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  • Cell Line  (50)
  • Rats, Inbred Strains  (30)
  • *Ecosystem
  • Crystallography, X-Ray
  • Phosphorylation
  • American Association for the Advancement of Science (AAAS)  (83)
  • American Meteorological Society
  • MDPI Publishing
  • 1995-1999
  • 1985-1989  (83)
  • 1985  (83)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (83)
  • American Meteorological Society
  • MDPI Publishing
Years
  • 1995-1999
  • 1985-1989  (83)
Year
  • 1
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    Identification of the protein encoded by the E6 transforming gene of bovine papillomavirus (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-25
    Description: Papillomaviruses (PV) contain several conserved genes that may encode nonstructural proteins; however, none of these predicted gene products have been identified. Papillomavirus E6 genes are retained and expressed as RNA in PV-associated human and animal carcinomas and cell lines. This suggests that the E6 gene product may be important in the maintenance of the malignant phenotype. The E6 open reading frame of the bovine papillomavirus (BPV) genome has been identified as one of two BPV genes that can independently transform mouse cells in vitro. A polypeptide encoded by this region of BPV was produced in a bacterial expression vector and used to raise antisera. The antisera specifically immunoprecipitated the predicted 15.5-kilodalton BPV E6 protein from cells transformed by the E6 gene. The E6 protein was identified in both the nuclear and membrane fractions of these transformed cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Androphy, E J -- Schiller, J T -- Lowy, D R -- 5-F32-CA-07237/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):442-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996134" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bovine papillomavirus 1/*genetics ; Cell Line ; Cell Transformation, Viral ; *Genes, Viral ; Mice ; Oncogenes ; Papillomaviridae/*genetics ; RNA, Messenger/genetics ; Rabbits ; Rats ; Tumor Virus Infections/genetics ; Viral Proteins/*genetics/isolation & purification
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Immunogenicity of synthetic peptides from circumsporozoite protein of Plasmodium falciparum (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-24
    Description: In a study of recombinant proteins that might be useful in developing a vaccine against malaria, synthetic peptides from the circumsporozoite (CS) protein of Plasmodium falciparum were found to be immunogenic for mice and rabbits. Antibody to peptides from the repeating region of the CS protein recognized native CS protein and blocked sporozoite invasion of human hepatoma cells in vitro. Antibodies to peptides from regions I and II had no biologic activity, although antibody to region I recognized processed CS protein by Western blot analysis. These data support the feasibility of developing a vaccine against the sporozoite stage of the malaria parasite by using synthetic peptides of the repeating region of the CS protein conjugated to a carrier protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ballou, W R -- Rothbard, J -- Wirtz, R A -- Gordon, D M -- Williams, J S -- Gore, R W -- Schneider, I -- Hollingdale, M R -- Beaudoin, R L -- Maloy, W L -- New York, N.Y. -- Science. 1985 May 24;228(4702):996-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2988126" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies/immunology ; Antibody Formation ; Antigens, Surface/*immunology ; Carcinoma, Hepatocellular ; Cell Line ; Cross Reactions ; Fluorescent Antibody Technique ; Humans ; Immune Sera/immunology ; Liver Neoplasms ; Malaria/prevention & control ; Mice ; Peptides/chemical synthesis/*immunology ; Plasmodium/immunology ; Plasmodium falciparum/*immunology/physiology ; Precipitin Tests ; *Protozoan Proteins ; Rabbits ; Vaccines/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Trigeminal-taste interaction in palatability processing (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-10
    Description: Peripheral transection of the sensory branches of the trigeminal nerve in rats unbalanced palatability, selectively reducing the ingestive actions elicited by preferred tastes but leaving unchanged the aversive actions elicited by unpreferred tastes. The reduction in the number of positive ingestive actions occurred even though the capacity to emit these actions remained unimpaired. These findings show that there is an interaction between somatosensation and gustation in the processing of palatability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berridge, K C -- Fentress, J C -- New York, N.Y. -- Science. 1985 May 10;228(4700):747-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Food Preferences ; Humans ; Male ; Rats ; Rats, Inbred Strains ; Taste/*physiology ; Tongue/physiology ; Trigeminal Nerve/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 4
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    Active T-cell receptor genes have intron deoxyribonuclease hypersensitive sites (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-08-09
    Description: The T-cell receptor beta-chain gene has a nuclease hypersensitive site in several kinds of T cells, which does not appear in B cells expressing immunoglobulins. Conversely, the kappa immunoglobulin gene shows a known hypersensitive site at its enhancer element in B cells, as expected, but this site is absent in T cells. As is the case with immunoglobulin genes, the T-cell receptor site lies within the gene, in the intron separating joining and constant region segments. These nuclease hypersensitive DNA configurations in the introns of active T-cell receptor and immunoglobulin genes may arise from control elements that share ancestry but have diverged to the extent that each normally acts only in lymphoid cells which use the proximal gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bier, E -- Hashimoto, Y -- Greene, M I -- Maxam, A M -- AI 19901/AI/NIAID NIH HHS/ -- CA 22427/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 9;229(4713):528-34.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3927483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Base Sequence ; Binding Sites ; Cell Line ; Chromosome Mapping ; Collodion ; Deoxyribonuclease I/*metabolism ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Humans ; Hybridomas ; Immunochemistry ; Immunoglobulin Fragments/*genetics ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin kappa-Chains/genetics ; Mice ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 5
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    Selective extraction of small and large molecules from the cerebrospinal fluid by Purkinje neurons (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-19
    Description: Cerebellar Purkinje neurons accumulated propidium iodide, granular blue, and horseradish peroxidase conjugated to wheat germ agglutinin but not unconjugated horseradish peroxidase, bisbenzimide, or Evans blue when these compounds were infused into the lateral cerebral ventricles of awake, unrestrained rats. Accumulation of propidium iodide by Purkinje neurons of the vermis was associated with a reproducible behavioral abnormality characterized by truncal tremor, ataxia, and nystagmus. Both the accumulation of propidium iodide in Purkinje cells and the behavioral abnormality were prevented by prior intracerebroventricular administration of ouabain or colchicine, drugs that block neuronal transport processes. The ability of cerebellar Purkinje neurons to extract small and large molecules from the cerebrospinal fluid has important implications for their physiology and pathology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borges, L F -- Elliott, P J -- Gill, R -- Iversen, S D -- Iversen, L L -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):346-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2580350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bisbenzimidazole/metabolism ; Cerebrospinal Fluid/*physiology ; Dendrites/physiology ; Evans Blue/metabolism ; Horseradish Peroxidase/metabolism ; Humans ; Male ; Propidium/metabolism/pharmacology ; Purkinje Cells/*metabolism/physiology ; Rats ; Rats, Inbred Strains ; Tremor/chemically induced/physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Hormonal control of the anatomical specificity of motoneuron-to-muscle innervation in rats (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-15
    Description: Motoneurons of the spinal nucleus of the bulbocavernosus innervate bulbocavernosus muscles in male rats. Adult female rats normally lack both the spinal nucleus and its target muscles. Prenatal treatment of females with testosterone propionate resulted in adults having, like males, both the spinal nucleus and its target muscles. However, prenatal treatment with dihydrotestosterone propionate preserves the muscles but not the motoneurons. This paradoxical condition might result from (i) bulbocavernosus muscles without innervation; (ii) muscles innervated by morphologically unrecognizable motoneurons; (iii) muscles innervated by a very few spinal nucleus cells, each innervating many bulbocavernosus fibers; or (iv) muscles innervated by motoneurons outside their normal anatomical locus in the spinal nucleus. The results of retrograde marker injections into the bulbocavernosus muscles of females treated with androgen refute the first three possibilities and confirm the last: the different androgen treatments result in anatomically distinct spinal motor nuclei innervating bulbocavernosus muscles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breedlove, S M -- NS19790/NS/NINDS NIH HHS/ -- RR07006/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1357-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dihydrotestosterone/analogs & derivatives/pharmacology ; Female ; Male ; Motor Neurons/anatomy & histology/drug effects/*physiology ; Muscles/drug effects/*innervation ; Pregnancy ; Rats ; Rats, Inbred Strains ; Sex Differentiation/drug effects ; Testosterone/*pharmacology
    Print ISSN: 0036-8075
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  • 7
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    Association of crossover points with topoisomerase I cleavage sites: a model for nonhomologous recombination (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-22
    Description: Nonhomologous DNA recombination is frequently observed in somatic cells upon the introduction of DNA into cells or in chromosomal events involving sequences already stably carried by the genome. In this report, the DNA sequences at the crossover points for excision of SV40 from chromosomes were shown to be associated with eukaryotic topoisomerase I cleavage sites in vitro. The precise location of the cleavage sites relative to the crossover points has suggested a general model for nonhomologous recombination mediated by topoisomerase I.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bullock, P -- Champoux, J J -- Botchan, M -- CA 30490/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Nov 22;230(4728):954-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2997924" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Transformation, Viral ; Chromatin/ultrastructure ; Chromosome Mapping ; DNA Topoisomerases, Type I/*metabolism ; Rats ; *Recombination, Genetic ; Simian virus 40/*genetics
