carcinogenesis from environmental sources is described from personal experience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugimura, T -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):312-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3088728" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Nitroquinoline-1-oxide/analysis ; Animals ; Biotransformation ; Carcinogens/*analysis ; Cyanobacteria/analysis ; Environmental Pollution/*analysis ; Food Additives ; Food Handling ; Furylfuramide/toxicity ; Health Policy ; Humans ; Indoles/metabolism ; Japan ; Lyngbya Toxins/toxicity ; Methods ; Methylnitronitrosoguanidine/toxicity ; Mutagenicity Tests ; Oncogenes ; Primary Prevention ; Rats ; Risk ; Stereoisomerism ; Stomach Neoplasms/chemically induced ; Streptomyces/analysis ; Structure-Activity Relationship ; Urinary Bladder Neoplasms/chemically induced
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-25
    Description: Electrophysiological recordings of inward currents from whole cells showed that vascular muscle cells have one type of sodium channel and two types of calcium channels. One of the calcium channels, the transient calcium channel, was activated by small depolarizations but then rapidly inactivated. It was equally permeable to calcium and barium and was blocked by cadmium, but not by tetrodotoxin. The other type, the sustained calcium channel, was activated by larger depolarizations, but inactivated very little; it was more permeable to barium than calcium. The sustained calcium channel was more sensitive to block by cadmium than the transient channel, but also was not blocked by tetrodotoxin. The sodium channel inactivated 15 times more rapidly than the transient calcium channel and at more negative voltages. This sodium channel, which is unusual because it is only blocked by a very high (60 microM) tetrodotoxin concentration but not by cadmium, is the first to be characterized in vascular muscle, and together with the two calcium channels, provides a basis for different patterns of excitation in vascular muscles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sturek, M -- Hermsmeyer, K -- HL 16328/HL/NHLBI NIH HHS/ -- HL 32295/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):475-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2425434" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Ion Channels/*physiology ; Membrane Potentials ; *Muscle Contraction ; Muscle, Smooth, Vascular/*physiology ; Rats ; Rats, Inbred WKY ; Sodium/*physiology
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-01-31
    Description: Contrary to the orthodox view that optical image quality should "match" the photoreceptor grain, anatomical data from the eyes of various animals suggest that the image quality is significantly superior to the potential resolution of the cone mosaic in most retinal regions. A new theory is presented to explain the existence of this relation and to better appreciate eye design. It predicts that photoreceptors are potentially visible through the natural optics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snyder, A W -- Bossomaier, T R -- Hughes, A -- New York, N.Y. -- Science. 1986 Jan 31;231(4737):499-501.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941914" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cats ; Humans ; Models, Neurological ; Photoreceptor Cells/*anatomy & histology ; Rats ; Snakes ; Species Specificity ; *Vision, Ocular ; *Visual Perception
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  • 12
    Publication Date: 1986-08-29
    Description: Epstein-Barr virus (EBV), a ubiquitous human herpesvirus, has the ability to transform human B lymphocytes. No other cell type has been experimentally transformed by EBV, either by intact virions or naked viral DNA and subgenomic fragments. Two immortalized human T-lymphoblastoid cell lines have now been established by transfecting cord blood lymphocytes with purified B95-8 viral DNA enclosed in fusogenic Sendai virus envelopes (RSVE) and then exposing the cells to EBV from a P3HR-1 cell subclone. One of these lines, which has been fully characterized, is termed HBD-1. This line is positive for EBV DNA and expresses surface OKT11, OKT4, and Tac receptors, but not M-1, mu immunoglobulin chains, EBV receptors, or B-1 surface markers. The cells contain fully rearranged T-cell receptor genes and germline immunoglobulin genes. The karyotype of the cells is normal, they do not require interleukin-2 for growth, and do not contain human T-lymphotropic virus type I. However, the HBD-1 cells contain incomplete EBV genomes and express several EBV-determined antigens, including the early antigen type D, membrane antigens, but not EBV-determined nuclear antigen (EBNA). This association of the EBV genome with permanently growing hematopoietic cells of non B-cell lineage should prove useful in studies on the mechanism of EBV-mediated cell transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevenson, M -- Volsky, B -- Hedenskog, M -- Volsky, D J -- CA33386/CA/NCI NIH HHS/ -- CA37465/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):980-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016899" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Survival ; DNA, Viral/*genetics ; Deltaretrovirus/genetics ; Herpesvirus 4, Human/*genetics ; Humans ; Nucleic Acid Hybridization ; T-Lymphocytes/*microbiology/physiology ; *Transfection
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  • 13
    Publication Date: 1986-04-18
    Description: In situ hybridization of an oligonucleotide probe complementary to vasopressin messenger RNA (mRNA) in sections from normal or Brattleboro rat hypothalami revealed hybridization densities in each of three vasopressin-rich nuclei: the supraoptic, paraventricular, and suprachiasmatic. When entrained to a daily light-dark cycle, each rat strain displayed diurnal variation in hybridizable mRNA in the suprachiasmatic, but not in the supraoptic or paraventricular nuclei. The higher values for suprachiasmatic mRNA in the morning correlate well with previously elucidated morning increases in vasopressin immunoreactivity in the cerebrospinal fluid. These results support the utility of in situ hybridization techniques for elucidating physiological influences on regional peptidergic function, are consistent with a prominent role for vasopressinergic suprachiasmatic neurons in generating the cerebrospinal fluid vasopressin rhythm, and suggest that regulation of this mRNA rhythm is not dependent on release of intact peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uhl, G R -- Reppert, S M -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):390-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3961487" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; *Circadian Rhythm ; Nucleic Acid Hybridization ; Paraventricular Hypothalamic Nucleus/analysis/physiology ; RNA, Messenger/*analysis/isolation & purification ; Rats ; Rats, Brattleboro ; Rats, Inbred Strains ; Suprachiasmatic Nucleus/*analysis/physiology ; Supraoptic Nucleus/analysis/physiology ; Vasopressins/genetics/*physiology
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  • 14
    Publication Date: 1986-11-21
    Description: The human T-lymphotropic retrovirus HTLV-III/LAV encodes a trans-activator that increases viral gene expression. We expressed this trans-activator in animal cells and studied its structural and functional characteristics. The putative trans-activator protein was immunoprecipitated from overproducing stable cell lines and shown to migrate as a 14-kilodalton polypeptide on sodium dodecyl sulfate-polyacrylamide gels. S1 nuclease mapping experiments showed that the trans-activator increases the levels of steady-state messenger RNA transcribed from the viral long terminal repeat promoter. Sequences within the R region of the HTLV-III/LAV long terminal repeat are essential for trans-activation. Quantitations of messenger RNA and protein showed that the protein increase was greater than the messenger RNA increase in CV1 and HeLa cells, indicating that more than one mechanism was responsible for the trans-activation and that cell type-specific factors may determine the final level of trans-activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, C M -- Felber, B K -- Paskalis, H -- Pavlakis, G N -- N01-CO-23909/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 21;234(4779):988-92.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3490693" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Electrophoresis, Polyacrylamide Gel ; Gene Products, rev ; HIV/*genetics ; Molecular Sequence Data ; Nucleic Acid Hybridization ; RNA, Messenger/analysis ; Retroviridae Proteins/*metabolism ; Transfection ; Viral Proteins/*biosynthesis ; Virus Activation ; rev Gene Products, Human Immunodeficiency Virus
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  • 15
    Publication Date: 1986-06-13
    Description: Administration of cholecystokinin (CCK) to rats caused a dose-dependent increase in plasma levels of the neurohypophyseal hormone oxytocin (OT). The OT secretion was comparable to that found in response to nausea-producing chemical agents that cause learned taste aversions. The effect of CCK on OT secretion was blunted after gastric vagotomy, as was the inhibition of food intake induced by CCK. Food ingestion also led to elevated plasma OT in rats, but CCK and aversive agents caused even greater OT stimulation. Thus, after administration of large doses of CCK, vagally mediated activation of central nausea pathways seems to be predominantly responsible for the subsequent decrease in food intake. Despite their dissimilar affective states, both nausea and satiety may activate a common hypothalamic oxytocinergic pathway that controls the inhibition of ingestion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verbalis, J G -- McCann, M J -- McHale, C M -- Stricker, E M -- AM-16166/AM/NIADDK NIH HHS/ -- MH-25140/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1417-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3715453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning/physiology ; Cholecystokinin/*pharmacology ; Feeding Behavior/*physiology ; Nausea/*physiopathology ; Oxytocin/*secretion ; Paraventricular Hypothalamic Nucleus/physiology ; Rats ; Satiation/*physiology ; Vagotomy
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  • 16
    Publication Date: 1986-05-09
    Description: Antigenic or mitogenic stimulation of T cells induces the secretion of an array of protein hormones that regulate immune responses. Molecular cloning has contributed strongly to our present understanding of the nature of this regulation. A complementary DNA (cDNA) library prepared from a cloned concanavalin A-activated mouse T-helper cell line was screened for abundant and induction-specific cDNA's. One such randomly chosen cDNA was found to encode mouse preproenkephalin messenger RNA (mRNA). Preproenkephalin mRNA represented about 0.4 percent of the mRNA in the activated cell line but was absent in resting cells of this line. Other induced T-helper cell lines have 0.1 to 0.5 percent of their mRNA as preproenkephalin mRNA. Induced T-helper cell culture supernatants have [Met]enkephalin-immunoreactive material. The production by activated T cells of a peptide neurotransmitter identifies a signal that can potentially permit T cells to modulate the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zurawski, G -- Benedik, M -- Kamb, B J -- Abrams, J S -- Zurawski, S M -- Lee, F D -- New York, N.Y. -- Science. 1986 May 9;232(4751):772-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938259" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cell Line ; Cloning, Molecular ; DNA/genetics ; Enkephalins/*biosynthesis/genetics ; Humans ; *Lymphocyte Activation ; Mice ; Protein Precursors/*biosynthesis/genetics ; RNA, Messenger/*biosynthesis ; Rats ; T-Lymphocytes, Helper-Inducer/drug effects/metabolism/*physiology
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  • 17
    Publication Date: 1986-09-05
    Description: Expression of the ras oncogene is thought to be one of the contributing events in the initiation of certain types of human cancer. To determine the cellular activities that are directly triggered by ras proteins, the early consequences of microinjection of the human H-ras proteins into quiescent rat embryo fibroblasts were investigated. Within 30 minutes to 1 hour after injection, cells show a marked increase in surface ruffles and fluid-phase pinocytosis. The rapid enhancement of membrane ruffling and pinocytosis is induced by both the proto-oncogenic and the oncogenic forms of the H-ras protein. The effects produced by the oncogenic protein persist for more than 15 hours after injection, whereas the effects of the proto-oncogenic protein are short-lived, being restricted to a 3-hour interval after injection. The stimulatory effect of the ras oncogene protein on ruffling and pinocytosis is dependent on the amount of injected protein and is accompanied by an apparent stimulation of phospholipase A2 activity. These rapid changes in cell membrane activities induced by ras proteins may represent primary events in the mechanism of action of ras proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bar-Sagi, D -- Feramisco, J R -- CA07896/CA/NCI NIH HHS/ -- CA39811/CA/NCI NIH HHS/ -- GM28277/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1061-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3090687" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Membrane/*drug effects/ultrastructure ; Cells, Cultured ; Culture Media ; DNA/biosynthesis ; GTP-Binding Proteins/*pharmacology ; Humans ; Microinjections ; Oncogene Proteins, Viral/*pharmacology ; Phospholipases A/metabolism ; Phospholipases A2 ; Phospholipids/metabolism ; Pinocytosis/*drug effects ; Rats ; Time Factors
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  • 18
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):155-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*anatomy & histology/growth & development ; Chickens ; Genes ; Humans ; Language Development ; Male ; Neurons/physiology ; Rats ; Synapses/physiology ; Visual Cortex/anatomy & histology/physiology
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  • 19
    Publication Date: 1986-08-08
    Description: The production and action of immunoregulatory cytokines, including interleukin-1 (IL-1), are inhibited by glucocorticoid hormones in vivo and in vitro. Conversely, glucocorticoid blood levels were increased by factors released by human leukocytes exposed to Newcastle disease virus preparations. This activity was neutralized by an antibody to IL-1. Therefore the capacity of IL-1 to stimulate the pituitary-adrenal axis was tested. Administration of subpyrogenic doses of homogeneous human monocyte-derived IL-1 or the pI 7 form of human recombinant IL-1 to mice and rats increased blood levels of adrenocorticotropic hormone (ACTH) and glucocorticoids. Another monokine, tumor necrosis factor, and the lymphokines IL-2 and gamma-interferon had no such effects when administered in doses equivalent to or higher than those of IL-1. The stimulatory effect of IL-1 on the pituitary-adrenal axis seemed not to be mediated by the secondary release of products from mature T lymphocytes since IL-1 was endocrinologically active when injected into athymic nude mice. These results strongly support the existence of an immunoregulatory feedback circuit in which IL-1 acts as an afferent and glucocorticoid as an efferent hormonal signal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Besedovsky, H -- del Rey, A -- Sorkin, E -- Dinarello, C A -- AI15614/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):652-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014662" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/blood/physiology ; Animals ; Corticosterone/blood/physiology ; Female ; Glucocorticoids/blood/immunology/*physiology ; Humans ; Interleukin-1/immunology/pharmacology/*physiology ; Leukocytes/drug effects/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Nude ; Newcastle disease virus/immunology ; Rats ; Rats, Inbred Strains