    Print ISSN: 0036-8075
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  • 8
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    Imaging elemental distribution and ion transport in cultured cells with ion microscopy (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-28
    Description: Both elemental distribution and ion transport in cultured cells have been imaged by ion microscopy. Morphological and chemical information was obtained with a spatial resolution of approximately 0.5 micron for sodium, potassium, calcium, and magnesium in freeze-fixed, cryofractured, and freeze-dried normal rat kidney cells and Chinese hamster ovary cells. Ion transport was successfully demonstrated by imaging Na+-K+ fluxes after the inhibition of Na+- and K+ -dependent adenosine triphosphatase with ouabain. This method allows measurements of elemental (isotopic) distribution to be related to cell morphology, thereby providing the means for studying ion distribution and ion transport under different physiological, pathological, and toxicological conditions in cell culture systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandra, S -- Morrison, G H -- R01GM24314/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1543-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis ; Cell Line ; Cells, Cultured ; Cricetinae ; Elements/*analysis ; Female ; Freeze Fracturing ; Kidney/*ultrastructure ; Magnesium/analysis ; Microscopy/methods ; Ouabain/pharmacology ; Ovary/*ultrastructure ; Potassium/analysis ; Rats ; Sodium/analysis ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Tissue Distribution
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  • 9
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    Disorganization of cultured vascular endothelial cell monolayers by fibrinogen fragment D (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-22
    Description: Fibrinogen fragment D, which is heterogeneous, has several important biological functions. Human fibrinogen fragments D94 (molecular weight, 94,000), D78 (78,000), and E (52,000) were purified. Fragments D78 and D94 but not purified fibrinogen or fragment E specifically caused disorganization of bovine aortic endothelial cells cultured as monolayers. Within 2 hours of exposure to pathophysiological concentrations of fragment D, the confluent endothelial cells retracted from each other and projected pseudopodia. These disturbed cells subsequently became rounded and detached from the substrate. The actin present in stress fibers in stationary monolayer cells was diffusely redistributed in cells with fragment D-induced alterations in morphology. This effect was not observed in monolayers of kidney epithelial cells. The results demonstrate a specific effect of fibrinogen fragment D on the disorganization of cultured vascular endothelial cell monolayers and suggest that fragment D plays a role in the pathogenesis of syndromes with vascular endothelial damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dang, C V -- Bell, W R -- Kaiser, D -- Wong, A -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1487-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4038818" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/analysis ; Animals ; Aorta ; Cattle ; Cell Adhesion/drug effects ; Cell Line ; Cells, Cultured ; Cytoskeleton/drug effects ; Endothelium/analysis/*cytology/drug effects/ultrastructure ; Epithelial Cells ; Fibrin Fibrinogen Degradation Products/*pharmacology ; Humans ; Kidney ; Pseudopodia/drug effects
    Print ISSN: 0036-8075
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  • 10
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    Inhibition of lymphocyte proliferation by a synthetic peptide homologous to retroviral envelope proteins (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-25
    Description: The retroviral transmembrane envelope protein p15E is immunosuppressive in that it inhibits immune responses of lymphocytes, monocytes, and macrophages. A region of p15E has been conserved among murine and feline retroviruses; a homologous region is also found in the transmembrane envelope proteins of the human retroviruses HTLV-I and HTLV-II and in a putative envelope protein encoded by an endogenous C-type human retroviral DNA. A peptide (CKS-17) was synthesized to correspond to this region of homology and was examined for its effects on lymphocyte proliferation. CKS-17 inhibited the proliferation of an interleukin-2-dependent murine cytotoxic T-cell line as well as alloantigen-stimulated proliferation of murine and human lymphocytes. Four other peptides, representing different regions of virus proteins, were inactive. These results suggest that the immunosuppressive portion of retroviral transmembrane envelope proteins may reside, at least in part, in a-conserved sequence represented by the CKS-17 peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cianciolo, G J -- Copeland, T D -- Oroszlan, S -- Snyderman, R -- P01-CA29589-02/CA/NCI NIH HHS/ -- R23-CA34671-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):453-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996136" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Deltaretrovirus/genetics ; Humans ; Leukemia Virus, Feline/genetics ; Leukemia Virus, Murine/genetics ; Lymphocyte Activation/*drug effects ; Lymphocyte Culture Test, Mixed ; Lymphocytes/drug effects ; Mice ; Mice, Inbred BALB C ; Peptides/*pharmacology ; Retroviridae/*genetics ; Spleen/cytology ; Viral Envelope Proteins/genetics/*pharmacology
    Print ISSN: 0036-8075
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  • 11
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    Vitamin E reversal of the effect of extracellular calcium on chemically induced toxicity in hepatocytes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-15
    Description: Isolated rat hepatocytes were incubated in the presence or absence of extracellular calcium and alpha-tocopherol succinate with three different toxic chemicals; namely, adriamycin in combination with 1,3-bis(2-chloroethyl)-1-nitrosourea, ethyl methanesulfonate, and the calcium ionophore A23187. In the absence of extracellular calcium these three compounds were far more toxic to the cells than in its presence. The addition of vitamin E to calcium-free medium, however, protected hepatocytes against toxic injury, whereas cells incubated in medium containing calcium were not protected. Hepatocyte viability during each toxic insult correlated well with the cellular alpha-tocopherol content but not with the presence or absence of extracellular calcium. These results suggest that cellular alpha-tocopherol maintains the viability of the cell during a toxic insult and that the presence or absence of vitamin E in the incubation medium probably explains the conflicting reports on the role of extracellular calcium in toxic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fariss, M W -- Pascoe, G A -- Reed, D J -- ES01978/ES/NIEHS NIH HHS/ -- ES07060/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):751-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3918345" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcimycin/toxicity ; Calcium/*physiology ; Carmustine/toxicity ; Cell Survival/*drug effects ; Cells, Cultured ; Doxorubicin/toxicity ; Ethyl Methanesulfonate/toxicity ; Liver/cytology/*drug effects ; Male ; Rats ; Rats, Inbred Strains ; Vitamin E/*physiology
    Print ISSN: 0036-8075
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  • 12
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    Interaction of calcitonin and calcitonin gene-related peptide at receptor sites in target tissues (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-15
    Description: Discrete receptor sites for calcitonin (CT) and calcitonin gene-related peptide (CGRP) were found in the nervous system and in peripheral tissues. Each peptide was capable of cross-reacting with the specific receptor of the other. In contrast to CT receptors, CGRP receptors were not linked to adenylate cyclase. However, CGRP could stimulate adenylate cyclase in CT target tissues apparently by interacting with CT receptors. The relative abilities of CGRP and mammalian CT to inhibit CT binding suggest that CGRP could serve as an endogenous ligand for CT receptors in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goltzman, D -- Mitchell, J -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1343-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2983422" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Adrenal Glands/metabolism ; Animals ; Bone and Bones/metabolism ; Brain/metabolism ; Calcitonin/*metabolism ; Calcitonin Gene-Related Peptide ; Kidney/metabolism ; Male ; Nerve Tissue Proteins/*metabolism ; Pituitary Gland/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Calcitonin ; Receptors, Cell Surface/*metabolism ; Spinal Cord/metabolism
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  • 13
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    Immunoglobulin heavy-chain enhancer requires one or more tissue-specific factors (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-18
    Description: Enhancer sequences are regulatory regions that greatly increase transcription of certain eukaryotic genes. An immunoglobulin heavy-chain variable gene segment is moved from a region lacking enhancer activity to a position adjacent to the known heavy-chain enhancer early in B-cell maturation. In lymphoid cells, the heavy-chain and SV40 enhancers bind a common factor essential for enhancer function. In contrast, fibroblast cells contain a functionally distinct factor that is used by the SV40 but not by the heavy-chain enhancer. The existence of different factors in these cells may explain the previously described lymphoid cell specificity of the heavy-chain enhancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mercola, M -- Goverman, J -- Mirell, C -- Calame, K -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 18;227(4684):266-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3917575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; B-Lymphocytes/immunology ; Base Sequence ; Cell Line ; *Enhancer Elements, Genetic ; Fibroblasts/immunology ; *Genes, Regulator ; Humans ; Immunoglobulin Constant Regions/genetics ; Immunoglobulin Heavy Chains/*genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Transcription, Genetic
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  • 14
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    Choline acetyltransferase activity in striatum of neonatal rats increased by nerve growth factor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-19