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  • 20
    Publication Date: 1986-06-27
    Description: Age-associated increases in collagen cross-linking and accumulation of advanced glycosylation products are both accelerated by diabetes, suggesting that glucose-derived cross-link formation may contribute to the development of chronic diabetic complications as well as certain physical changes of aging. Aminoguanidine, a nucleophilic hydrazine compound, prevented both the formation of fluorescent advanced nonenzymatic glycosylation products and the formation of glucose-derived collagen cross-links in vitro. Aminoguanidine administration to rats was equally effective in preventing diabetes-induced formation of fluorescent advanced nonenzymatic glycosylation products and cross-linking of arterial wall connective tissue protein in vivo. The identification of aminoguanidine as an inhibitor of advanced nonenzymatic glycosylation product formation now makes possible precise experimental definition of the pathogenetic significance of this process and suggests a potential clinical role for aminoguanidine in the future treatment of chronic diabetic complications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brownlee, M -- Vlassara, H -- Kooney, A -- Ulrich, P -- Cerami, A -- AM 19655/AM/NIADDK NIH HHS/ -- R01-AM 33861/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 27;232(4758):1629-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3487117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arteries/*drug effects/metabolism ; Collagen/metabolism ; Connective Tissue/drug effects/metabolism ; Diabetes Mellitus, Experimental/*drug therapy/metabolism ; Glucose/metabolism ; Guanidines/*pharmacology/therapeutic use ; Male ; Rats ; Rats, Inbred Lew ; Serum Albumin, Bovine/metabolism
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  • 21
    Publication Date: 1986-04-25
    Description: Nerve growth factor (NGF) and its receptor are important in the development of cells derived from the neural crest. Mouse L cell transformants have been generated that stably express the human NGF receptor gene transfer with total human DNA. Affinity cross-linking, metabolic labeling and immunoprecipitation, and equilibrium binding with 125I-labeled NGF revealed that this NGF receptor had the same size and binding characteristics as the receptor from human melanoma cells and rat PC12 cells. The sequences encoding the NGF receptor were molecularly cloned using the human Alu repetitive sequence as a probe. A cosmid clone that contained the human NGF receptor gene allowed efficient transfection and expression of the receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chao, M V -- Bothwell, M A -- Ross, A H -- Koprowski, H -- Lanahan, A A -- Buck, C R -- Sehgal, A -- NS-17551/NS/NINDS NIH HHS/ -- NS-23343-01/NS/NINDS NIH HHS/ -- NS21072/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):518-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic/drug effects ; *Cloning, Molecular ; DNA, Recombinant ; Genes ; Humans ; Melanoma/metabolism ; Mice ; Oncogenes ; Rats ; Receptors, Cell Surface/*genetics ; Receptors, Nerve Growth Factor ; Repetitive Sequences, Nucleic Acid ; Tunicamycin/pharmacology
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  • 22
    Publication Date: 1986-07-25
    Description: Rat thyroid cells in culture, rendered quiescent by hormone deprivation, can be stimulated to undergo DNA synthesis in the absence of serum by the addition of purified thyrotropin. The primary effect in response to thyrotropin action in thyroid cells is the induction of the c-fos oncogene, followed by c-myc expression. This suggests that thyrotropin acts as a competence growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colletta, G -- Cirafici, A M -- Vecchio, G -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):458-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726540" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Division/drug effects ; Cells, Cultured ; Cycloheximide/pharmacology ; DNA/biosynthesis ; Oncogenes/*drug effects ; Rats ; Thyroid Gland/*cytology/drug effects/metabolism ; Thyrotropin/*pharmacology
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  • 23
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-03-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Easton, T A -- New York, N.Y. -- Science. 1986 Mar 14;231(4743):1235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3945820" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Homosexuality ; Humans ; Male ; *Perfume ; Rats ; *Sexual Behavior
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  • 24
    Publication Date: 1986-06-20
    Description: The hormone 17 beta-estradiol acts through its receptor system to induce MCF-7 human breast cancer cells to form tumors in athymic mice. In vitro studies have identified the production of estrogen-induced growth factors from MCF-7 cells that may have a role in growth control. These induced growth factors were sufficient to stimulate MCF-7 tumor growth in ovariectomized athymic mice, thus partially replacing estradiol. Growth factors may act as estrogen-induced "second messengers" in estrogen-responsive growth of human breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickson, R B -- McManaway, M E -- Lippman, M E -- New York, N.Y. -- Science. 1986 Jun 20;232(4757):1540-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3715461" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*pathology ; Cell Division ; Cell Line ; Culture Media ; Estradiol/*physiology ; Female ; Humans ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Ovariectomy ; Receptors, Estradiol/*physiology ; Receptors, Estrogen/*physiology ; Transplantation, Heterologous
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  • 25
    Publication Date: 1986-06-20
    Description: In many viral infections the host cell carries the viral genome without producing viral particles, a phenomenon known as viral latency. The cellular mechanisms by which viral latency is maintained or viral replication is induced are not known. The modulation of intracellular calcium concentrations by calcium ionophores induced Epstein-Barr viral antigens in lymphoblastoid cell lines that carry the virus. When calcium ionophores were used in conjunction with direct activators of protein kinase C (12-O-tetradecanoyl phorbol-13-acetate and a synthetic diacylglycerol), a greater induction of viral antigens was observed than with either agent alone. Activation of protein kinase C may be required for the expression of the viral genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faggioni, A -- Zompetta, C -- Grimaldi, S -- Barile, G -- Frati, L -- Lazdins, J -- New York, N.Y. -- Science. 1986 Jun 20;232(4757):1554-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3012779" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Burkitt Lymphoma ; Calcimycin/pharmacology ; Calcium/*pharmacology ; Cell Line ; Cell Transformation, Viral/*drug effects ; Culture Media ; Ethers/pharmacology ; Fluorescent Dyes ; Genes, Viral/*drug effects ; Herpesvirus 4, Human/drug effects/*genetics ; Humans ; Ionomycin ; Kinetics ; Tetradecanoylphorbol Acetate/pharmacology
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  • 26
    Publication Date: 1986-05-02
    Description: Cardiocytes in the atria contain a prohormone that gives rise to atrial natriuretic peptides (ANP's), which have intrinsic hemodynamic regulatory activity. The distribution of ANP's in the brain suggests the involvement of these peptides in central cardiovascular regulation. In conscious rats with chronic indwelling catheters, volume loading with isotonic saline or glucose increased the amount of circulating immunoreactive ANP's by a factor of 4 to 5, as determined by radioimmunoassay. Hyperosmotic challenge with a hypertonic NaCl solution or anesthesia with halothane caused similar increases in plasma ANP's. Results obtained with the denervated-heart preparation indicate that neuronal influences are important in the release of ANP's induced by volume loading. As judged from reversed-phase high-performance liquid chromatography of extracted plasma and radioimmunoassay of collected fractions, the circulating physiologically important ANP's in the conscious rodent appear to be alpha-rANP(5-28) (atriopeptin III) and either alpha-rANP(3-28) [ANF(8-33)] or alpha-rANP(1-28) (ANF).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eskay, R -- Zukowska-Grojec, Z -- Haass, M -- Dave, J R -- Zamir, N -- New York, N.Y. -- Science. 1986 May 2;232(4750):636-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938258" target="_blank"〉PubMed〈/a〉
    Keywords: Anesthesia ; Animals ; Atrial Natriuretic Factor/blood/isolation & purification/physiology/*secretion ; Blood Volume ; Chromatography, High Pressure Liquid ; Consciousness/physiology ; Halothane/pharmacology ; Heart/innervation ; Heart Atria/drug effects/secretion ; Male ; Osmotic Pressure ; Pentobarbital/pharmacology ; Peptide Fragments/isolation & purification ; Radioimmunoassay ; Rats ; Rats, Inbred Strains
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  • 27
    Publication Date: 1986-02-07
    Description: When the human T-cell line A3.01 is infected with HTLV-III/LAV, the virus associated with the acquired immune deficiency syndrome (AIDS), most of the cells are killed. However, a small number of cells that lack the Leu-3 surface marker survive. Under normal conditions these surviving cells do not produce virus, nor can they be infected by the virus, but they can be induced to produce virus by treatment with 5-iodo-2'-deoxyuridine. This response can be induced for as long as 3 months after the initial infection, suggesting that the cells may harbor a latent form of HTLV-III/LAV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Folks, T -- Powell, D M -- Lightfoote, M M -- Benn, S -- Martin, M A -- Fauci, A S -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):600-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003906" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/microbiology ; Cell Line ; Deltaretrovirus/*growth & development ; Humans ; Idoxuridine/pharmacology ; Models, Genetic ; T-Lymphocytes/drug effects/*microbiology ; Time Factors ; *Virus Activation/drug effects
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  • 28
    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
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  • 29
    Publication Date: 1986-05-16
    Description: A specific DNA probe was used to study the effect of recombinant rat, mouse, and human gamma-interferon (gamma-IFN) on the course of sporozoite-induced malaria infections. In mice and rats infected with sporozoites of Plasmodium berghei, mouse and rat gamma-IFN's strongly inhibited the development of the exoerythrocytic forms in the liver liver cells of the hosts, but not the development of the erythrocytic stages. The degree of inhibition of the exoerythrocytic forms was proportional to the dose of gamma-IFN administered, but was independent of the number of sporozoites used for challenge. A 30 percent reduction in the development of exoerythrocytic forms in rat liver was achieved when 150 units (about 15 nanograms of protein) of rat gamma-IFN were injected a few hours before sporozoite challenge; the reduction was 90 percent or more with higher doses of gamma-IFN. The effect was less pronounced if the gamma-IFN was administered 18 hours before or a few hours after challenge. Human gamma-IFN also diminished the parasitemia in chimpanzees infected with sporozoites of the human malaria parasite Plasmodium vivax. The target of gamma-IFN activity may be the infected hepatocytes themselves, as shown by in vitro experiments in which small doses of the human lymphokine inhibited the development of exoerythrocytic forms of Plasmodium berghei in a human hepatoma cell line. These results suggest that immunologically induced interferon may be involved in controlling malaria infection under natural conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, A -- Schofield, L -- Enea, V -- Schellekens, H -- van der Meide, P -- Collins, W E -- Nussenzweig, R S -- Nussenzweig, V -- New York, N.Y. -- Science. 1986 May 16;232(4752):881-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3085218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Humans ; Interferon-gamma/pharmacology/*therapeutic use ; Liver/cytology ; Malaria/*drug therapy ; Mice ; Pan troglodytes ; Plasmodium berghei/drug effects ; Plasmodium vivax/drug effects ; Toxoplasma/drug effects
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  • 30
    Publication Date: 1986-01-24
    Description: Steady-state cellular levels of phosphatidylinositol-4,5-bisphosphate (PIP2), 1,2-diacylglycerol (DAG), and inositol phosphates have been measured in two different fibroblast cell lines (NIH 3T3 and NRK cells) before and after transformation with three different ras genes. At high cell density the ratio of DAG to PIP2 was 2.5- to 3-fold higher in the ras-transformed cells than in their untransformed counterparts. The sum of the water-soluble breakdown products of the polyphosphoinositides, inositol-1,4-bisphosphate and inositol-1,4,5-trisphosphate, was also elevated in ras-transformed NRK cells compared with nontransformed NRK cells. These findings suggest that the ras (p21) protein may act by affecting these levels, possibly as a regulatory element in the PIP2 breakdown pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fleischman, L F -- Chahwala, S B -- Cantley, L -- GM 36133/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):407-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3001936" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic/*analysis ; Diglycerides/analysis ; Humans ; Inositol 1,4,5-Trisphosphate ; Inositol Phosphates/analysis ; *Oncogenes ; Phosphatidylinositol 4,5-Diphosphate ; Phosphatidylinositols/*analysis ; Rats
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  • 31
    Publication Date: 1986-12-05
    Description: Clonal cell lines derived from specific types of central neurons can be used to identify and characterize properties specific to those neurons. With somatic cell fusion techniques, nine clonal hybrid cell lines have been developed from the septal region of the mouse basal forebrain. Two lines express characteristics typical of cholinergic neurons--choline acetyltransferase activity and immunoreactivity, neurite formation with neurofilament protein immunoreactivity, and aggregation in rotation-mediated cell culture. These cell lines may be useful for studying the trophic interactions that support the development and maintenance of central cholinergic connections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hammond, D N -- Wainer, B H -- Tonsgard, J H -- Heller, A -- HD04583/HD/NICHD NIH HHS/ -- NS07195/NS/NINDS NIH HHS/ -- NS17661/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1237-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775382" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology ; Cell Line ; Choline O-Acetyltransferase/metabolism ; Cholinergic Fibers/*physiology ; Clone Cells ; Hybrid Cells ; Mice ; Mice, Inbred C57BL ; Neuroblastoma/metabolism ; Neurons/*physiology
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  • 32
    Publication Date: 1986-04-25