    Description: Some neurodegenerative disorders may be caused by abnormal synthesis or utilization of trophic molecules required to support neuronal survival. A test of this hypothesis requires that trophic agents specific for the affected neurons be identified. Cholinergic neurons in the corpus striatum of neonatal rats were found to respond to intracerebroventricular administration of nerve growth factor with prominent, dose-dependent, selective increases in choline acetyltransferase activity. Cholinergic neurons in the basal forebrain also respond to nerve growth factor in this way. These actions of nerve growth factor may indicate its involvement in the normal function of forebrain cholinergic neurons as well as in neurodegenerative disorders involving such cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mobley, W C -- Rutkowski, J L -- Tennekoon, G I -- Buchanan, K -- Johnston, M V -- ES07094/ES/NIEHS NIH HHS/ -- NS00603/NS/NINDS NIH HHS/ -- NS17642/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):284-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2861660" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Alzheimer Disease/metabolism ; Animals ; Animals, Newborn/metabolism ; Brain/drug effects/enzymology ; Choline O-Acetyltransferase/*metabolism ; Corpus Striatum/cytology/drug effects/*enzymology ; Dose-Response Relationship, Drug ; Glutamate Decarboxylase/metabolism ; Humans ; Huntington Disease/metabolism ; Nerve Growth Factors/*pharmacology/physiology ; Neurons/enzymology/physiology ; Rats ; Rats, Inbred Strains ; Tyrosine 3-Monooxygenase/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    AIDS virology: a battle on many fronts (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norman, C -- New York, N.Y. -- Science. 1985 Nov 1;230(4725):518-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2413546" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/diagnosis/*microbiology ; Antibodies, Monoclonal ; Antibodies, Viral/analysis ; Antigens, Viral/analysis/immunology ; Cell Line ; Cross Reactions ; Culture Techniques/methods ; Cytopathogenic Effect, Viral ; Deltaretrovirus/immunology/*isolation & purification ; Homosexuality ; Humans ; Lymphatic Diseases/microbiology ; Microscopy, Electron ; Patents as Topic/legislation & jurisprudence ; RNA-Directed DNA Polymerase/analysis ; Reagent Kits, Diagnostic ; T-Lymphocytes/microbiology ; Terminology as Topic ; United States ; Viral Core Proteins/immunology ; Viral Envelope Proteins/immunology
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  • 16
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    Differential control of U1 small nuclear RNA expression during mouse development (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-20
    Description: During normal mouse development the relative amounts of two types of U1 small nuclear RNA's (U1 RNA) change significantly. Fetal tissues have comparable levels of the two major types of mouse U1 RNA's, mU1a and mU1b, whereas most differentiated adult tissues contain only mU1a RNA's. Those adult tissues that also accumulate detectable amounts of embryonic (mU1b) RNA's (for example, testis, spleen, and thymus) contain a significant proportion of stem cells capable of further differentiation. Several strains of mice express minor sequence variants of U1 RNA's that are subject to the same developmental controls as the major types of adult and embryonic U1 RNA. The differential accumulation of embryonic U1 RNA's may influence the pattern of gene expression during early development and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lund, E -- Kahan, B -- Dahlberg, J E -- CA 33453/CA/NCI NIH HHS/ -- GM 30220/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 20;229(4719):1271-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2412294" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Base Sequence ; Brain/*growth & development/metabolism ; Cell Line ; Embryonic and Fetal Development ; Liver/*growth & development/metabolism ; Male ; Mice ; Mice, Inbred ICR ; Neoplastic Stem Cells/metabolism ; Nucleic Acid Hybridization ; RNA/*biosynthesis ; RNA, Messenger/biosynthesis ; RNA, Small Nuclear ; Testis/*growth & development/metabolism
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  • 17
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    U1 small nuclear RNA genes are subject to dosage compensation in mouse cells (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-19
    Description: Multiple copies of a gene that encodes human U1 small nuclear RNA were introduced into mouse C127 cells with bovine papilloma virus as the vector. For some recombinant constructions, the human U1 gene copies were maintained extrachromosomally on the viral episome in an unrearranged fashion. The relative abundance of human and mouse U1 small nuclear RNA varied from one cell line to another, but in some lines human U1 RNA accounted for as much as one-third of the total U1. Regardless of the level of human U1 expression, the total amount of U1 RNA (both mouse and human) in each cell line was nearly the same relative to endogenous mouse 5S or U2 RNA. This result was obtained whether measurements were made of total cellular U1 or of only the U1 in small nuclear ribonucleoprotein particles that could be precipitated with antibody directed against the Sm antigen. The data suggest that the multigene families encoding mammalian U1 RNA are subject to some form of dosage compensation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mangin, M -- Ares, M Jr -- Weiner, A M -- GM09148/GM/NIGMS NIH HHS/ -- GM31073/GM/NIGMS NIH HHS/ -- GM31335/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):272-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2409601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Bovine papillomavirus 1/genetics ; Cell Line ; DNA, Recombinant ; *Dosage Compensation, Genetic ; Electrophoresis, Polyacrylamide Gel ; Genetic Vectors ; Humans ; Mice ; Plasmids ; RNA/*genetics/isolation & purification ; RNA, Small Nuclear ; Xenopus
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  • 18
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    Measles virus matrix protein synthesized in a subacute sclerosing panencephalitis cell line (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-07
    Description: Measles virus generally produces acute illness. Rarely, however, persistent infection of brain cells occurs, resulting in a chronic and fatal neurological disease, subacute sclerosing panencephalitis (SSPE). Evidence indicates that expression of the measles virus matrix protein is selectively restricted in this persistent infection, but the mechanism underlying this restriction has not been identified. Defective translation of matrix messenger RNA has been described in one SSPE cell line. This report presents evidence that in a different SSPE tissue culture cell line IP-3-Ca, the matrix protein is synthesized but fails to accumulate. A general scheme is proposed to reconcile the different levels at which restriction of matrix protein has been observed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheppard, R D -- Raine, C S -- Bornstein, M B -- Udem, S A -- CA13330-12/CA/NCI NIH HHS/ -- NS 08952/NS/NINDS NIH HHS/ -- NS 11920/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 7;228(4704):1219-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4001938" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Gene Expression Regulation ; Humans ; Hydrolysis ; Measles virus/genetics/growth & development/*metabolism ; Molecular Weight ; Mutation ; Protein Processing, Post-Translational ; Subacute Sclerosing Panencephalitis/*microbiology ; Viral Matrix Proteins ; Viral Proteins/*biosynthesis/genetics ; Virus Replication
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  • 19
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    Studies of the putative transforming protein of the type I human T-cell leukemia virus (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-21
    Description: The putative transforming protein of the type I human T-cell leukemia virus (HTLV-1) is a 40-kilodalton protein encoded by the X region and is termed p40XI. On the basis of both subcellular fractionation techniques and immunocytochemical analysis, it is now shown that p40XI is a nuclear protein with a relatively short half-life (120 minutes). It is synthesized de novo in considerable quantities in a human T-cell line infected with and transformed by the virus in vitro, and it is not packaged in detectable amounts in the extracellular virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Press, M F -- Souza, L M -- Murdock, D C -- Cline, M J -- Golde, D W -- Gasson, J C -- Chen, I S -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 21;228(4706):1427-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990027" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Polyomavirus Transforming ; Antigens, Viral, Tumor/immunology/*metabolism ; Cell Fractionation ; Cell Line ; Cell Nucleus/metabolism ; Cell Transformation, Viral ; Deltaretrovirus/*metabolism ; Half-Life ; Humans ; Immune Sera ; Precipitin Tests ; Viral Proteins/immunology/*metabolism
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  • 20
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    Dissociation of antitumor potency from anthracycline cardiotoxicity in a doxorubicin analog (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-28
    Description: The search for new congeners of the leading anticancer drug doxorubicin has led to an analog that is approximately 1000 times more potent, noncardiotoxic at therapeutic dose levels, and non-cross-resistant with doxorubicin. The new anthracycline, 3'-deamino-3'-(3-cyano-4-morpholinyl)doxorubicin (MRA-CN), is produced by incorporation of the 3' amino group of doxorubicin in a new cyanomorpholinyl ring. The marked increase in potency was observed against human ovarian and breast carcinomas in vitro; it was not accompanied by an increase in cardiotoxicity in fetal mouse heart cultures. Doxorubicin and MRA-CN both produced typical cardiac ultrastructural and biochemical changes, but at equimolar concentrations. In addition, MRA-CN was not cross-resistant with doxorubicin in a variant of the human sarcoma cell line MES-SA selected for resistance to doxorubicin. Thus antitumor efficacy was dissociated from both cardiotoxicity and cross-resistance by this modification of anthracycline structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikic, B I -- Ehsan, M N -- Harker, W G -- Friend, N F -- Brown, B W -- Newman, R A -- Hacker, M P -- Acton, E M -- CA 24543/CA/NCI NIH HHS/ -- CA 32250/CA/NCI NIH HHS/ -- CA 33303/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1544-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012308" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antineoplastic Agents ; Breast Neoplasms/drug therapy ; Cell Line ; Chemical Phenomena ; Chemistry ; Dose-Response Relationship, Drug ; Doxorubicin/adverse effects/*analogs & derivatives/therapeutic use ; Female ; Heart/drug effects ; Humans ; Isoenzymes ; L-Lactate Dehydrogenase/analysis ; Mice ; Myocardium/enzymology ; Ovarian Neoplasms/drug therapy ; Pregnancy
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  • 21
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    Trans-acting transcriptional regulation of human T-cell leukemia virus type III long terminal repeat (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-11