    Description: Monocytes are a subpopulation of peripheral blood leukocytes, which when appropriately activated by the regulatory hormones of the immune system, are capable of becoming macrophages--potent effector cells for immune response to tumors and parasites. A complementary DNA for the T lymphocyte-derived lymphokine, granulocyte-macrophage colony-stimulating factor (GM-CSF), has been cloned, and recombinant GM-CSF protein has been expressed in yeast and purified to homogeneity. This purified human recombinant GM-CSF stimulated peripheral blood monocytes in vitro to become cytotoxic for the malignant melanoma cell line A375. Another T cell-derived lymphokine, gamma-interferon (IFN-gamma), also stimulated peripheral blood monocytes to become tumoricidal against this malignant cell line. When IFN-gamma activates monocytes to become tumoricidal, additional stimulation by exogenously added lipopolysaccharide is required. No such exogenous signals were required for the activation of monocytes by GM-CSF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grabstein, K H -- Urdal, D L -- Tushinski, R J -- Mochizuki, D Y -- Price, V L -- Cantrell, M A -- Gillis, S -- Conlon, P J -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):506-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3083507" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Colony-Stimulating Factors/biosynthesis/*pharmacology ; Cytotoxicity, Immunologic/*drug effects ; Humans ; Interferon-gamma/biosynthesis/pharmacology ; Macrophages/*drug effects ; Melanoma/immunology ; Monocytes/drug effects ; Neoplasms/*immunology ; Recombinant Proteins/biosynthesis/pharmacology
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  • 33
    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
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-12-12
    Description: Transformation of C3H10T1/2 cells by exposure to ultraviolet (UV) irradiation followed by tetradecanoyl phorbol acetate (TPA) has been used as a model of two-stage carcinogenesis. However, cells cloned from UV-TPA-induced foci (UV-TDTx cells) had a unique phenotype. Cloned UV-TDTx cells appeared transformed in pure culture but were unable to form foci when cocultured with C3H10T1/2 cells. However, in the presence of TPA, UV-TDTx cells form foci in mixed culture with C3H10T1/2 cells. This phenotype was the only one observed for UV-TPA transformants. These data suggest that communal suppression of cell division is a discrete phenomenon that must be overcome as one step in the multistage process of transformation, and this protocol permits the routine isolation of transformed cells responsive to density-dependent growth suppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herschman, H R -- Brankow, D W -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1385-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3787250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic/drug effects/radiation effects ; Clone Cells ; Mice ; Mice, Inbred C3H ; Phenotype ; Tetradecanoylphorbol Acetate/pharmacology ; *Ultraviolet Rays
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-12-19
    Description: Thyroid hormones stimulate the rate of cell division by poorly understood mechanisms. The possibility that thyroid hormones increase cell growth by stimulating secretion of a growth factor was investigated. Thyroid hormones are nearly an absolute requirement for the division of GH4C1 rat pituitary tumor cells plated at low density. Conditioned media from cells grown with or without L-triiodothyronine (T3) were treated with an ion exchange resin to remove T3 and were tested for ability to stimulate the division of GH4C1 cells. Conditioned medium from T3-treated cells was as active as thyroid hormone at promoting GH4C1 cell growth but did not elicit other thyroid hormone responses, induction of growth hormone, and down-regulation of thyrotropin-releasing hormone receptors, as effectively as T3 did. A substance or substances associated with T3-induced growth stimulatory activity migrated at high molecular weight at neutral pH and was different from known growth-promoting hormones induced by T3. The results demonstrate that thyroid hormones stimulate the division of GH4C1 pituitary cells by stimulating the secretion of an autocrine growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinkle, P M -- Kinsella, P A -- AM 32847/AM/NIADDK NIH HHS/ -- AM/NS 00827/AM/NIADDK NIH HHS/ -- CA 11198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 19;234(4783):1549-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3097825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; Epidermal Growth Factor/metabolism ; Growth Hormone/metabolism ; Growth Substances/*secretion ; Nerve Growth Factors/metabolism ; Pituitary Neoplasms/*metabolism/pathology ; Rats ; Thyrotropin-Releasing Hormone/metabolism ; Triiodothyronine/*pharmacology
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  • 36
    Publication Date: 1986-05-30
    Description: Glutamate decarboxylase (GAD; E.C. 4.1.1.15) converts glutamate to gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the vertebrate central nervous system. This report describes the isolation of a GAD complementary DNA clone by immunological screening of a lambda gt-11 brain complementary DNA expression library. The fusion protein produced by this clone catalyzes the conversion of glutamate to GABA and carbon dioxide, confirming its identity as GAD. Antibodies to beta-galactosidase remove GAD enzymatic activity from solution, showing that this activity is associated with the fusion protein. In immunoblotting experiments all three available antisera to GAD reacted with the fusion polypeptide and with two major polypeptides (molecular size, 60,000 and 66,000 daltons) in brain extracts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaufman, D L -- McGinnis, J F -- Krieger, N R -- Tobin, A J -- HD05615/HD/NICHD NIH HHS/ -- NS20356/NS/NINDS NIH HHS/ -- NS22256/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 30;232(4754):1138-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3518061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*enzymology ; Cloning, Molecular ; DNA/genetics ; Escherichia coli/metabolism ; Glutamate Decarboxylase/biosynthesis/genetics/*metabolism ; Humans ; Mice ; Rats ; Recombinant Proteins/biosynthesis/metabolism ; gamma-Aminobutyric Acid/*biosynthesis
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  • 37
    Publication Date: 1986-01-10
    Description: To characterize the precursor of mammalian thyrotropin-releasing hormone (TRH), a rat hypothalamic lambda gt11 library was screened with an antiserum directed against a synthetic peptide representing a portion of the rat TRH prohormone. The nucleotide sequence of the immunopositive complementary DNA encoded a protein with a molecular weight of 29,247. This protein contained five copies of the sequence Gln-His-Pro-Gly flanked by paired basic amino acids and could therefore generate five TRH molecules. In addition, potential cleavage sites in the TRH precursor could produce other non-TRH peptides, which may be secreted. In situ hybridization to rat brain sections demonstrated that the pre-proTRH complementary DNA detected neurons concentrated in the parvocellular division of the paraventricular nucleus, the same location as cells detected by immunohistochemistry. These findings indicate that mammalian TRH arises by posttranslational processing of a larger precursor protein. The ability of the TRH prohormone to generate multiple copies of the bioactive peptide may be an important mechanism in the amplification of hormone production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lechan, R M -- Wu, P -- Jackson, I M -- Wolf, H -- Cooperman, S -- Mandel, G -- Goodman, R H -- AM 34540/AM/NIADDK NIH HHS/ -- CA 37370/CA/NCI NIH HHS/ -- P30 AM 39428/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):159-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3079917" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/*physiology ; DNA/genetics ; Hypothalamus/physiology ; Molecular Weight ; Protein Precursors/genetics/*physiology ; Pyrrolidonecarboxylic Acid/analogs & derivatives ; Rats ; Rats, Inbred Strains ; Thyrotropin-Releasing Hormone/genetics/*physiology
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-04-25
    Description: The acoustic startle response in rats shows both short-term habituation, which recovers in seconds or minutes, and long-term habituation, which is effectively permanent. Lesions of the cerebellar vermis significantly attenuated long-term habituation without affecting the short-term process or altering initial response levels. In this response system the cerebellar vermis is part of an essential circuit for long-term habituation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leaton, R N -- Supple, W F Jr -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):513-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3961494" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Animals ; Auditory Pathways/anatomy & histology/physiology ; Cerebellum/anatomy & histology/*physiology ; Habituation, Psychophysiologic/*physiology ; Male ; Rats ; Reflex, Startle/*physiology ; Reticular Formation/analysis/physiology
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  • 39
    Publication Date: 1986-02-07
    Description: In mammals different isoforms of myosin heavy chain are encoded by the members of a multigene family. The expression of each gene of this family is regulated in a tissue- and developmental stage-specific manner as well as by hormonal and various pathological stimuli. In this study the molecular basis of isoform switches induced in myosin heavy chain by thyroid hormone was investigated. The expression of the myosin heavy chain gene family was analyzed in seven different muscles of adult rats subjected to hypo- or hyperthyroidism with complementary DNA probes specific for six different myosin heavy chain genes. The results demonstrate that all six genes are responsive to thyroid hormone. More interestingly, the same myosin heavy chain gene can be regulated by thyroid hormone in highly different modes, even in opposite directions, depending on the tissue in which it is expressed. Furthermore, the skeletal embryonic and neonatal myosin heavy chain genes, so far considered specific to these two developmental stages, can be reinduced by hypothyroidism in specific adult muscles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Izumo, S -- Nadal-Ginard, B -- Mahdavi, V -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):597-600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3945800" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diaphragm/drug effects/growth & development/metabolism ; Genes/*drug effects ; Heart/drug effects/growth & development ; Hyperthyroidism/metabolism ; Hypothyroidism/metabolism ; Male ; Muscle Development ; Muscles/drug effects/metabolism ; Myocardium/metabolism ; Myosins/*genetics ; Rats ; Thyroid Hormones/*pharmacology
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  • 40
    Publication Date: 1986-11-07
    Description: Lipopolysaccharide, a component of the outer membrane of Gram-negative bacteria, activates B lymphocytes and macrophages. Pertussis toxin, which inactivates several members of the G protein family of signaling components, including Gi and transducin, was found to inhibit the lipopolysaccharide-induced responses of the WEHI-231 B lymphoma cell line and the P388D1 macrophage cell line. These results, combined with the demonstration that lipopolysaccharide inhibits adenylate cyclase activity in P388D1 cells, strongly argues that lipopolysaccharide activation of cells is mediated by a Gi-like receptor-effector coupling protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jakway, J P -- DeFranco, A L -- AI-20038/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):743-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095921" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenylate Cyclase Toxin ; Antibodies, Anti-Idiotypic/immunology ; B-Lymphocytes/*physiology ; Cell Line ; Dose-Response Relationship, Drug ; Escherichia coli ; GTP-Binding Proteins/*physiology ; Immunoglobulin M/immunology ; Interleukin-1/metabolism ; Lipopolysaccharides/*antagonists & inhibitors/immunology ; Lymphocyte Activation/drug effects ; Macrophage Activation/drug effects ; Macrophages/*physiology ; *Pertussis Toxin ; Virulence Factors, Bordetella/*pharmacology
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  • 41
    Publication Date: 1986-01-10
    Description: In rat hippocampal pyramidal cells tested in situ by iontophoresis of several neurotransmitters, ethanol significantly enhanced excitatory responses to acetylcholine and inhibitory responses to somatostatin-14 but had no statistically significant effect on excitatory responses to glutamate or inhibitory responses to gamma-aminobutyric acid or, in preliminary tests, to norepinephrine or serotonin. The effects of ethanol on responses to acetylcholine and somatostatin-14 may provide insight into synaptic mechanisms underlying the behavioral consequences of ethanol intoxication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mancillas, J R -- Siggins, G R -- Bloom, F E -- AA-06420/AA/NIAAA NIH HHS/ -- AM-26741/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):161-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2867600" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*pharmacology ; Action Potentials/drug effects ; Animals ; Ethanol/*pharmacology ; Goldfish ; Hippocampus/*drug effects ; Male ; Neurons/drug effects/physiology ; Norepinephrine/pharmacology ; Rats ; Rats, Inbred Strains ; Serotonin/pharmacology ; Somatostatin/*pharmacology ; Synaptic Membranes/drug effects ; gamma-Aminobutyric Acid/pharmacology
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-09-19
    Description: Prenatal exposure to alcohol produces many developmental defects of the central nervous system, such as microcephaly, mental retardation, motor dysfunction, and cognitive deficiencies. Therefore, the generation of neurons in the cerebral cortex was examined in the offspring of female rats fed a diet containing ethanol. Prenatal exposure to ethanol delayed and extended the period during which cortical neurons were generated, reduced the number of neurons in the nature cortex with the same time of origin, and altered the distribution of neurons generated on a particular day. Thus, the proliferation and migration of cortical neurons are profoundly affected by in utero exposure to ethanol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, M W -- AA 06916/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 1986 Sep 19;233(4770):1308-11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3749878" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/*drug effects/embryology ; Ethanol/*pharmacology ; Female ; Gestational Age ; Humans ; Motor Cortex/drug effects/embryology ; Neurons/*drug effects/embryology ; Pregnancy ; Rats
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  • 43
    Publication Date: 1986-07-11
    Description: The mechanism by which sex steroids rapidly modulate the excitability of neurons was investigated by intracellular recording of neurons in rat medial amygdala brain slices. Brief hyperpolarization and increased potassium conductance were produced by 17 beta-estradiol. This effect persisted after elimination of synaptic input and after suppression of protein synthesis. Thus, 17 beta-estradiol directly changes the ionic conductance of the postsynaptic membrane of medial amygdala neurons. In addition, a greater proportion of the neurons from females than from males responded to 17 beta-estradiol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nabekura, J -- Oomura, Y -- Minami, T -- Mizuno, Y -- Fukuda, A -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):226-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726531" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/*drug effects ; Animals ; Cycloheximide/pharmacology ; Dactinomycin/pharmacology ; Estradiol/*pharmacology ; Female ; Male ; Membrane Potentials/drug effects ; Neurons/drug effects/physiology ; Rats ; Rats, Inbred Strains
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, T -- Lucignani, G -- Sokoloff, L -- New York, N.Y. -- Science. 1986 May 9;232(4751):776-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008340" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Brain Chemistry ; Deoxy Sugars/*metabolism ; Deoxyglucose/*metabolism ; Glucose-6-Phosphatase/metabolism ; *Glucose-6-Phosphate/*analogs & derivatives ; Glucosephosphates/analysis ; *Magnetic Resonance Spectroscopy ; Rats
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  • 45
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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
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  • 46
    Publication Date: 1986-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paul, S M -- Schwartz, R D -- Creveling, C R -- Hollingsworth, E B -- Daly, J W -- Skolnick, P -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):228-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Brain/*metabolism ; Cell Membrane/metabolism/*physiology ; Chick Embryo ; Chlorides/*metabolism ; Guinea Pigs ; Mice ; Rats ; Receptors, GABA-A/metabolism/*physiology ; Synaptosomes/metabolism
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  • 47
    Publication Date: 1986-01-24
    Description: Human probes identifying the cellular homologs of the v-ets gene, Hu-ets-1 and Hu-ets-2, and two panels of rodent-human cell hybrids were used to study specific translocations occurring in acute leukemias. The human ets-1 gene was found to translocate from chromosome 11 to 4 in the t(4;11)(q21;23), a translocation characteristic of a subtype of leukemia that represents the expansion of a myeloid/lymphoid precursor cell. Similarly, the human ets-2 gene was found to translocate from chromosome 21 to chromosome 8 in the t(8;21)(q22;q22), a nonrandom translocation commonly found in patients with acute myeloid leukemia with morphology M2 (AML-M2). Both translocations are associated with expression different from the expression in normal lymphoid cells of ets genes, raising the possibility that these genes play a role in the pathogenesis of these leukemias.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sacchi, N -- Watson, D K -- Guerts van Kessel, A H -- Hagemeijer, A -- Kersey, J -- Drabkin, H D -- Patterson, D -- Papas, T S -- AG00029/AG/NIA NIH HHS/ -- HD17449/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):379-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes, Human, 21-22 and Y ; Chromosomes, Human, 6-12 and X ; Cricetinae ; Cricetulus ; Humans ; Hybrid Cells ; Leukemia/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; *Translocation, Genetic
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  • 48
    Publication Date: 1986-03-14
    Description: Human malignant melanoma cells express specific chondroitin sulfate proteoglycans (mel-CSPG) on the surface, both in vivo and in vitro. Melanocytes in normal skin show no detectable mel-CSPG but can be induced to express the antigen when cultured in the presence of cholera toxin and the tumor promoter 12-O-tetradecanoylphorbol-13-acetate. Most other cell types do not express mel-CSPG either in vivo or in vitro. A study was designed to examine regulatory signals controlling mel-CSPG expression. The gene encoding mel-CSPG was mapped to human chromosome 15, and this chromosome was introduced into rodent cells derived from distinct differentiation lineages. Three types of mel-CSPG--expressing hybrids were found: (i) hybrids derived from human melanomas; (ii) hybrids derived from human cells that do not express mel-CSPG; and (iii) hybrids derived from human cells expressing mel-CSPG that are antigen-negative but that are induced to express mel-CSPG when cultured on extracellular matrix instead of plastic surfaces. Thus, mel-CSPG expression can be controlled both through intrinsic signals, provided by the differentiation program of the rodent fusion partner, and through extrinsic signals, provided by specific cell-matrix interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rettig, W J -- Real, F X -- Spengler, B A -- Biedler, J L -- Old, L J -- CA-08748/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 14;231(4743):1281-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3633135" target="_blank"〉PubMed〈/a〉
    Keywords: Aggrecans ; Animals ; Antibodies, Monoclonal ; Cell Line ; Cholera Toxin/pharmacology ; Chromosome Mapping ; Chromosomes, Human, 13-15 ; Cricetinae ; Cricetulus ; *Extracellular Matrix Proteins ; Gene Expression Regulation/drug effects ; Glycoproteins/*biosynthesis/genetics ; Humans ; Hybrid Cells/drug effects/*metabolism ; Lectins, C-Type ; Lymphocytes/metabolism ; Melanocytes/drug effects/metabolism ; Melanoma/*metabolism ; Mice ; Neoplasm Proteins/*biosynthesis/genetics ; Neuroblastoma/metabolism ; *Proteoglycans ; Rats ; Tetradecanoylphorbol Acetate/pharmacology
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  • 49
    Publication Date: 1986-07-25
    Description: Bovine papillomavirus (BPV-1) contains two independent transforming genes that have been mapped to the E5 and E6 open reading frames (ORF's). The E5 transforming protein was identified by means of an antiserum against a synthetic peptide corresponding to the 20 COOH-terminal amino acids of the E5 ORF. The E5 polypeptide is the smallest viral transforming protein yet characterized; it had an apparent size of 7 kilodaltons. The transforming polypeptide is encoded entirely within the second half of the E5 ORF and its predicted amino acid composition is very unusual; 68% of the amino acids are strongly hydrophobic and 34% are leucine. Cell fractionation studies localized this polypeptide predominantly to cellular membranes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlegel, R -- Wade-Glass, M -- Rabson, M S -- Yang, Y C -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):464-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bovine papillomavirus 1/*genetics ; Cell Line ; Cell Transformation, Viral ; *Genes, Viral ; Mice ; Oncogene Proteins, Viral/*genetics ; Papillomaviridae/*genetics
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  • 50
    Publication Date: 1986-06-13
    Description: Tissue welding is a potentially important biomedical application of laser technology. The structural alterations basic to this phenomenon were studied in experimental repair of lesions of the rat carotid artery and sciatic nerve. A modified neodymiumdoped yttrium-aluminum-garnet laser operating at a wavelength of 1.319 micrometers was used in conjunction with conventional suture techniques. Histological and fine-structural analysis revealed a homogenizing change in collagen with interdigitation of altered individual fibrils that appeared to be the structural basis of the welding effect.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schober, R -- Ulrich, F -- Sander, T -- Durselen, H -- Hessel, S -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1421-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3715454" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carotid Arteries/*radiation effects ; *Collagen ; Dose-Response Relationship, Radiation ; Extracellular Matrix/radiation effects ; *Lasers ; Rats ; Sciatic Nerve/*radiation effects
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  • 51
    Publication Date: 1986-02-07
    Description: In the adult castrated male rat, exposure to inescapable, intermittent electroshocks inhibited the pulsatile pattern of luteinizing hormone release and markedly lowered its plasma concentrations. The central administration of the corticotropin-releasing factor (CRF) antagonist alpha-helical ovine CRF residues 9 to 41 reversed the inhibitory action of stress. Neither its peripheral injection, nor the intraventricular injection of the inactive CRF analog des-Glu to Arg ovine CRF was effective. These results suggest that endogenous CRF may mediate some deleterious effects of noxious stimuli on reproduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rivier, C -- Rivier, J -- Vale, W -- AA03504/AA/NIAAA NIH HHS/ -- AM26741/AM/NIADDK NIH HHS/ -- HD13527/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):607-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003907" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/physiology ; Animals ; Corticotropin-Releasing Hormone/pharmacology/*physiology ; Electroshock ; Female ; Humans ; Luteinizing Hormone/blood ; Male ; Orchiectomy ; Rats ; *Reproduction/drug effects ; Stress, Psychological/*physiopathology
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  • 52
    Publication Date: 1986-02-21
    Description: A 4-week assay for screening tumor promoters of bladder cancer has been developed in which increased agglutinability of isolated rat bladder cells with concanavalin A is used as an indicator. On the basis of this assay system, L-isoleucine and L-leucine were suspected of being possible tumor promoters. Results of 40- to 60-week carcinogenesis experiments in which N-butyl-N-(4-hydroxybutyl)nitrosamine was used as an initiator demonstrate that L-isoleucine and L-leucine promote bladder cancer in rats. This finding may be relevant to the high incidence of human bladder cancer in Western countries, where the diet is rich in protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishio, Y -- Kakizoe, T -- Ohtani, M -- Sato, S -- Sugimura, T -- Fukushima, S -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):843-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3945812" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogens ; Carcinoma/*chemically induced ; *Isoleucine ; *Leucine ; Papilloma/*chemically induced ; Precancerous Conditions/*chemically induced ; Rats ; Rats, Inbred F344 ; Urinary Bladder Neoplasms/*chemically induced
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  • 53
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-18
    Description: Protein kinase C, an enzyme that is activated by the receptor-mediated hydrolysis of inositol phospholipids, relays information in the form of a variety of extracellular signals across the membrane to regulate many Ca2+-dependent processes. At an early phase of cellular responses, the enzyme appears to have a dual effect, providing positive forward as well as negative feedback controls over various steps of its own and other signaling pathways, such as the receptors that are coupled to inositol phospholipid hydrolysis and those of some growth factors. In biological systems, a positive signal is frequently followed by immediate negative feedback regulation. Such a novel role of this protein kinase system seems to give a logical basis for clarifying the biochemical mechanism of signal transduction, and to add a new dimension essential to our understanding of cell-to-cell communication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishizuka, Y -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):305-12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014651" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Animals ; Blood Platelets/metabolism ; Calcimycin/pharmacology ; Calcium-Transporting ATPases/metabolism ; Carrier Proteins/metabolism ; *Cation Transport Proteins ; Cell Membrane/physiology ; Cyclic AMP/metabolism ; Diglycerides/metabolism ; Electric Conductivity ; Enzyme Activation ; Fluorescent Antibody Technique ; Isoenzymes/metabolism ; Models, Biological ; Phosphatidylinositols/*metabolism ; Potassium/metabolism ; Protein Kinase C/*metabolism ; Purkinje Cells/enzymology ; Rats ; Serotonin/blood ; Sodium/metabolism ; Sodium-Hydrogen Antiporter ; Tetradecanoylphorbol Acetate/pharmacology ; Time Factors
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  • 54
    Publication Date: 1986-07-18
    Description: The myb gene is the transforming oncogene of the avian myeloblastosis virus (AMV); its normal cellular homolog, c-myb, is conserved across a broad span of evolution. In humans, c-myb is expressed in malignant hematopoietic cell lines and in primary hematopoietic tumors. Partial complementary DNA clones were generated from blast cells of patients with acute myelogenous leukemia. The sequences of the clones were compared to the c-myb of other species, as well as the v-myb of AMV. In addition, the carboxyl terminal region of human c-myb was placed in an expression vector to obtain protein for the generation of antiserum, which was used to identify the human c-myb gene product. Like v-myb, this protein was found within the nucleus of leukemic cells where it was associated with the nuclear matrix. These studies provide further evidence that c-myb might be involved in human leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Boone, T C -- Murdock, D C -- Keith, D E -- Press, M F -- Larson, R A -- Souza, L M -- CA36827/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):347-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014652" target="_blank"〉PubMed〈/a〉
    Keywords: *Aspartate Carbamoyltransferase ; Avian Leukosis Virus/*genetics ; Avian Myeloblastosis Virus/*genetics ; Base Sequence ; *Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) ; Cell Line ; Cloning, Molecular ; DNA/analysis ; DNA Restriction Enzymes/metabolism ; *Dihydroorotase ; Escherichia coli/genetics ; Hematopoietic Stem Cells/microbiology ; Humans ; Leukemia, Myeloid, Acute/*genetics ; Molecular Weight ; *Multienzyme Complexes ; *Oncogenes ; Proteins/analysis
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  • 55
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-10
    Description: Polypeptide growth factors, regulatory peptides, and a variety of pharmacological agents acting alone or synergistically induce mitogenesis in cultured fibroblasts. The early signals in the membrane, cytosol, and nucleus promoted by these extracellular factors, together with their mitogenic effectiveness, are integrated in a unified hypothesis for the regulation of fibroblast growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rozengurt, E -- New York, N.Y. -- Science. 1986 Oct 10;234(4773):161-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3018928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bombesin/pharmacology ; Cell Line ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Cyclic AMP/metabolism ; Cytosol/metabolism ; DNA/biosynthesis ; Enzyme Activation ; Growth Substances/*pharmacology ; Interphase ; Ions/metabolism ; Mitogens/*pharmacology ; Mitosis ; Models, Biological ; Oncogenes ; Phosphorylation ; Platelet-Derived Growth Factor/*pharmacology ; Protein Kinase C/metabolism ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism
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  • 56
    Publication Date: 1986-09-05