    Description: Human T-cell leukemia virus type III (HTLV-III) was recently identified as the probable etiologic agent of the acquired immune deficiency syndrome (AIDS). Here it is shown that, in human T-cell lines infected with HTLV-III, gene expression directed by the long terminal repeat sequence of this virus is stimulated by more than two orders of magnitude compared to matched uninfected cells. The rate of transcription of the HTLV-III long terminal repeat is more than 1000 times that of the SV40 early promoter in one infected cell line. Thus, HTLV-III, like HTLV-I, HTLV-II, and the bovine leukemia virus, is characterized by trans-activation of transcription in infected cells. The efficiency of trans-activation in the case of HTLV-III may account, at least in part, for the virulent nature of HTLV-III infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sodroski, J -- Rosen, C -- Wong-Staal, F -- Salahuddin, S Z -- Popovic, M -- Arya, S -- Gallo, R C -- Haseltine, W A -- CA07094/CA/NCI NIH HHS/ -- CA07580/CA/NCI NIH HHS/ -- CA36974/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 11;227(4683):171-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2981427" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics/metabolism ; Cell Line ; Chloramphenicol O-Acetyltransferase ; DNA, Recombinant ; Deltaretrovirus/*genetics ; *Gene Expression Regulation ; Humans ; Operon ; Plasmids ; Transcription, Genetic ; Transfection
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  • 22
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    A strong influence of serotonin axons on beta-adrenergic receptors in rat brain (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-18
    Description: The role of serotonin axons in modulating the norepinephrine neurotransmission system in rat brain was investigated. Selective lesions of the forebrain serotonergic system were made by injecting 5,7-dihydroxytryptamine into the midbrain raphe nuclei. Four to six weeks after the lesion, the uptake of 3H-labeled serotonin in the frontal cortex and the hippocampus was reduced by more than 90 percent, while neither the uptake of 3H-labeled norepinephrine nor the content of norepinephrine was affected in either tissue. The number of beta-adrenergic receptors, as measured by radioligand binding with 3H-labeled dihydroalprenolol, was increased in the frontal cortex and hippocampus of rats with lesions. Similarly, specific lesions of central serotonin axons produced by systemically administered p-chloramphetamine resulted in an increase in the binding of 3H-labeled dihydroalprenolol to beta-adrenergic receptors and in the production of adenosine 3',5'-monophosphate in response to isoproterenol. These results indicate that serotonin axons may regulate beta-adrenergic receptor number and function in brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stockmeier, C A -- Martino, A M -- Kellar, K J -- MH08982/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):323-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cerebral Cortex/*metabolism ; Clonidine/analogs & derivatives/metabolism ; Dihydroalprenolol/metabolism ; Hippocampus/*metabolism ; Kinetics ; Male ; Norepinephrine/metabolism ; Prazosin/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, beta/*metabolism ; Serotonin/*physiology
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  • 23
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    Recombinant human tumor necrosis factor-alpha: effects on proliferation of normal and transformed cells in vitro (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-22
    Description: Modulation of the growth of human and murine cell lines in vitro by recombinant human tumor necrosis factor-alpha (rTNF-alpha) and recombinant human interferon-gamma (rIFN-gamma) was investigated. rTNF-alpha had cytostatic or cytolytic effects on only some tumor cell lines. When administered together with rIFN-gamma, rTNF-alpha showed enhanced antiproliferative effects on a subset of the cell lines tested. In contrast to its effects on sensitive tumor cells, rTNF-alpha augmented the growth of normal diploid fibroblasts. Variations in the proliferative response induced by rTNF-alpha were apparently not due to differences in either the number of binding sites per cell or their affinity for rTNF-alpha. These observations indicate that the effects of rTNF-alpha on cell growth are not limited to tumor cells, but rather that this protein may have a broad spectrum of activities in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugarman, B J -- Aggarwal, B B -- Hass, P E -- Figari, I S -- Palladino, M A Jr -- Shepard, H M -- New York, N.Y. -- Science. 1985 Nov 22;230(4728):943-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3933111" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/*drug effects ; Cell Line ; Cell Survival/drug effects ; Cell Transformation, Neoplastic/pathology ; Drug Synergism ; Glycoproteins/*pharmacology ; Humans ; Interferon-gamma/pharmacology ; Mice ; Recombinant Proteins/*pharmacology ; Tumor Necrosis Factor-alpha
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  • 24
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    Reversal of oncogenesis by the expression of a major histocompatibility complex class I gene (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-05
    Description: The classical transplantation antigens (the major histocompatibility complex class I antigens) play a key role in host defense against cells expressing foreign antigens. Several naturally occurring tumors and virally transformed cells show an overall suppression of these surface antigens. Since the class I molecules are required in the presentation of neoantigens on tumor cells to the cytotoxic T lymphocytes, their absence from the cell surface may lead to the escape of these tumors from immunosurveillance. To test this possibility, a functional class I gene was transfected into human adenovirus 12-transformed mouse cells that do not express detectable levels of class I antigens; the transformants were tested for expression of the transfected gene and for changes in oncogenicity. The expression of a single class I gene, introduced by DNA-mediated gene transfer into highly tumorigenic adenovirus 12-transformed cells, was sufficient to abrogate the oncogenicity of these cells. This finding has important implications for the regulation of the malignant phenotype in certain tumors and for the potential modulation of oncogenicity through derepression of the endogenous class I genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, K -- Isselbacher, K J -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):26-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975631" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; Cell Line ; Immunization ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Neoplasms, Experimental/genetics/*immunology ; Rats
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  • 25
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    Bovine leukemia virus-related antigens in lymphocyte cultures infected with AIDS-associated viruses (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-22
    Description: An earlier finding that lymphocytes from African patients with the acquired immune deficiency syndrome (AIDS) react with rabbit antiserum to purified antigens of bovine leukemia virus (BLV) prompted a study of the possible cross-reactions between a BLV-infected ovine cell line and human lymphocytes inoculated with a strain of lymphadenopathy syndrome-associated virus (LAV). A solid-phase radioimmunoassay was used to detect antigenic markers of the retroviruses. Crude extracts from short-term cultures of lymphocytes infected with LAV bound rabbit antisera to the LAV glycoprotein gp13 (molecular weight 13,000) and the BLV proteins p24 and gp51, but did not bind antibodies to the p24 of human T-cell leukemia virus type I (HTLV-I). Antiserum to LAV gp13 reacted with an ovine cell line producing BLV but also weakly with virus-free ovine cells. Lymphocyte cultures from four African patients with AIDS expressed BLV-related antigens within 6 to 10 days of culture, at the moment when particle-bound reverse transcriptase was produced. BLV-related antigens were induced in lymphocyte cultures from healthy individuals by addition of filtered supernatant or irradiated cells of the original culture. The antisera to BLV used in this study may prove useful for the detection of AIDS-associated viruses in short-term cultures of lymphocytes from AIDS patients or their contacts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thiry, L -- Sprecher-Goldberger, S -- Jacquemin, P -- Cogniaux, J -- Burny, A -- Bruck, C -- Portetelle, D -- Cran, S -- Clumeck, N -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1482-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2579433" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Animals ; Antigens, Viral/analysis/*immunology ; Cell Line ; Cells, Cultured ; Cross Reactions ; Deltaretrovirus/*immunology ; Epitopes/immunology ; Humans ; Leukemia Virus, Bovine/*immunology ; Lymph Nodes/microbiology ; Lymphocytes/immunology/*microbiology ; Radioimmunoassay ; Retroviridae/*immunology ; Sheep ; Viral Proteins/immunology
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  • 26
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    Endogenous anticonvulsant substance in rat cerebrospinal fluid after a generalized seizure (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-31
    Description: Cerebrospinal fluid taken from rats subjected to electroshock-induced seizures and injected into the cerebral ventricles of rats that had not been shocked increased the seizure threshold of the recipients. The anticonvulsant activity of the donor cerebrospinal fluid was antagonized by opioid antagonists and enhanced by peptidase inhibitors. These results suggest the existence of an endogenous anticonvulsant substance in rat cerebrospinal fluid, possibly opioid in nature, which is activated as a consequence of a seizure and which may play a critical role in postseizure inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tortella, F C -- Long, J B -- New York, N.Y. -- Science. 1985 May 31;228(4703):1106-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2986292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticonvulsants/*cerebrospinal fluid ; Electroshock ; Enkephalin, Leucine/analogs & derivatives/pharmacology ; Male ; Naloxone/pharmacology ; Narcotic Antagonists/pharmacology ; Peptide Hydrolases ; Rats ; Rats, Inbred Strains ; Receptors, Opioid/drug effects ; Receptors, Opioid, delta ; Seizures/*cerebrospinal fluid
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  • 27
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    Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-aspartate antagonist (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-08
    Description: The possibility that neuronal damage due to hypoglycemia is induced by agonists acting on the N-methyl-D-aspartate (NMDA) receptor was investigated in the rat caudate nucleus. Local injections of an NMDA receptor antagonist, 2-amino-7-phosphonoheptanoic acid, were performed before induction of 30 minutes of reversible, insulin-induced, hypoglycemic coma. Neuronal necrosis in these animals after 1 week of recovery was reduced 90 percent compared to that in saline-injected animals. The results suggest that hypoglycemic neuronal damage is induced by NMDA receptor agonists, such as the excitatory amino acids or related compounds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wieloch, T -- New York, N.Y. -- Science. 1985 Nov 8;230(4726):681-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996146" target="_blank"〉PubMed〈/a〉