    Description: The oral administration of peptide drugs is well known to be precluded by their digestion in the stomach and small intestine. As a new approach to oral delivery, peptide drugs were coated with polymers cross-linked with azoaromatic groups to form an impervious film to protect orally administered drugs from digestion in the stomach and small intestine. When the azopolymer-coated drug reached the large intestine, the indigenous microflora reduced the azo bonds, broke the cross-links, and degraded the polymer film, thereby releasing the drug into the lumen of the colon for local action or for absorption. The ability of the azopolymer coating to protect and deliver orally administered peptide drugs was demonstrated in rats with the peptide hormones vasopressin and insulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saffran, M -- Kumar, G S -- Savariar, C -- Burnham, J C -- Williams, F -- Neckers, D C -- AI 18710/AI/NIAID NIH HHS/ -- SO-7-RR05700-15/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1081-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3526553" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Azo Compounds ; Blood Glucose/metabolism ; Diabetes Mellitus, Experimental/drug therapy ; Enterobacteriaceae/metabolism ; Insulin/*administration & dosage ; Lypressin/administration & dosage ; Peptides/*administration & dosage ; Polymers ; Rats ; *Tablets, Enteric-Coated
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  • 57
    Publication Date: 1986-10-31
    Description: A novel human B-lymphotropic virus (HBLV) was isolated from the peripheral blood leukocytes of six individuals: two HTLV-III seropositive patients from the United States (one with AIDS-related lymphoma and one with dermatopathic lymphadenopathy), three HTLV-III seronegative patients from the United States (one with angioimmunoblastic lymphadenopathy, one with cutaneous T-cell lymphoma, and one with immunoblastic lymphoma), and one HTLV-III seronegative patient with acute lymphocytic leukemia from Jamaica. All six isolates were closely related by antigenic analysis, and sera from all six virus-positive patients reacted immunologically with each virus isolate. In contrast, only four sera from 220 randomly selected healthy donors and none from 12 AIDS patients without associated lymphoma were seropositive. The virus selectively infected freshly isolated human B cells and converted them into large, refractile mono- or binucleated cells with nuclear and cytoplasmic inclusion bodies. HBLV is morphologically similar to viruses of the herpesvirus family but is readily distinguishable from the known human and nonhuman primate herpesviruses by host range, in vitro biological effects, and antigenic features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salahuddin, S Z -- Ablashi, D V -- Markham, P D -- Josephs, S F -- Sturzenegger, S -- Kaplan, M -- Halligan, G -- Biberfeld, P -- Wong-Staal, F -- Kramarsky, B -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):596-601.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2876520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/microbiology ; Cell Line ; Deltaretrovirus Infections/microbiology ; Fluorescent Antibody Technique ; Haplorhini ; Herpesviridae/*isolation & purification ; Herpesviridae Infections/*microbiology ; Humans ; Lymphoproliferative Disorders/*microbiology ; Microscopy, Electron ; T-Lymphocytes/microbiology
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  • 58
    Publication Date: 1986-08-01
    Description: Transforming growth factor-beta (TGF-beta) is a multifunctional peptide that controls proliferation, differentiation, and other functions in many cell types. Many cells synthesize TGF-beta and essentially all of them have specific receptors for this peptide. TGF-beta regulates the actions of many other peptide growth factors and determines a positive or negative direction of their effects. Its marked ability to enhance formation of connective tissue in vivo suggests several therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sporn, M B -- Roberts, A B -- Wakefield, L M -- Assoian, R K -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):532-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3487831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Epidermal Growth Factor/metabolism ; Genes ; Humans ; Peptides/genetics/metabolism/pharmacology/*physiology ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Transforming Growth Factors
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  • 59
    Publication Date: 1986-04-04
    Description: The human metallothionein-IIA (hMT-IIA) gene contains an enhancer element within its 5' regulatory region. This enhancer element can compete with the SV40 enhancer for one or more cellular factors in vivo. The competition between the two elements is modulated by cadmium, an inducer of hMT-IIA transcription. The data presented are consistent with a model in which heavy metal ions control the ability of the hMT-IIA enhancer to bind a positive factor, leading to increased transcription. The same factor is required for maximal activity of the SV40 enhancer, which suggests that viruses utilize factors that have a normal role in cellular gene expression to control their own genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scholer, H -- Haslinger, A -- Heguy, A -- Holtgreve, H -- Karin, M -- ES03222/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):76-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006253" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Base Sequence ; Cadmium/pharmacology ; Cell Line ; Cercopithecus aethiops ; Chloramphenicol O-Acetyltransferase ; *Enhancer Elements, Genetic ; *Genes ; *Genes, Regulator ; *Genes, Viral ; Humans ; Kidney ; Kinetics ; Metallothionein/*genetics ; Plasmids ; Simian virus 40/*genetics ; Transcription, Genetic/drug effects ; Transfection
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  • 60
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-16
    Description: The adrenergic control of glucose homeostasis is mediated in part through variations in the release of pancreatic hormones. In this study, purified pancreatic A and B cells were used to identify the recognition and messenger units involved in the adrenergic regulation of glucagon and insulin release. Catecholamines induced beta-adrenergic receptor activity in A cells and alpha 2-adrenergic receptor activity in B cells. The two recognition units provoked opposite variations in the production of cellular cyclic adenosine monophosphate, the beta-adrenergic unit enhancing the nucleotide's permissive effect on amino acid-induced glucagon release and the alpha 2-adrenergic unit inhibiting that upon glucose-induced insulin release. In both cell types, catecholamines interact powerfully with the synergistic control of hormone release by nutrient- and (neuro)hormone-driven messenger systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schuit, F C -- Pipeleers, D G -- New York, N.Y. -- Science. 1986 May 16;232(4752):875-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2871625" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Animals ; Cyclic AMP/analysis ; Epinephrine/pharmacology ; Glucagon/secretion ; Insulin/secretion ; Islets of Langerhans/analysis/drug effects/*physiology ; Male ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, beta/drug effects/*physiology
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  • 61
    Publication Date: 1986-04-11
    Description: Second-passage rat embryo cells were transfected with a neomycin resistance gene and the activated form of the c-Ha-ras I gene, or with these two genes plus the adenovirus type 2 E1a gene. Foci of morphologically transformed cells were observed in both cases; however, the frequency of transformation was at least ten times higher with two oncogenes than with the ras gene alone. All the transformed cell lines gave rise to rapidly growing tumors when injected subcutaneously into nude mice. All but one of the cell lines transformed by the ras oncogene alone formed metastatic nodules in the lungs of animals that had been injected subcutaneously with transformed cells. When transformed cells were injected intravenously, all the ras single-gene transformants gave rise to many metastatic lung nodules. In contrast, cell lines transformed with ras and E1a did not generate metastases after subcutaneous injection and gave rise to very few metastatic lung nodules after intravenous injection. These data demonstrate that a fully malignant cell with metastatic potential, as measured in an immunodeficient animal, can be obtained from early passage embryo cells by the transfection of the ras oncogene alone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pozzatti, R -- Muschel, R -- Williams, J -- Padmanabhan, R -- Howard, B -- Liotta, L -- Khoury, G -- 3F32CA07245-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 11;232(4747):223-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3456644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma/genetics ; Cell Line ; Cell Transformation, Neoplastic/*metabolism ; Cricetinae ; Genetic Engineering ; Mice ; Mice, Nude ; *Oncogenes ; Plasmids ; Rats/embryology ; Rats, Inbred Strains/embryology ; Transfection ; Urinary Bladder Neoplasms/genetics
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  • 62
    Publication Date: 1986-12-05
    Description: Ethanol, at pharmacologically relevant concentrations of 20 to 100 mM, stimulates gamma-aminobutyric (GABA) receptor-mediated uptake of 36Cl-labeled chlorine into isolated brain vesicles. One drug that acts at GABA-benzodiazepine receptors, the imidazobenzodiazepine Ro15-4513, has been found to be a potent antagonist of ethanol-stimulated 36Cl- uptake into brain vesicles, but it fails to antagonize either pentobarbital- or muscimol-stimulated 36Cl- uptake. Pretreatment of rats with Ro15-4513 blocks the anticonflict activity of low doses of ethanol (but not pentobarbital) as well as the behavioral intoxication observed with higher doses of ethanol. The effects of Ro15-4513 in antagonizing ethanol-stimulated 36Cl- uptake and behavior are completely blocked by benzodiazepine receptor antagonists. However, other benzodiazepine receptor inverse agonists fail to antagonize the actions of ethanol in vitro or in vivo, suggesting a novel interaction of Ro15-4513 with the GABA receptor-coupled chloride ion channel complex. The identification of a selective benzodiazepine antagonist of ethanol-stimulated 36Cl- uptake in vitro that blocks the anxiolytic and intoxicating actions of ethanol suggests that many of the neuropharmacologic actions of ethanol may be mediated via central GABA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzdak, P D -- Glowa, J R -- Crawley, J N -- Schwartz, R D -- Skolnick, P -- Paul, S M -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1243-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3022383" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/drug effects ; Azides/*pharmacology ; Benzodiazepines/*pharmacology ; Chlorides/metabolism ; Ethanol/*antagonists & inhibitors ; Flumazenil/pharmacology ; Male ; Pyrazoles/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, GABA-A/drug effects ; Synaptosomes/drug effects
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  • 63
    Publication Date: 1986-06-27
    Description: The posttranslational maturation of a complex precursor polyprotein, human proenkephalin, was assessed by infection of a wide spectrum of cell types with a recombinant vaccinia virus that expressed human proenkephalin. The infected cells rapidly produced both cellular and secreted Met-enkephalin immunoreactivity. Although each cell line could secrete intact proenkephalin, only a mouse pituitary line was capable of processing proenkephalin to mature enkephalin peptides. The quantity of intact proenkephalin secreted from BSC-40 cells (derived from African Green monkey kidney) was sufficient to establish the value of vaccinia virus as a mammalian cell expression vector.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, G -- Herbert, E -- Hruby, D E -- 7 RO1 DA04154-01/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 27;232(4758):1641-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cercopithecus aethiops ; Enkephalin, Methionine/biosynthesis ; Enkephalins/*biosynthesis/genetics ; Genetic Vectors ; Humans ; Mice ; Protein Precursors/*biosynthesis/genetics ; Rats ; Recombinant Proteins/*biosynthesis ; Vaccinia virus/*genetics
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  • 64
    Publication Date: 1986-10-24
    Description: Cachectin (tumor necrosis factor), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. Recombinant human cachectin was infused into rats in an effort to determine whether cachectin, by itself, can elicit the derangements of host physiology caused by administration of endotoxin. When administered in quantities similar to those produced endogenously in response to endotoxin, cachectin causes hypotension, metabolic acidosis, hemoconcentration, and death within minutes to hours, as a result of respiratory arrest. Hyperglycemia and hyperkalemia were also observed after infusion. At necropsy, diffuse pulmonary inflammation and hemorrhage were apparent on gross and histopathologic examination, along with ischemic and hemorrhagic lesions of the gastrointestinal tract, and acute renal tubular necrosis. Thus, it appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tracey, K J -- Beutler, B -- Lowry, S F -- Merryweather, J -- Wolpe, S -- Milsark, I W -- Hariri, R J -- Fahey, T J 3rd -- Zentella, A -- Albert, J D -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):470-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764421" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Endotoxins/toxicity ; Female ; Glycoproteins/*toxicity ; Humans ; Potassium/blood ; Rats ; Recombinant Proteins ; Shock/*chemically induced/pathology/physiopathology ; Sodium/blood ; Tumor Necrosis Factor-alpha
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, M -- New York, N.Y. -- Science. 1986 Sep 12;233(4769):1143-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3738527" target="_blank"〉PubMed〈/a〉
    Keywords: Acetamides/*adverse effects ; Animals ; *Government Agencies ; Herbicides/*adverse effects ; Humans ; Neoplasms/chemically induced ; Rats ; United States ; *United States Environmental Protection Agency
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wehrenberg, W B -- Ehlers, C L -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1271-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3085220" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arousal/drug effects ; Brain/*drug effects ; Electroencephalography ; Growth Hormone/blood ; Growth Hormone-Releasing Hormone/administration & dosage/*pharmacology ; Injections, Intraventricular ; Motor Activity/drug effects ; Rats
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  • 67
    Publication Date: 1986-11-14
    Description: Interleukin-2 (IL-2) binds to both high- and low-affinity classes of IL-2 receptors on activated T lymphocytes. Only the high-affinity receptors are involved in receptor-mediated endocytosis and normally transduce the mitogenic signals of IL-2; however, the structural features distinguishing the high- and low-affinity receptors are unknown. When 125I-labeled IL-2 was chemically cross-linked to activated human T lymphocytes, two major bands were identified. First, as predicted, a 68- to 72-kilodalton band, consisting of IL-2 (15.5 kilodaltons) cross-linked to the IL-2 receptor (55 kilodaltons), was observed. Second, an unpredicted 85- to 92-kilodalton moiety was detected. This band was not present when IL-2 was cross-linked to transfected C127 cells, which exclusively express low-affinity receptors. The data presented are most consistent with the existence of a 70- to 77-kilodalton glycoprotein subunit (p70) which, upon associating with the 55-kilodalton low-affinity receptor (p55), transforms it into a high-affinity site. It is proposed that p55 and p70 be referred to as the alpha and beta subunits, respectively, of the high-affinity IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharon, M -- Klausner, R D -- Cullen, B R -- Chizzonite, R -- Leonard, W J -- New York, N.Y. -- Science. 1986 Nov 14;234(4778):859-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095922" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cross-Linking Reagents ; Humans ; Immunosorbent Techniques ; Interleukin-2/metabolism ; Leukemia, Lymphoid/metabolism ; Lymphocyte Activation ; Mice ; Molecular Weight ; Receptors, Immunologic/*metabolism ; Receptors, Interleukin-2 ; Succinimides ; T-Lymphocytes/metabolism
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  • 68
    Publication Date: 1986-01-24
    Description: Parathyroid hormone-like factors have been found in extracts of tumors associated with humoral hypercalcemia of malignancy, many of which are of squamous epithelial origin. Cultured, nonmalignant human keratinocytes were examined for the production of similar factors. Keratinocyte-conditioned medium from ten cultures stimulated the production of cyclic adenosine monophosphate in clonally derived rat osteosarcoma cells sensitive to parathyroid hormone. Bovine [Nle8,18, Tyr34]PTH-(3-34)NH2, a competitive inhibitor of parathyroid hormone, stopped the adenylate cyclase production stimulated by keratinocyte-conditioned medium, but antisera to parathyroid hormone had no effect on such adenylate cyclase activity. The active component of keratinocyte-conditioned medium has a molecular weight exceeding that of native parathyroid hormone. These characteristics are shared by the parathyroid hormone receptor agonists associated with humoral hypercalcemia of malignancy, which suggests that normal human keratinocytes may produce a factor related to that produced by malignant tumors associated with humoral hypercalcemia of malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merendino, J J Jr -- Insogna, K L -- Milstone, L M -- Broadus, A E -- Stewart, A F -- AM 30102/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):388-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2417317" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Cattle ; Cells, Cultured ; Cyclic AMP/metabolism ; Epidermis/*cytology/metabolism/physiology ; Humans ; Isoproterenol/pharmacology ; Keratins/*metabolism ; Mice ; Osteosarcoma/metabolism ; Parathyroid Hormone/pharmacology/*physiology ; Peptide Fragments/pharmacology ; Rats ; Teriparatide
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  • 69
    Publication Date: 1986-08-29
    Description: Insulin action may involve the intracellular generation of low molecular weight substances that modulate certain key enzymes. The production of two substances that regulate the activity of adenosine 3',5'-monophosphate phosphodiesterase was evaluated in cultured myocytes by incorporation of radiolabeled precursors. Insulin caused the rapid hydrolysis of a chemically undefined membrane glycolipid, resulting in the production of two related complex carbohydrates as well as diacylglycerol. Both the glycolipid precursor and the aqueous products were monitored by labeling with radioactive inositol and glucosamine. Depletion of the labeled precursor and the appearance of labeled water-soluble products and diacylglycerol occurred within 30 seconds after hormone treatment and was followed by rapid resynthesis of the precursor. The aqueous products that were radioactively labeled appeared chromatographically and electrophoretically identical to phosphodiesterase modulating activities produced by insulin from the same cells. The purified radiolabeled and bioactive substances had similar chemical properties. Hydrolysis of the glycolipid precursor and subsequent generation of products could be reproduced by incubation of extracted lipids with a phosphatidylinositol-specific phospholipase C. These studies suggest that insulin stimulates an endogenous, selective phospholipase C activity that hydrolyzes a novel glycolipid, resulting in the generation of a complex carbohydrate-phosphate substance containing inositol and glucosamine that may mediate some of the actions of the hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saltiel, A R -- Fox, J A -- Sherline, P -- Cuatrecasas, P -- AM33804/AM/NIADDK NIH HHS/ -- F32 AI07185/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):967-72.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016898" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/*metabolism ; Animals ; Cell Line ; Glucosamine/metabolism ; Glycolipids/*metabolism ; Hydrolysis ; Inositol/metabolism ; Insulin/*pharmacology ; Liver/metabolism ; Mice ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoinositide Phospholipase C ; Phosphoric Diester Hydrolases/metabolism ; Staphylococcus aureus/enzymology
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  • 70
    Publication Date: 1986-02-07
    Description: Rat optic and sciatic nerves were crushed, and 10 minutes to 3 days later nerve segments between the crushed site and the cell body were removed and assayed for posttranslational protein modification by amino acid addition. Protein modification was comparable in intact optic and sciatic nerves, but in sciatic nerves increased to 1.6 times control levels 10 minutes after crushing and reached a maximum of ten times control levels by 2 hours. In optic nerves activity was decreased throughout the time course studied. The results indicate that, in a nerve which is capable of regeneration (sciatic), protein modification by the addition of amino acids increases immediately after injury, but a nerve incapable of regeneration (optic) is incapable of activating the modification reaction. These findings may be important in understanding the reasons for the lack of a regenerative response after injury to central mammalian nerves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shyne-Athwal, S -- Riccio, R V -- Chakraborty, G -- Ingoglia, N A -- NS19148/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):603-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3080804" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/*metabolism ; Animals ; Arginine/metabolism ; Decapodiformes ; Goldfish ; Leucine/metabolism ; Lysine/metabolism ; Nerve Regeneration ; Nerve Tissue Proteins/*metabolism ; Optic Nerve/*metabolism/physiology ; Optic Nerve Injuries ; Rats ; Sciatic Nerve/injuries/*metabolism/physiology ; Time Factors
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-07-18
    Description: Excitability is generated in developing skeletal muscle by the incorporation of sodium-selective ion channels into the surface membrane. Whole-cell and patch voltage-clamp recording from myotubes and their embryologic precursors, myoblasts, indicated that voltage-activated sodium current in myoblasts was more resistant to block by tetrodotoxin (TTX) than that in myotubes. Single-channel recording from both cell types showed two classes of sodium channels. One class had a lower single-channel conductance, activated at more hyperpolarized voltages, and was more resistant to TTX than the other. The proportion of TTX-resistant to TTX-sensitive sodium channels was higher in myoblasts than in myotubes. Thus, the difference in TTX sensitivity between myoblasts and myotubes can be explained by a difference in the proportion of the two classes of sodium channels. In addition, the lower conductance of TTX-resistant channels provides insight into the relationship between the TTX binding site and the external mouth of the sodium channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, R E -- Horn, R -- NS 00703/NS/NINDS NIH HHS/ -- NS 18608/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Jul 18;233(4761):361-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2425432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Drug Resistance ; Electric Conductivity ; Electric Stimulation ; Ion Channels/drug effects/*physiology ; *Muscle Development ; Muscles/metabolism ; Rats ; Sodium/*metabolism ; Tetrodotoxin/pharmacology
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  • 72
    Publication Date: 1986-11-07
    Description: This work was aimed at understanding the mechanisms of T-lymphocyte function by studying the cellular distribution and traffic of molecules of the T-cell receptor complex. The accumulation of specific molecules in intracytoplasmic vesicles is related to the activation of T lymphocytes. Some of these molecules include acid hydrolases, the transferrin receptor, and class I antigens of the major histocompatibility complex. Molecules of the T-cell receptor complex have now also been found in intracytoplasmic vesicles in a human T-cell line derived from a lymphoblastic leukemia. Such vesicles were tightly associated with the cytoplasmic microtubule network. One functional aspect of this association is a cellular pathway by which vesicles traveling to and from the cell surface converge in an area of the cells that is rich in processing enzymes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tse, D B -- Al-Haideri, M -- Pernis, B -- Cantor, C R -- Wang, C Y -- CA39782/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):748-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3490690" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cell Compartmentation ; Cell Line ; Cytoplasmic Granules/metabolism ; HLA Antigens/metabolism ; Humans ; Microtubules/ultrastructure ; Receptors, Antigen, T-Cell/*metabolism ; Receptors, Transferrin/metabolism ; T-Lymphocytes/immunology/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-29
    Description: Cardiac gap junctions consist of arrays of integral membrane proteins joined across the intercellular cleft at points of cell-to-cell contact. These junctional proteins are thought to form pores through which ions can diffuse from cytosol to cytosol. By monitoring whole-cell currents in pairs of embryonic heart cells with two independent patch-clamp circuits, the properties of single gap junction channels have been investigated. These channels had a conductance of about 165 picosiemens and underwent spontaneous openings and closings that were independent of voltage. Channel activity and macroscopic junctional conductance were both decreased by the uncoupling agent 1-octanol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Veenstra, R D -- DeHaan, R L -- HL-06909/HL/NHLBI NIH HHS/ -- HL-27385/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):972-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2426781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chick Embryo ; Electric Conductivity ; Guinea Pigs ; Heart/embryology ; Intercellular Junctions/*physiology ; Ion Channels/*cytology ; Myocardium/*cytology ; Rats
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  • 74
    Publication Date: 1986-11-14
    Description: The expression of the cellular src gene product pp60c-src was examined in an embryonal carcinoma cell line that differentiates in vitro into neuronlike cells after being treated with retinoic acid. Quantitative and qualitative changes in c-src expression accompanied the events associated with neuronal differentiation. The levels of pp60c-src increased 8- to 20-fold during the period when the cells elaborated neuritic processes and expressed neuron-specific proteins. The electrophoretic mobility of pp60c-src induced in these cells was retarded in comparison with that in untreated cells or in treated cells before neurite elaboration. The shift in electrophoretic mobility was due to an alteration in the amino terminal 16,000 daltons of pp60c-src and similar to an alteration of c-src protein found in neural tissues and in pure primary cultures of neuronal cells. These results indicate that expression of pp60c-src induced by retinoic acid in these embryonal carcinoma cells mimics the expression of c-src in developing neurons. Therefore, this embryonal carcinoma cell line provides a model system to investigate the function of the src protein in neuronal differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, S A -- Brugge, J S -- Levine, J M -- CA 28146/CA/NCI NIH HHS/ -- NS 21198/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 14;234(4778):873-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095923" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation/drug effects ; Cell Line ; Embryonal Carcinoma Stem Cells ; Gene Expression Regulation ; Neoplastic Stem Cells/cytology/*metabolism ; Neurons/cytology ; Oncogene Protein pp60(v-src) ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Retroviridae Proteins/genetics/*metabolism ; Tretinoin/pharmacology
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  • 75
    Publication Date: 1986-04-18
    Description: Suppressor cells specific for acetylcholine receptor (AChR) were induced in a population of lymphocytes previously sensitized to AChR, obtained from rats with experimental autoimmune myasthenia gravis (EAMG). The lymphocytes were cultured with the immunosuppressive drug cyclosporin A plus purified AChR for 7 days. These cells, when mixed with lymphocytes from rats with EAMG in vitro, strongly suppressed the antibody response to AChR. They did not inhibit antibody responses to an unrelated antigen, an indication that suppression was specific for AChR. This approach should be a useful way to induce specific suppressor cells from sensitized populations of lymphocytes and may be applicable in the treatment of autoimmune diseases such as myasthenia gravis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McIntosh, K R -- Drachman, D B -- 5RO1 HD04817-16/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):401-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclosporins/pharmacology ; Female ; Lymph Nodes/cytology ; Lymphocytes/drug effects ; Myasthenia Gravis/*immunology ; Rats ; Rats, Inbred Lew ; Receptors, Cholinergic/*immunology ; Spleen/cytology ; T-Lymphocytes, Regulatory/*immunology
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  • 76
    Publication Date: 1986-01-24
    Description: Human T-lymphotropic virus type III (HTLV-III) or lymphadenopathy-associated virus (LAV) is tropic for human T cells with the helper-inducer phenotype, as defined by reactivity with monoclonal antibodies specific for the T4 molecule. Treatment of T4+ T cells with monoclonal antibodies to T4 antigen blocks HTLV-III/LAV binding, syncytia formation, and infectivity. Thus, it has been inferred that the T4 molecule itself is a virus receptor. In the present studies, the surfaces of T4+ T cells were labeled radioactively, and then the cells were exposed to virus. After the cells were lysed, HTLV-III/LAV antibodies were found to precipitate a surface protein with a molecular weight of 58,000 (58K). By blocking and absorption experiments, this 58K protein was identified as the T4 molecule. No cell-surface structures other than the T4 molecule were involved in the antibody-antigen complex formation. Two monoclonal antibodies, each reactive with a separate epitope of the T4 molecule, were tested for their binding capacities in the presence of HTLV-III/LAV. When HTLV-III/LAV was bound to T4+ T cells, the virus blocked the binding of one of the monoclonal antibodies, T4A (OKT4A), but not of the other, T4 (OKT4). When HTLV-III/LAV was internally radiolabeled and bound to T4+ T cells which were then lysed, a viral glycoprotein of 110K (gp110) coprecipitated with the T4 molecule. The binding of gp110 to the T4 molecule may thus be a major factor in HTLV-III/LAV tropism and may prove useful in developing therapeutic or preventive measures for the acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougal, J S -- Kennedy, M S -- Sligh, J M -- Cort, S P -- Mawle, A -- Nicholson, J K -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):382-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3001934" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Antibodies, Monoclonal ; Cell Line ; Deltaretrovirus/*metabolism ; Humans ; T-Lymphocytes/metabolism/*microbiology ; Viral Proteins/*metabolism
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-16