    Keywords: *2-Amino-5-phosphonovalerate/*analogs & derivatives ; Amino Acids/*pharmacology ; Animals ; Aspartic Acid/*analogs & derivatives/antagonists & inhibitors ; Caudate Nucleus/cytology ; Electroencephalography ; Hypoglycemia/*metabolism/pathology ; Male ; N-Methylaspartate ; Necrosis ; Neurons/*drug effects/metabolism/pathology ; Rats ; Rats, Inbred Strains ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/metabolism
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  • 28
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    Human GM-CSF: molecular cloning of the complementary DNA and purification of the natural and recombinant proteins (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-17
    Description: Clones of complementary DNA encoding the human lymphokine known as granulocyte-macrophage colony-stimulating factor (GM-CSF) were isolated by means of a mammalian cell (monkey COS cell) expression screening system. One of these clones was used to produce recombinant GM-CSF in mammalian cells. The recombinant hematopoietin was similar to the natural product that was purified to apparent homogeneity from medium conditioned by a human T-cell line. The human T-cell GM-CSF was found to be 60 percent homologous with the GM-CSF recently cloned from murine lung messenger RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, G G -- Witek, J S -- Temple, P A -- Wilkens, K M -- Leary, A C -- Luxenberg, D P -- Jones, S S -- Brown, E L -- Kay, R M -- Orr, E C -- New York, N.Y. -- Science. 1985 May 17;228(4701):810-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3923623" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; *Cloning, Molecular ; Colony-Stimulating Factors/biosynthesis/*genetics/isolation & purification ; *Dna ; DNA, Recombinant ; *Granulocytes ; Haplorhini ; Humans ; *Macrophages ; RNA, Messenger/genetics ; T-Lymphocytes ; Transfection
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  • 29
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    Transformation of human bronchial epithelial cells transfected by Harvey ras oncogene (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-08
    Description: Transfection of normal human bronchial epithelial (NHBE) cells with a plasmid carrying the ras oncogene of Harvey murine sarcoma virus (v-Ha ras) changed the growth requirements, terminal differentiation, and tumorigenicity of the recipient cells. One of the cell lines isolated after transfection (TBE-1) was studied extensively and shown to contain v-Ha ras DNA. Total cellular RNA from TBE-1 cells hybridized to v-Ha ras structural gene fragment probes five to eight times more than RNA from parental NHBE cells. The TBE-1 cells expressed phosphorylated v-Ha ras polypeptide p21, showed a reduced requirement for growth-factor supplements, and became aneuploid as an early cellular response to v-Ha ras expression. As the transfectants acquire an indefinite life-span and anchorage independence they became transplantable tumor cells and showed many phenotypic changes suggesting a pleiotropic mechanism for the role of Ha ras in human carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoakum, G H -- Lechner, J F -- Gabrielson, E W -- Korba, B E -- Malan-Shibley, L -- Willey, J C -- Valerio, M G -- Shamsuddin, A M -- Trump, B F -- Harris, C C -- New York, N.Y. -- Science. 1985 Mar 8;227(4691):1174-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bronchi/*cytology/microbiology ; Carcinoma, Bronchogenic/genetics ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; *Cell Transformation, Viral ; Culture Media ; DNA, Neoplasm/genetics ; Epithelial Cells ; Epithelium/microbiology ; Humans ; Lung Neoplasms/genetics ; Mice ; Mice, Nude ; Nucleic Acid Hybridization ; *Oncogenes ; Rats ; *Transfection
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  • 30
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    Expression of Plasmodium falciparum circumsporozoite proteins in Escherichia coli for potential use in a human malaria vaccine (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-24
    Description: The circumsporozoite (CS) protein of the human malaria parasite Plasmodium falciparum may be the most promising target for the development of a malaria vaccine. In this study, proteins composed of 16, 32, or 48 tandem copies of a tetrapeptide repeating sequence found in the CS protein were efficiently expressed in the bacterium Escherichia coli. When injected into mice, these recombinant products resulted in the production of high titers of antibodies that reacted with the authentic CS protein on live sporozoites and blocked sporozoite invasion of human hepatoma cells in vitro. These CS protein derivatives are therefore candidates for a human malaria vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, J F -- Hockmeyer, W T -- Gross, M -- Ballou, W R -- Wirtz, R A -- Trosper, J H -- Beaudoin, R L -- Hollingdale, M R -- Miller, L H -- Diggs, C L -- New York, N.Y. -- Science. 1985 May 24;228(4702):958-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2988125" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Formation ; Antigens, Surface/genetics/*immunology ; Carcinoma, Hepatocellular ; Cell Line ; Cloning, Molecular ; Cross Reactions ; DNA, Recombinant ; Escherichia coli/genetics ; Humans ; Liver Neoplasms ; Malaria/*prevention & control ; Mice ; Plasmodium/immunology ; Plasmodium falciparum/genetics/*immunology/physiology ; *Protozoan Proteins ; Vaccines/*immunology
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  • 31
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    Regional myocardial substrate uptake in hypertensive rats: a quantitative autoradiographic measurement (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-22
    Description: Severe hypertension causes global and regional changes in myocardial perfusion and substrate utilization. Regional perfusion and fatty acid utilization were evaluated by dual-tracer autoradiography in normotensive and hypertensive rats of the Dahl strain. The regional distributions of perfusion and fatty acid utilization were homogeneous in normotensive rats. Severe hypertension was associated with a homogeneous pattern of regional perfusion, but fatty acid utilization was focally decreased in the free wall of the left ventricle. The decrease in fatty acid uptake was associated with a concomitant increase in glucose utilization. These findings suggest that severe hypertension is associated with uniform myocardial perfusion and focal alterations in the substrates used for the performance of myocardial work.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yonekura, Y -- Brill, A B -- Som, P -- Yamamoto, K -- Srivastava, S C -- Iwai, J -- Elmaleh, D R -- Livni, E -- Strauss, H W -- Goodman, M M -- HL29636/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1494-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Deoxyglucose/analogs & derivatives/metabolism ; Endocardium/metabolism ; Fatty Acids/*metabolism ; Fluorodeoxyglucose F18 ; Glucose/*metabolism ; Heart Septum/metabolism ; Hypertension/*metabolism ; Myocardium/*metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred Strains ; Tissue Distribution
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  • 32
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    Distribution of enkephalin immunoreactivity in germinative cells of developing rat cerebellum (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-01
    Description: The cellular distribution of enkephalin, an endogenous opioid, in the developing rat cerebellum was determined by immunocytochemistry. Methionine and leucine enkephalin were concentrated in the external germinal layer, a matrix of proliferative cells; staining was confined to the cortical cytoplasm. Enkephalin was not detected by immunocytochemistry in differentiated neural cells. These results indicate that endogenous opioids are involved specifically in early phases of nervous system development, particularly cell proliferation and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zagon, I S -- Rhodes, R E -- McLaughlin, P J -- NS-20500/NS/NINDS NIH HHS/ -- NS-20623/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 1;227(4690):1049-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3883485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cerebellum/cytology/*growth & development/physiology ; Enkephalin, Leucine/immunology/physiology ; Enkephalin, Methionine/immunology/physiology ; Enkephalins/immunology/*physiology ; Fluorescent Antibody Technique ; Rats ; Rats, Inbred Strains
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  • 33
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    Superinduction of c-fos by nerve growth factor in the presence of peripherally active benzodiazepines (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-09-20
    Description: Alterations in proto-oncogene expression after stimulation of rat pheochromocytoma (PC12) cells by nerve growth factor (NGF) have been investigated. A specific stimulation of c-fos messenger RNA and protein was detected 30 minutes after treatment. This induction was enhanced more than 100-fold in the presence of peripherally active benzodiazepines. The effect was specific as very little change was observed in the levels of c-rasHa, c-rasKi, c-myc, and N-myc messenger RNA's. Under the conditions used here, NGF treatment ultimately results in neurite outgrowth, with a reduction or cessation of cell division. Thus, stimulation of the c-fos gene in this system appeared to be associated with differentiation and not with cellular proliferation. The effect of benzodiazepines was stereospecific and represents a novel action of these compounds at the level of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curran, T -- Morgan, J I -- New York, N.Y. -- Science. 1985 Sep 20;229(4719):1265-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4035354" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepines/*pharmacology ; Cell Line ; Cell Transformation, Neoplastic/drug effects ; Gene Expression Regulation/*drug effects ; Nerve Growth Factors/*pharmacology ; *Oncogenes ; Pheochromocytoma/genetics/metabolism ; RNA, Messenger/biosynthesis ; Rats
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  • 34
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    Plasticity of hippocampal circuitry in Alzheimer's disease (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-12-06