    Description: The activities of both chymotrypsin and amylase in individual zymogen granules of rat pancreas were measured by means of micromanipulation and microfluorometric methods. The enzyme content and the ratio of amylase to chymotrypsin varied widely among granules taken from the same animal. These results are compatible with short-term nonparallel bulk secretion of the two enzymes through exocytosis. The distribution of each enzyme activity in a population of granules suggests quantal packaging of amylase and chymotrypsinogen into the granules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mroz, E A -- Lechene, C -- AM26488/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 May 16;232(4752):871-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422756" target="_blank"〉PubMed〈/a〉
    Keywords: Amylases/*analysis ; Animals ; Chymotrypsin/*analysis ; Cytoplasmic Granules/*analysis ; Exocytosis ; Female ; Pancreas/*secretion ; Rats ; Rats, Inbred Strains
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  • 78
    Publication Date: 1986-04-18
    Description: Efforts to investigate the progression of events that lead human cells of epithelial origin to become neoplastic in response to carcinogenic agents have been aided by the development of tissue culture systems for propagation of epithelial cells. In the present study, nontumorigenic human epidermal keratinocytes immortalized by adenovirus 12 and simian virus 40 (Ad 12-SV40) were transformed by treatment with the chemical carcinogens N-methyl-N'-nitro-N-nitrosoguanidine or 4-nitroquinoline-1-oxide. Such transformants showed morphological alterations and induced carcinomas when transplanted into nude mice, whereas primary human epidermal keratinocytes treated with these chemical carcinogens failed to show any evidence of transformation. This in vitro system may be useful in assessing environmental carcinogens for human epithelial cells and in detecting new human oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhim, J S -- Fujita, J -- Arnstein, P -- Aaronson, S A -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):385-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2421406" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Nitroquinoline-1-oxide/*pharmacology ; Adenoviruses, Human/*metabolism ; Animals ; Cell Line ; Cell Transformation, Neoplastic/*chemically induced/metabolism ; Cell Transformation, Viral ; Epidermis/*cytology ; Humans ; *Keratins ; Methylnitronitrosoguanidine/*pharmacology ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Nitroquinolines/*pharmacology ; Oncogenes ; Simian virus 40/*metabolism ; Skin Neoplasms/chemically induced/*etiology/microbiology
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  • 79
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-10
    Description: The secretion of follicle-stimulating hormone (FSH) by the anterior pituitary gland is regulated by the interaction of hypothalamic and gonadal hormones. Recently, proteins termed inhibins that selectively suppress FSH secretion have been purified and characterized from the gonadal fluids of several species. Antibodies to a synthetic peptide encompassing the amino terminal 25 residues of the recently characterized porcine inhibin were used to develop a specific radioimmunoassay (RIA) for inhibin and to neutralize endogenous inhibin during the estrous cycle of the rat. The administration of 20 international units of pregnant mare serum gonadotropin (PMSG) stimulated the secretion of inhibin in intact immature female rats, whereas ovariectomy caused an abrupt decrease in plasma inhibin concentrations that were not prevented by the injection of PMSG. The infusion of a polyclonal antiserum to inhibin, from 12 noon on proestrus to 1 a.m. on the morning of estrus, as well as its acute intravenous injection during diestrus I or II, caused an increase in plasma FSH (but not luteinizing hormone) concentrations. These results support the hypothesis of a feedback loop between the release of ovarian inhibin and FSH in the female rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rivier, C -- Rivier, J -- Vale, W -- HD13527/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 10;234(4773):205-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3092356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estrus ; Female ; Follicle Stimulating Hormone/blood/*secretion ; Gonadotropins, Equine/pharmacology ; Immune Sera ; Inhibins/blood/immunology/*secretion ; Luteinizing Hormone/blood ; Ovariectomy ; Proestrus ; Rats ; Rats, Inbred Strains
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  • 80
    Publication Date: 1986-05-09
    Description: In multidrug resistance, which is observed clinically and in tissue culture, cells that are challenged with certain cytotoxic drugs develop resistance not only to the selective agent but also to other, seemingly unrelated, agents. The multidrug-resistant phenotype is associated with DNA sequence amplification and with the overproduction of a number of cytosolic and membrane glycoproteins. The differential amplification and altered expression of at least two related genes, termed multidrug-resistant associated genes has been shown in multidrug-resistant Chinese hamster cells. In multidrug-resistant mouse and human cells, genes homologous to those in Chinese hamster cells are also amplified. The level of expression of these genes varied and did not correlate with their copy number. Furthermore, in Chinese hamster cells, the development of resistance to a single drug and multidrug resistance were closely related, but uncoupled, events. The overexpression of the multidrug-resistant genes was better correlated with the degree of resistance to the selective agent than it was with the extent of multidrug resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scotto, K W -- Biedler, J L -- Melera, P W -- CA-08748/CA/NCI NIH HHS/ -- CA-09207/CA/NCI NIH HHS/ -- CA-28595/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 9;232(4751):751-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2421411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Molecular ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA/genetics ; Dactinomycin/pharmacology ; Daunorubicin/pharmacology ; *Drug Resistance ; Gene Amplification/*drug effects ; Gene Expression Regulation/*drug effects ; Humans ; Lung/cytology/drug effects ; Mice ; Nucleic Acid Hybridization ; RNA/genetics ; Vincristine/pharmacology
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  • 81
    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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  • 82
    Publication Date: 1986-08-15
    Description: Growth cones are specialized structures that form the distal tips of growing axons. During both normal development of the nervous system and regeneration of injured nerves, growth cones are essential for elongation and guidance of growing axons. Developmental and regenerative axon growth is frequently accompanied by elevated synthesis of a protein designated GAP-43. GAP-43 has now been found to be a major component of growth-cone membranes in developing rat brains. Relative to total protein, GAP-43 is approximately 12 times as abundant in growth-cone membranes as in synaptic membranes from adult brains. Immunohistochemical localization of GAP-43 in frozen sections of developing brain indicates that the protein is specifically associated with neuropil areas containing growth cones and immature synaptic terminals. The results support the proposal that GAP-43 plays a role in axon growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skene, J H -- Jacobson, R D -- Snipes, G J -- McGuire, C B -- Norden, J J -- Freeman, J A -- EY01117/EY/NEI NIH HHS/ -- EY03718/EY/NEI NIH HHS/ -- NS18103/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):783-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3738509" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Anura ; Axons/physiology ; Brain/growth & development/*physiology ; Cell Membrane/metabolism ; Fetus ; GAP-43 Protein ; Growth Substances/*biosynthesis/isolation & purification ; Membrane Proteins/*biosynthesis/isolation & purification ; *Nerve Regeneration ; Nerve Tissue Proteins/*biosynthesis/isolation & purification ; Optic Nerve/cytology/*physiology ; Rats ; Synaptic Membranes/metabolism
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  • 83
    Publication Date: 1986-08-01
    Description: Whether growth hormone stimulates longitudinal bone growth by a direct effect at the site of the growth plate or indirectly by increasing the concentration of circulating somatomedins (insulin-like growth factors) has been the subject of controversy. Immunohistochemical methods were used to explore the localization and distribution of insulin-like growth factor I (IGF-I) immunoreactivity in the epiphyseal growth plate of the proximal tibia of male rats. Cells in the proliferative zone of the growth plate of normal rats exhibited a bright immunofluorescence, whereas cells in the germinal and hypertrophic zones stained only weakly. In rats subjected to hypophysectomy, the number of fluorescent cells was markedly reduced. When the hypophysectomized rats were treated with growth hormone, either systemically or at the site of the growth plate, the number of IGF-I-immunoreactive cells in the proliferative zone was increased. The results show that IGF-I is produced in proliferative chondrocytes in the growth plate and that the number of IGF-I-containing cells is directly regulated by growth hormone. These findings suggest that IGF-I has a specific role in the clonal expansion of differentiated chondrocytes and exerts its function locally through autocrine or paracrine mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nilsson, A -- Isgaard, J -- Lindahl, A -- Dahlstrom, A -- Skottner, A -- Isaksson, O G -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):571-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3523759" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fluorescent Antibody Technique ; Growth Hormone/pharmacology/*physiology ; Growth Plate/*cytology/drug effects/growth & development ; Hypophysectomy ; Insulin-Like Growth Factor I/pharmacology/*physiology ; Male ; Rats ; Rats, Inbred Strains ; Somatomedins/*physiology ; Tibia
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  • 84
    Publication Date: 1986-12-05
    Description: Transient stimulation of target tissues by sex steroids can cause long-lasting changes that may facilitate or alter responses to subsequent hormonal treatment. How these altered characteristics are propagated during cell division in the absence of the stimulating hormone is unknown. The human hepatocarcinoma cell line HepG2 was used as a model to examine the effects of estrogen on the synthesis of serum apolipoproteins in vitro. Treatment with low concentrations of estrogen for 24 to 48 hours resulted in long-lasting alterations in the kinetics with which the cells responded to subsequent stimulation with estrogen. Manifestation of this memory effect was correlated quantitatively with the induction and propagation of a moderate-affinity, nuclear, estrogen-binding protein with the characteristics of a type II estrogen receptor. The data indicate that transient exposure of these cells to estrogen can induce changes in their response characteristics and composition of nuclear proteins that are inherited by daughter cells grown in the absence of hormone for more than ten generations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tam, S P -- Hache, R J -- Deeley, R G -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1234-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3022381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins B/pharmacology ; Apolipoproteins E/pharmacology ; Carcinoma, Hepatocellular/metabolism ; Cell Division ; Cell Line ; Chick Embryo ; Estradiol/pharmacology ; Estrogens/*pharmacology ; Humans ; Liver/*cytology/drug effects ; Liver Neoplasms/metabolism ; Receptors, Estrogen/drug effects
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-29
    Description: Study of the neurobiology of learning and memory is in a most exciting phase. Behavioral studies in animals are characterizing the categories and properties of learning and memory; essential memory trace circuits in the brain are being defined and localized in mammalian models; work on human memory and the brain is identifying neuronal systems involved in memory; the neuronal, neurochemical, molecular, and biophysical substrates of memory are beginning to be understood in both invertebrate and vertebrate systems; and theoretical and mathematical analysis of basic associative learning and of neuronal networks in proceeding apace. Likely applications of this new understanding of the neural bases of learning and memory range from education to the treatment of learning disabilities to the design of new artificial intelligence systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, R F -- New York, N.Y. -- Science. 1986 Aug 29;233(4767):941-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3738519" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/physiology ; Brain/physiology ; Cerebellum/physiology ; Cerebral Cortex/physiology ; Conditioning, Classical/physiology ; Hippocampus/physiology ; Humans ; Learning/*physiology ; Memory/*physiology ; Neural Pathways/physiology ; Neurons/physiology ; Primates ; Rats ; Synapses/physiology
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-11-21
    Description: Long-term potentiation (LTP), a long-lasting enhancement of synaptic efficacy, is considered a model for learning and memory. In anesthetized rats, activation of dentate granule cells by stimulating either the medial or lateral perforant pathway at frequencies of 100 to 400 Hz produced LTP of the stimulated pathway preferentially at 400 Hz. However, hippocampal pathways do not normally fire at this high rate. Stimuli at 200 Hz were then applied to either the medial or lateral pathway separately, to both pathways simultaneously, or to the two pathways asynchronously so that the composite stimulus applied to the granule cell dendrite was 400 Hz. LTP was produced preferentially in the asynchronous condition. Thus, lower frequency, physiological input volleys arriving asynchronously at medial and lateral synapses can induce LTP by activating a 400-Hz sensitive mechanism capable of integrating spatially separated granule cell inputs. This may reflect how LTP is normally produced in the dentate gyrus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winson, J -- Dahl, D -- 5-K02-MH00232/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 21;234(4779):985-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775372" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Evoked Potentials ; Hippocampus/*physiology ; Neurons, Afferent/physiology ; Rats
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  • 87
    Publication Date: 1986-02-07
    Description: Protein kinase C activity in rat hippocampal membranes and cytosol was determined 1 minute and 1 hour after induction of the synaptic plasticity of long-term potentiation. At 1 hour after long-term potentiation, but not at 1 minute, protein kinase C activity was increased twofold in membranes and decreased proportionately in cytosol, suggesting translocation of the activity. This time-dependent redistribution of enzyme activity was directly related to the persistence of synaptic plasticity, suggesting a novel mechanism regulating the strength of synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akers, R F -- Lovinger, D M -- Colley, P A -- Linden, D J -- Routtenberg, A -- MH25281/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):587-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/enzymology ; Cytosol/enzymology ; Enzyme Activation ; Hippocampus/*enzymology/physiology ; Male ; Neuronal Plasticity ; Protein Kinase C/metabolism/*physiology ; Rats ; Synaptic Membranes/enzymology ; Synaptic Transmission