    Description: Two markers of neuronal plasticity were used to compare the response of the human central nervous system to neuronal loss resulting from Alzheimer's disease with the response of rats to a similar neuronal loss induced by lesions. In rats that had received lesions of the entorhinal cortex, axon sprouting of commissural and associational fibers into the denervated molecular layer of the dentate gyrus was paralleled by a spread in the distribution of tritiated kainic acid-binding sites. A similar expansion of kainic acid receptor distribution was observed in hippocampal samples obtained postmortem from patients with Alzheimer's disease. An enhancement of acetylcholinesterase activity in the dentate gyrus molecular layer, indicative of septal afferent sprouting, was also observed in those patients with a minimal loss of cholinergic neurons. These results are evidence that the central nervous system is capable of a plastic response in Alzheimer's disease. Adaptive growth responses occur along with the degenerative events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geddes, J W -- Monaghan, D T -- Cotman, C W -- Lott, I T -- Kim, R C -- Chui, H C -- AG00538/AG/NIA NIH HHS/ -- MH 19691/MH/NIMH NIH HHS/ -- P50AG5142/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1179-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4071042" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/metabolism ; Alzheimer Disease/*pathology ; Animals ; Hippocampus/enzymology/*pathology ; Humans ; Kainic Acid/metabolism ; Male ; *Neuronal Plasticity ; Neurons/pathology ; Rats ; Rats, Inbred Strains
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  • 35
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    Contribution of promoter to tissue-specific expression of the mouse immunoglobulin kappa gene (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-09-13
    Description: The immunoglobulin kappa (kappa) gene promoter was activated by a "neutral" enhancer derived from Harvey murine sarcoma virus (HaMuSV) in immunoglobulin-producing myeloma cells, regardless of the enhancer's orientation or position in the vector. In one fibroblast line (3T3) the immunoglobulin kappa gene promoter was completely inactive when linked to the HaMuSV enhancer, whereas in mouse L cells, promoter activity was observed only with the HaMuSV enhancer in tandem with the immunoglobulin kappa gene promoter. The differential behavior of the gene promoter, when activated by a neutral enhancer in these three murine cell lines, suggests that promoter sequences contribute to the tissue-specific expression of this gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gopal, T V -- Shimada, T -- Baur, A W -- Nienhuis, A W -- New York, N.Y. -- Science. 1985 Sep 13;229(4718):1102-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994213" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Viral ; Fibroblasts/analysis ; *Gene Expression Regulation ; Immunoglobulin Light Chains/*genetics ; Immunoglobulin kappa-Chains/*genetics ; Mice ; Multiple Myeloma/metabolism ; *Operon ; Sarcoma Viruses, Murine
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    The insulin receptor contains a calmodulin-binding domain (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-15
    Description: Substantial evidence suggests that calcium has a pivotal role in regulating the initial events through which insulin alters plasma membrane metabolism. Because binding of insulin to its receptor represents the initial site of insulin action in the plasma membrane, studies were undertaken to determine whether the insulin receptor is a calmodulin-binding protein. Preparations enriched in the insulin receptor and calmodulin-binding proteins were isolated from detergent-solubilized rat adipocyte membranes by chromatography with wheat germ agglutinin agarose and calmodulin-conjugated Sepharose, respectively. Substantial purification of a manganese-dependent, insulin-sensitive phosphoprotein of 95K identified as the beta subunit of the insulin receptor was accomplished. Binding and photocovalent cross-linking of iodine-125-labeled calmodulin to these affinity-purified preparations and to isolated plasma membranes, followed by immunoadsorption with insulin receptor antibodies bound to protein A Sepharose, resulted in significant purification of a binding complex of 110K to 140K. These results indicate that the adipocyte insulin receptor or a polypeptide closely associated with the receptor is a calmodulin-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graves, C B -- Goewert, R R -- McDonald, J M -- AM-25897/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Nov 15;230(4727):827-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3904001" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology ; Animals ; Calmodulin/metabolism ; Calmodulin-Binding Proteins/isolation & purification/*metabolism ; Cell Membrane/metabolism ; Insulin/metabolism ; Phosphorylation ; Rats ; Receptor, Insulin/isolation & purification/*metabolism
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  • 37
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    cis- and trans-acting transcriptional regulation of visna virus (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-08-02
    Description: Visna virus is a pathogenic lentivirus of sheep that is related to human T-cell lymphotropic virus type III (HTLV-III), the probable etiologic agent of the acquired immune deficiency syndrome (AIDS). The transcriptional activity of visna virus promoter and enhancer sequences was studied by means of an assay based on the transient expression of the bacterial gene chloramphenicol acetyltransferase (CAT). The results suggest that the high level of expression of visna virus is due in part to cis-acting enhancer sequences that give the viral promoter a high level of transcriptional activity. In addition, the rate of transcription from the visna virus promoter situated in a plasmid expressing the CAT gene was much greater in infected than uninfected cells. This phenomenon of trans-acting transcriptional activation may involve either virally or cellularly encoded factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hess, J L -- Clements, J E -- Narayan, O -- NS-15721/NS/NINDS NIH HHS/ -- NS-16145/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 2;229(4712):482-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990051" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Base Sequence ; Cell Line ; Chloramphenicol O-Acetyltransferase ; Choroid Plexus ; Chromosome Mapping ; Enhancer Elements, Genetic ; *Genes, Regulator ; Goats ; Humans ; L Cells (Cell Line) ; Macrophages ; Mice ; Plasmids ; Promoter Regions, Genetic ; Sheep ; Synovial Membrane ; T-Lymphocytes ; *Transcription, Genetic ; Transfection ; Visna-maedi virus/*genetics
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  • 38
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    Effect of vanadate on elevated blood glucose and depressed cardiac performance of diabetic rats (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-22
    Description: The trace element vanadium has an unclear biological function. Vanadate, an oxidized form of vanadium, appears to have an insulin-like action. The effect of vanadate on blood glucose and cardiac performance was assessed in female Wistar rats 6 weeks after they were made diabetic with streptozotocin. When vanadate was administered for a 4-week period to the diabetic rats, their blood glucose was not significantly different from that of nondiabetic controls despite a low serum insulin. In contrast, blood glucose was increased about threefold in the diabetic rats that were not treated with vanadate; these rats also had low insulin levels. Cardiac performance was depressed in the untreated diabetic animals, but the cardiac performance of the vanadate-treated diabetic animals was not significantly different from that of nondiabetic controls. Thus vanadate controlled the high blood glucose and prevented the decline in cardiac performance due to diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heyliger, C E -- Tahiliani, A G -- McNeill, J H -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1474-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3156405" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/*analysis ; Calcium-Transporting ATPases/antagonists & inhibitors ; Diabetes Mellitus, Experimental/blood/*physiopathology ; Drinking ; Female ; Insulin/blood ; Myocardial Contraction/*drug effects ; Myocardium/enzymology ; Rats ; Rats, Inbred Strains ; Sarcoplasmic Reticulum/enzymology ; Vanadates ; Vanadium/*pharmacology
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  • 39
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    The human gene encoding GM-CSF is at 5q21-q32, the chromosome region deleted in the 5q- anomaly (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-12-13
    Description: Human granulocyte-macrophage colony-stimulating factor (GM-CSF) is a 22,000-dalton glycoprotein that stimulates the growth of myeloid progenitor cells and acts directly on mature neutrophils. A full-length complementary DNA clone encoding human GM-CSF was used as a probe to screen a human genomic library and isolate the gene encoding human GM-CSF. The human GM-CSF gene is approximately 2.5 kilobase pairs in length with at least three intervening sequences. The GM-CSF gene was localized by somatic cell hybrid analysis and in situ hybridization to human chromosome region 5q21-5q32, which is involved in interstitial deletions in the 5q- syndrome and acute myelogenous leukemia. An established, human promyelocytic leukemia cell line, HL60, contains a rearranged, partially deleted GM-CSF allele and a candidate 5q- marker chromosome, indicating that the truncated GM-CSF allele may reside at the rejoining point for the interstitial deletion on the HL60 marker chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huebner, K -- Isobe, M -- Croce, C M -- Golde, D W -- Kaufman, S E -- Gasson, J C -- CA-10805/CA/NCI NIH HHS/ -- CA-16685/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Dec 13;230(4731):1282-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2999978" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia/genetics ; Base Sequence ; Cell Line ; Chromosome Aberrations/*genetics ; Chromosome Deletion ; Chromosome Disorders ; Chromosome Mapping ; *Chromosomes, Human, 4-5 ; Colony-Stimulating Factors/*genetics ; DNA Restriction Enzymes ; Genes ; Granulocytes ; Humans ; Leukemia, Myeloid, Acute/genetics ; Macrophages ; Syndrome
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  • 40
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    Partial primary structure of the alpha and beta chains of human tumor T-cell receptors (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-01-18
    Description: The T-cell receptor for antigen (Ti) was purified from the human tumor cell line HPB-ALL. Amino-terminal sequence analysis of an acid-cleaved peptide of the Ti alpha chain showed that it is highly homologous to a putative murine alpha chain recently described. Amino-terminal sequence analysis of the Ti beta chain revealed that it shares 50 percent homology with the Ti beta chain amino acid sequences from two other human T-cell tumors. Nucleotide sequence analysis of a complementary DNA clone encoding the Ti beta chain from the HPB-MLT cell line showed that this chain represents a second human constant region gene segment and suggested that it arises from direct joining of the variable and joining gene segments without any intervening D region sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, N -- Leiden, J -- Dialynas, D -- Fraser, J -- Clabby, M -- Kishimoto, T -- Strominger, J L -- Andrews, D -- Lane, W -- Woody, J -- 5 R01 AI15669/AI/NIAID NIH HHS/ -- AI10736/AI/NIAID NIH HHS/ -- Y001CP00502/CP/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 18;227(4684):311-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3871253" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Humans ; Immunoglobulin Constant Regions/genetics ; Leukemia, Lymphoid/immunology ; Lymphoma/immunology ; Mice ; Nucleic Acid Hybridization ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/*immunology
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    Control of cytochrome P1-450 gene expression by dioxin (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-22
    Description: The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may produce its effects by altering gene expression in susceptible cells. In mouse hepatoma cells, TCDD induces the transcription of the cytochrome P1-450 gene, whose product, aryl hydrocarbon hydroxylase, contributes both to the detoxification and to the metabolic activation of carcinogenic polycyclic aromatic hydrocarbons. A DNA fragment containing sequences flanking the 5' end of the cytochrome P1-450 gene was isolated and analyzed. This DNA fragment contains a cis-acting control element with at least three functional domains: a putative promoter, an inhibitory domain upstream from the promoter that blocks its function, and a TCDD-responsive domain still farther (1265 to 1535 base pairs) upstream of the promoter. These findings, together with results from earlier studies, imply that transcription of the cytochrome P1-450 gene is under both positive and negative control by at least two trans-acting regulatory factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, P B -- Galeazzi, D R -- Fisher, J M -- Whitlock, J P Jr -- CA09302/CA/NCI NIH HHS/ -- CA32786/CA/NCI NIH HHS/ -- GM07149/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1499-502.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856321" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/biosynthesis/genetics ; Animals ; Cell Line ; Chloramphenicol O-Acetyltransferase ; Cytochrome P-450 Enzyme System/*genetics ; DNA, Recombinant ; Dioxins/*pharmacology ; Enzyme Induction ; Gene Expression Regulation/*drug effects ; *Genes, Regulator ; Liver Neoplasms, Experimental ; Mice ; *Promoter Regions, Genetic ; Tetrachlorodibenzodioxin/*pharmacology ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; Transfection
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  • 42
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    Human dioxin-inducible cytochrome P1-450: complementary DNA and amino acid sequence (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-05
    Description: Induction of cytochrome P1-450 has been linked to susceptibility to certain chemically induced cancers in mouse and man. Treatment of the human cell line MCF-7 with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in high levels of aryl hydrocarbon (benzo[a]pyrene) hydroxylase (P1-450) activity. This cell line was used to isolate a human P1-450 full-length complementary DNA (cDNA) clone. The cDNA is 2566 nucleotides in length, encodes a polyadenylated messenger RNA (2.8 kilobases in length), and has a continuous reading frame producing a protein with 512 residues (molecular weight, 58,151). The human P1-450 cDNA and protein are 63 percent and 80 percent similar to mouse P1-450 cDNA and protein, respectively. Whereas the mouse TCDD-inducible P-450 gene subfamily has two members (P1-450 and P3-450), the human TCDD-inducible gene subfamily appears to have only one gene (P1-450).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaiswal, A K -- Gonzalez, F J -- Nebert, D W -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):80-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838385" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carcinogens/pharmacology ; Cell Line ; Cricetinae ; Cytochrome P-450 Enzyme System/*genetics ; DNA/*genetics ; Dioxins/*pharmacology ; Enzyme Induction ; Humans ; Mice ; Nucleic Acid Hybridization ; Rabbits ; Tetrachlorodibenzodioxin/*pharmacology
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  • 43
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    Transfection of v-rasH DNA into MCF-7 human breast cancer cells bypasses dependence on estrogen for tumorigenicity (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-10
    Description: The natural history of estrogen-responsive breast cancers often involves a phenotypic change to an estrogen-unresponsive, more aggressive tumor. The human breast cancer cell line, MCF-7, which requires estradiol for tumor formation in vivo and shows growth stimulation in response to estradiol in vitro, is a model for hormone-responsive tumors. The v-rasH onc gene was transfected into MCF-7 cells. The cloned MCF-7ras transfectants, which expressed the v-rasH messenger RNA and v-rasH p21 protein (21,000 daltons), were characterized. In contrast to the parental cell line, MCF-7ras cells no longer responded to exogenous estrogen in culture and their growth was minimally inhibited by exogenous antiestrogens. When tested in the nude mouse, the MCF-7ras cells were fully tumorigenic in the absence of estrogen supplementation. Thus, cells acquiring an activated onc gene can bypass the hormonal regulatory signals that trigger the neoplastic growth of a human breast cancer cell line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, A -- Lippman, M E -- Papageorge, A G -- Lowy, D R -- Gelmann, E P -- New York, N.Y. -- Science. 1985 May 10;228(4700):725-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4039465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/chemically induced/*genetics ; Cell Line ; Cell Transformation, Neoplastic/*chemically induced ; DNA, Neoplasm/genetics ; Estrogens/*pharmacology ; Female ; Humans ; Mice ; Mice, Nude ; Neoplasms, Experimental/chemically induced/genetics ; *Oncogenes ; Pyrrolidines/pharmacology ; Repetitive Sequences, Nucleic Acid ; Thiophenes/pharmacology ; *Transfection
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  • 44
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    Molecular cloning of a complementary DNA encoding human macrophage-specific colony-stimulating factor (CSF-1) (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-18
    Description: Complementary DNA (cDNA) clones encoding human macrophage-specific specific colony-stimulating factor (CSF-1) were isolated. One cDNA clone codes for a mature polypeptide of 224 amino acids and a putative leader of 32 amino acids. This cDNA, which was cloned in the Okayama-Berg expression vector, specifies the synthesis of biologically active CSF-1 in COS cells, as determined by a specific radioreceptor assay, macrophage bone marrow colony formation, and antibody neutralization. Most of the cDNA isolates contain part of an intron sequence that changes the reading frame, resulting in an abrupt termination of translation; these cDNA's were inactive in COS cells. The CSF-1 appears to be encoded by a single-copy gene, but its expression results in the synthesis of several messenger RNA species, ranging in size from about 1.5 to 4.5 kilobases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawasaki, E S -- Ladner, M B -- Wang, A M -- Van Arsdell, J -- Warren, M K -- Coyne, M Y -- Schweickart, V L -- Lee, M T -- Wilson, K J -- Boosman, A -- C32551/PHS HHS/ -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):291-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996129" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; *Cloning, Molecular ; Colony-Stimulating Factors/*genetics ; DNA/*metabolism ; DNA Restriction Enzymes ; *Genes ; Humans ; Macrophages/*metabolism ; Pancreatic Neoplasms ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 45
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    Pathways of protein secretion in eukaryotes (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-10-04
    Description: Protein secretion from cells can take several forms. Secretion is constitutive if proteins are secreted as fast as they are synthesized. In regulated secretion newly synthesized proteins destined for secretion are stored at high concentration in secretory vesicles until the cell receives an appropriate stimulus. When both constitutive and regulated protein secretion can take place in the same cell a mechanism must exist for sorting the correct secretory protein into the correct secretory vesicle. The secretory vesicle must then be delivered to the appropriate region of plasma membrane. Transfection of DNA encoding foreign secretory proteins into regulated secretory cells has provided insight into the specificity of sorting into secretory vesicles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelly, R B -- New York, N.Y. -- Science. 1985 Oct 4;230(4721):25-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994224" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/secretion ; Animals ; Calcium/metabolism ; Calmodulin/metabolism ; Carrier Proteins/physiology ; Cell Compartmentation ; Cell Fusion ; Cell Line ; Cells/*secretion ; Cytoplasmic Granules/metabolism ; Eukaryotic Cells/cytology/*secretion ; Exocytosis ; Golgi Apparatus/ultrastructure ; Half-Life ; Leukemia Virus, Murine/genetics ; Lysosomes/enzymology ; Membrane Proteins/genetics/metabolism ; Microscopy, Electron ; Models, Biological ; Peptide Hydrolases/metabolism ; Pituitary Gland/cytology ; Pro-Opiomelanocortin/secretion ; Proteins/*secretion ; Transfection
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  • 46
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    Amplification of a novel v-erbB-related gene in a human mammary carcinoma (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-06
    Description: The cellular gene encoding the receptor for epidermal growth factor (EGF) has considerable homology to the oncogene of avian erythroblastosis virus. In a human mammary carcinoma, a DNA sequence was identified that is related to v-erbB but amplified in a manner that appeared to distinguish it from the gene for the EGF receptor. Molecular cloning of this DNA segment and nucleotide sequence analysis revealed the presence of two putative exons in a DNA segment whose predicted amino acid sequence was closely related to, but different from, the corresponding sequence of the erbB/EGF receptor. Moreover, this DNA segment identified a 5-kilobase transcript distinct from the transcripts of the EGF receptor gene. Thus, a new member of the tyrosine kinase proto-oncogene family has been identified on the basis of its amplification in a human mammary carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, C R -- Kraus, M H -- Aaronson, S A -- New York, N.Y. -- Science. 1985 Sep 6;229(4717):974-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2992089" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Breast Neoplasms/*genetics ; Cell Line ; Cloning, Molecular ; DNA, Neoplasm/*genetics ; Female ; *Gene Amplification ; Gene Expression Regulation ; Humans ; *Oncogenes ; Protein Kinases/*genetics ; Protein-Tyrosine Kinases ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/*genetics
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  • 47
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    Insertion mutagenesis of embryonal carcinoma cells by retroviruses (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-03