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  • 88
    Publication Date: 1986-11-07
    Description: Dense, focal injections of wheat germ agglutinin conjugated-horseradish peroxidase in the locus coeruleus of rats labeled afferent neurons in unexpectedly few brain regions. Major inputs emanate from only two nuclei--the paragigantocellularis and the prepositus hypoglossi, both in the rostral medulla. The dorsal cap of the paraventricular hypothalamic nucleus and the spinal intermediate gray are possible minor afferents to locus coeruleus. Other areas reported to project to locus coeruleus (for example, amygdala, nucleus tractus solitarius, and spinal dorsal horn) did not exhibit consistent retrograde labeling. Anterograde tracing and electrophysiologic experiments confirmed the absence of input to locus coeruleus from these areas, which instead terminate in targets adjacent to locus coeruleus. These findings redefine the anatomic organization of the locus coeruleus, and have implications for hypotheses concerning the functions of this noradrenergic brain nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aston-Jones, G -- Ennis, M -- Pieribone, V A -- Nickell, W T -- Shipley, M T -- NS20643/NS/NINDS NIH HHS/ -- NS22320/NS/NINDS NIH HHS/ -- NS23348/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):734-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775363" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; Efferent Pathways ; Electric Stimulation ; Locus Coeruleus/anatomy & histology/*physiology ; Male ; Medulla Oblongata/cytology ; Paraventricular Hypothalamic Nucleus/cytology ; Rats ; Spinal Cord/cytology ; Wheat Germ Agglutinins
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  • 89
    Publication Date: 1986-02-28
    Description: Differentiation of lymphoid precursor cells in a variety of species is induced by polypeptide hormones such as thymopoietin for T cells and bursin for B cells. In the present experiments, bursin isolated from the bursa of Fabricius of chicken was found to induce the phenotypic differentiation of mammalian and avian B precursor cells but not of T precursor cells in vitro. Similarly, bursin increased cyclic guanosine monophosphate in cells of the human B-cell line Daudi but not in cells of the human T-cell line CEM. These inducing properties of bursin are the reverse of the inducing properties of thymopoietin produced by the thymus and are appropriate to a physiological B-cell-inducing hormone. A tripeptide sequence (lysyl-histidyl-glycyl-amide) was determined for bursin and confirmed by synthesizing this proposed structure and demonstrating chemical identity of the natural and synthetic peptides. Similarity of biological action was indicated in induction assays by elevation of cyclic adenosine monophosphate and guanosine monophosphate in Daudi B cells but not in CEM T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Audhya, T -- Kroon, D -- Heavner, G -- Viamontes, G -- Goldstein, G -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):997-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3484838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*physiology ; Bursa of Fabricius/*physiology ; Cell Line ; Chickens ; Chromatography, High Pressure Liquid ; Chromatography, Thin Layer ; Humans ; Mass Spectrometry ; Oligopeptides/*isolation & purification/pharmacology/physiology ; Rats ; T-Lymphocytes/drug effects
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  • 90
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, B M -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1505.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952493" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Brain/cytology/*embryology ; Cell Differentiation ; Nerve Tissue/transplantation ; Peripheral Nerves/*cytology ; Rats
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  • 91
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-11-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1986 Nov 21;234(4779):938-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3022378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiopathology ; Disease Models, Animal ; Epilepsy/*physiopathology ; Humans ; Kindling, Neurologic ; Neural Inhibition ; Rats ; *Synaptic Transmission
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  • 92
    Publication Date: 1986-01-10
    Description: In rats infected with the parasite Schistosoma mansoni, the concentration of C-reactive protein in the serum increases after the lung stage of infection and is at its highest at the time of terminal worm rejection. The peak of platelet-mediated cytotoxicity induced by infected serum that has been heated (and is free of immunoglobulin E) as well as the time course for the development of platelet cytotoxic activity in infected rats was found to be correlated with the concentration of C-reactive protein. Rat and human platelets treated with homologous serum obtained during an acute phase of inflammation or with purified C-reactive protein were able to kill the immature forms of the worm in vitro. Platelets treated with C-reactive protein were furthermore capable of conferring significant protection against schistosomiasis in transfer experiments. Collectively these data indicate that a system that includes C-reactive protein and platelets participates in the natural resistance of the rat to schistosomal infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bout, D -- Joseph, M -- Pontet, M -- Vorng, H -- Deslee, D -- Capron, A -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):153-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3079916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/*drug effects/immunology ; C-Reactive Protein/blood/immunology/*pharmacology ; Cytotoxicity, Immunologic/*drug effects ; Dose-Response Relationship, Drug ; Immunity, Innate/drug effects ; Rats ; Schistosomiasis mansoni/*immunology ; Turpentine/pharmacology
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  • 93
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-02-28
    Description: gamma-Aminobutyric acid (GABA) is one of the major inhibitory neurotransmitters in the central nervous system. In the cerebral cortex, GABA-containing cells represent a subpopulation of interneurons. With semithin frozen sections, it is possible to demonstrate that most GABA neurons in the rat somatosensory cortex contain the calcium-binding protein parvalbumin and that parvalbumin is found virtually only in GABA neurons. Parvalbumin seems to influence the electrical properties and enzymatic machinery to modulate neuronal excitability and activity. The specific role of parvalbumin in GABA-containing cortical cells may be related to controlling the effectiveness of their inhibitory action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Celio, M R -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):995-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3945815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/analysis/*cytology ; Electrophysiology ; Male ; Muscle Proteins/*analysis ; Neurons/*analysis/physiology ; Parvalbumins/*analysis ; Rats ; gamma-Aminobutyric Acid/*physiology
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  • 94
    Publication Date: 1986-08-22
    Description: A new family of protein kinase C-related genes has been identified in bovine, human, and rat genomes. The alpha-, beta-, and gamma-type protein kinase sequences are highly homologous, include a kinase domain, and potential calcium-binding sites, and they contain interspersed variable regions. The corresponding genes are located on distinct human chromosomes; the possibility of even greater genetic complexity of this gene family is suggested by Northern and Southern hybridization analyses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coussens, L -- Parker, P J -- Rhee, L -- Yang-Feng, T L -- Chen, E -- Waterfield, M D -- Francke, U -- Ullrich, A -- New York, N.Y. -- Science. 1986 Aug 22;233(4766):859-66.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3755548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Chromosome Mapping ; Chromosomes, Human, 16-18 ; Dna ; Genes ; Humans ; Nucleic Acid Hybridization ; Protein Kinase C/*genetics ; Rats
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-02-07
    Description: Measurements confirm the quantitative theoretical prediction that the autonomic nonendocrine abnormality of rapid daytime gastric emptying is the major primary cause of the obesity resulting from ventromedial hypothalamic lesions in rats. Therapy for obesity could include slowing of stomach emptying.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duggan, J P -- Booth, D A -- New York, N.Y. -- Science. 1986 Feb 7;231(4738):609-11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3511527" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Feeding and Eating Disorders/*physiopathology ; *Gastric Emptying/drug effects ; Humans ; Hyperphagia/etiology/*physiopathology ; Insulin/pharmacology ; Obesity/etiology/*physiopathology ; Rats ; Rats, Inbred Strains ; Time Factors ; Ventromedial Hypothalamic Nucleus/*physiology
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  • 96
    Publication Date: 1986-05-16
    Description: The human T-lymphotropic viruses types I and II (HTLV-I and -II) have been etiologically linked with certain T-cell leukemias and lymphomas that characteristically display membrane receptors for interleukin-2. The relation of these viruses to this growth factor receptor has remained unexplained. It is demonstrated here that introduction of the trans-activator (tat) gene of HTLV-II into the Jurkat T-lymphoid cell line results in the induction of both interleukin-2 receptor and interleukin-2 gene expression. The coexpression of these cellular genes may play a role in the altering T-cell growth following retroviral infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, W C -- Leonard, W J -- Wano, Y -- Svetlik, P B -- Peffer, N J -- Sodroski, J G -- Rosen, C A -- Goh, W C -- Haseltine, W A -- 1R01CA369974-01AI/CA/NCI NIH HHS/ -- CA07580/CA/NCI NIH HHS/ -- CA40658/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 16;232(4752):877-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010456" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Deltaretrovirus/*genetics ; Gene Expression Regulation ; *Genes, Viral ; Humans ; Interleukin-2/biosynthesis/*genetics ; Leukemia/microbiology ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-2
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-01
    Description: The relative stability of amplified DNA in drug-resistant Leishmania major was previously reported to be dependent on location, that is, unstable amplified DNA was extrachromosomal and stable amplified DNA was chromosomal. Leishmanial chromosomes have now been directly examined by means of orthogonal-field-alternation gel electrophoresis (OFAGE). The amplified DNA's in three resistant cell lines displayed unusual migration and were clearly extrachromosomal, regardless of whether the amplified DNA's were stable or unstable. Thus, contrary to conclusions from earlier studies of drug resistance in cultured animal cells, stable amplified DNA in Leishmania can be extrachromosomal. In addition, these amplified DNA's were shown to be circular on the basis of their resistance to exonuclease III digestion and their behavior on OFAGE. Their mobility was also greatly changed after treatment with topoisomerase II, suggesting that the amplified DNA's were either supercoiled or concatenated circles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garvey, E P -- Santi, D V -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):535-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726545" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosomes ; DNA/*genetics ; Drug Resistance, Microbial ; Electrophoresis ; *Extrachromosomal Inheritance ; Gene Amplification/drug effects ; Leishmania tropica/drug effects/*genetics ; Methotrexate/pharmacology ; Nucleic Acid Hybridization
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 1986-09-26
    Description: The potential utility of cultured neuroblastoma cells as donor tissue for neutral implants into the mammalian brain has been examined. Cells from a human neuroblastoma cell line, IMR-32, were labeled with [3H]thymidine and chemically rendered amitotic. These differentiated IMR-32 cells were grafted into the hippocampi of five adult African Green monkeys, and graft survival was evaluated for up to 270 days after transplantation. Autoradiographically labeled grafted cells were identified in four animals. Processes from grafted cells could be followed for distances of up to 150 micrometers into the host brain. No evidence for neoplastic growth of the transplant was found. Thus, grafted neuroblastoma cells can survive for prolonged periods in the primate brain and may serve as a practical source of donor tissue for neural implants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gash, D M -- Notter, M F -- Okawara, S H -- Kraus, A L -- Joynt, R J -- New York, N.Y. -- Science. 1986 Sep 26;233(4771):1420-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3749886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Brain/*cytology ; Cell Line ; Cercopithecus aethiops ; DNA Replication ; Female ; Humans ; Male ; Neoplasm Transplantation ; Neuroblastoma/*pathology ; Neurons/*transplantation ; Thymidine/metabolism ; Tritium
    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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  • 99
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-03
    Description: Cholinergic agonists rapidly and transiently induced transcription of the c-fos protooncogene and one or more actin genes in neuronally differentiated PC12 cells. Transcription was activated within minutes after stimulation of the nicotinic acetylcholine receptor and required an influx of extracellular Ca2+ ions through voltage-sensitive calcium channels. Nicotine activation proceeded by a different pathway from activation by nerve growth factor, whose stimulation of these genes is independent of extracellular Ca2+ ions. These findings suggest that neurotransmitters may rapidly activate specific gene transcription in nondividing neuronally differentiated cells. They also suggest a functional role for neurotransmitter induction of c-fos and actin expression in the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenberg, M E -- Ziff, E B -- Greene, L A -- GM 30760/GM/NIGMS NIH HHS/ -- NS16036/NS/NINDS NIH HHS/ -- P30 CA 16087/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):80-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3749894" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Adrenal Gland Neoplasms/metabolism ; Animals ; Calcium/metabolism ; Cell Line ; Dose-Response Relationship, Drug ; Nerve Growth Factors/pharmacology ; Nicotine/pharmacology ; Pheochromocytoma/metabolism ; Rats ; Receptors, Cholinergic/*drug effects ; Transcription, Genetic/*drug effects
    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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  • 100
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolata, G -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1198-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775379" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholic Intoxication/*drug therapy ; Animals ; Azides/*pharmacology/therapeutic use ; Benzodiazepines/*pharmacology/therapeutic use ; Ethanol/*antagonists & inhibitors ; Humans ; Rats
    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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