    Description: Mutagenesis was studied in cultured F9 embryonal carcinoma cells infected with a variant of Moloney murine leukemia virus. Proviral insertion induced the inactivation of the hypoxanthine phosphoribosyltransferase locus, and the virus was used to isolate the mutated genes rapidly. Mutagenesis by these methods may be useful for the genetic dissection of the various mammalian cell phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, W -- Patel, M D -- Lobel, L I -- Goff, S P -- Nguyen-Huu, M C -- New York, N.Y. -- Science. 1985 May 3;228(4699):554-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; DNA/genetics ; DNA, Neoplasm/genetics ; DNA, Recombinant/metabolism ; DNA, Viral/genetics ; Mice ; Moloney murine leukemia virus/physiology ; *Mutation ; Nucleic Acid Hybridization ; Rats ; Retroviridae/*physiology ; Teratoma/*genetics/microbiology
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  • 48
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    Platelet-mediated cholesterol accumulation in cultured aortic smooth muscle cells (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-08
    Description: Cholesterol accumulates within smooth muscle cells and macrophages in atherosclerotic lesions, thereby contributing to the progressive enlargement of these lesions. The mechanism of this cellular accumulation of cholesterol is not known. The possibility that platelets may have a role in the cellular cholesterol accumulation that occurs during atherogenesis was investigated. Incubation of thrombin-activated washed rat platelets (or platelet-free supernatants prepared from thrombin-activated platelets) with cultured rat aortic smooth muscle cells induced cholesteryl ester lipid droplet accumulation within the smooth muscle cells. No cholesteryl ester lipid droplets accumulated when smooth muscle cells were incubated with unactivated platelets. Smooth muscle cell lipid droplet accumulation occurred in the absence of serum lipoproteins and was not inhibited by mevinolin, a drug that blocks cholesterol synthesis. These findings suggest that activated platelets may release cholesterol, which can be accumulated by cells and stored as lipid droplets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kruth, H S -- New York, N.Y. -- Science. 1985 Mar 8;227(4691):1243-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/physiopathology ; Arteriosclerosis/*physiopathology ; Blood Platelets/*physiology ; Cells, Cultured ; Cholesterol/*physiology ; Male ; Muscle, Smooth, Vascular/*cytology/physiopathology ; Platelet Aggregation ; Rats ; Rats, Inbred Strains ; Thrombin/physiology
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  • 49
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    Antibodies to peptides detect new hepatitis B antigen: serological correlation with hepatocellular carcinoma (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-25
    Description: The expression of a previously unidentified gene product, encoded by the hepatitis B virus (HBV) genome, has been achieved with a recombinant SV40 expression vector. Antibodies against synthetic peptides representing defined regions of this protein were used to screen cells infected with recombinant virus as well as tissues naturally infected with HBV. A 24,000-dalton protein (p24) was detected in cells infected with recombinant virus and a 28,000-dalton protein (p28) was detected in tissues infected with HBV. The peptides or recombinant-derived protein were used as antigens to screen sera from individuals infected with HBV. Specific antibodies were detected predominantly in sera from patients with hepatocellular carcinoma. The presence of p28 in tissues infected with HBV and the appearance of specific antibodies in infectious sera establish the existence of an additional marker for HBV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moriarty, A M -- Alexander, H -- Lerner, R A -- Thornton, G B -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):429-33.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2981434" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Hepatocellular/diagnosis/*immunology ; Cell Line ; Cloning, Molecular ; Enzyme-Linked Immunosorbent Assay ; Genetic Vectors ; Hepatitis B/diagnosis/*immunology ; Hepatitis B Antibodies/*analysis/immunology ; Hepatitis B Antigens/*analysis/immunology ; Humans ; Liver/*immunology ; Liver Neoplasms/diagnosis/*immunology ; Molecular Weight ; Peptides/immunology ; Simian virus 40/genetics ; Viral Proteins/immunology
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  • 50
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    Reexamination of glucose-6-phosphatase activity in the brain in vivo: no evidence for a futile cycle (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-05
    Description: Glucose-6-phosphatase activity in the rat brain in vivo was estimated by measuring the differential loss of tritium and carbon-14 from the glucose pool labeled by a mixture of [2-3H]glucose and [U-14C]glucose. The results provide no evidence of significant dephosphorylation of glucose-6-phosphate and do not support the hypothesis of a futile cycle involving glucose-6-phosphatase activity in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, T -- Lucignani, G -- Atlas, S -- Crane, A M -- Dienel, G A -- Sokoloff, L -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):60-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Glucose/metabolism ; Glucose-6-Phosphatase/*metabolism ; Glucosephosphates/*metabolism ; Glycolysis ; Male ; Rats ; Rats, Inbred Strains
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  • 51
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    Enhanced transcription of c-myc in bursal lymphoma cells requires continuous protein synthesis (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-06
    Description: In several bursal lymphoma cell lines in which c-myc transcription is regulated by avian leukosis virus (ALV) long terminal repeat (LTR) sequences, protein synthesis inhibition decreases the transcriptional activity of c-myc as well as other LTR driven viral genes. This decrease in transcription is associated with a change in the chromatin structure of c-myc, as measured by deoxyribonuclease I (DNase I) hypersensitivity, and a shift of transcription from the LTR to the normal c-myc promoter. In contrast, cycloheximide had little or no effect on the transcription of LTR driven genes in infected chicken embryo fibroblasts treated with the drug. These results suggest that a labile, cell type-specific protein may interact with the retroviral LTR and regulate transcription of genes under LTR control. Further, the results demonstrate that the increase in intracellular concentration of c-myc RNA induced by cycloheximide treatment of normal cells is the result of stabilization of this message.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linial, M -- Gunderson, N -- Groudine, M -- CA 18282/CA/NCI NIH HHS/ -- CA 28151/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1126-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2999973" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Leukosis/genetics ; Avian Leukosis Virus ; Bursa of Fabricius/cytology ; Cell Line ; Chick Embryo ; Chickens ; Chromatin/drug effects ; Cycloheximide/pharmacology ; Dactinomycin/pharmacology ; Emetine/pharmacology ; Lymphoma/*genetics ; Neoplasm Proteins/*biosynthesis ; *Oncogenes ; RNA, Neoplasm/metabolism ; Repetitive Sequences, Nucleic Acid ; *Transcription, Genetic/drug effects
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  • 52
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    Blood-brain barrier: endogenous modulation by adrenal-cortical function (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-29
    Description: The blood-brain barrier restricts the passage of molecules from the blood to the brain. The permeability of the barrier to iodine-125-labeled bovine serum albumin was examined in rats that had undergone adrenalectomy, adrenal demedullation, and corticosterone replacement. Adrenalectomy, but not adrenal demedullation, increased the permeability of brain tissue to the isotopically labeled macromolecule; corticosterone replacement reversed this effect. These results indicate that the blood-brain barrier may be hormonally regulated; that is, the pituitary-adrenal axis may physiologically modulate the permeability of the brain microvasculature to macromolecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, J B -- Holaday, J W -- New York, N.Y. -- Science. 1985 Mar 29;227(4694):1580-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975627" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/*physiology ; Adrenal Medulla/physiology ; Adrenalectomy ; Animals ; Blood Pressure ; *Blood-Brain Barrier ; Central Nervous System/physiology ; Corticosterone/blood/physiology ; Male ; Pituitary-Adrenal System/physiology ; Rats ; Rats, Inbred Strains ; Serum Albumin, Bovine/metabolism
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  • 53
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    Site-specific increased phosphorylation of pp60v-src after treatment of RSV-transformed cells with a tumor promoter (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-09-27
    Description: When vole cells that had been transformed by Rous sarcoma virus were treated with the tumor-promoting phorbol ester 12-O-tetradecanoyl-13-acetate (TPA), specific phosphorylation of pp60v-src was increased. Partial V8 protease mapping indicated that the increased phosphorylation occurred exclusively on serine residues located in the amino terminus of the molecule. Treatment of cells with dimethyl sulfoxide or 4 alpha-phorbol-12,13-didecanoate did not elicit this response. Two-dimensional tryptic phosphopeptide mapping of pp60v-src immunoprecipitated from untreated and TPA-treated cells indicated that a specific tryptic amino-terminal peptide was hyperphosphorylated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Purchio, A F -- Shoyab, M -- Gentry, L E -- New York, N.Y. -- Science. 1985 Sep 27;229(4720):1393-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994221" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arvicolinae ; Carcinogens/*pharmacology ; Cell Transformation, Neoplastic/metabolism ; Cells, Cultured ; Dimethyl Sulfoxide/pharmacology ; Mice ; Mice, Inbred BALB C ; Oncogene Protein pp60(v-src) ; Phorbol Esters/pharmacology ; Phosphorylation ; Protein Kinase C ; Protein Kinases/metabolism ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism ; Sarcoma, Avian/*genetics ; Tetradecanoylphorbol Acetate/pharmacology ; Viral Proteins/*metabolism
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  • 54
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    Ascorbic acid and the behavioral response to haloperidol: implications for the action of antipsychotic drugs (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-25
    Description: Haloperidol, a widely used antipsychotic drug, was tested for its ability to block the behavioral response to amphetamine and to elicit catalepsy in rats treated with saline or ascorbic acid (1000 milligrams per kilogram of body weight). By itself, ascorbic acid failed to exert significant behavioral effects, but it enhanced the antiamphetamine and cataleptogenic effects of haloperidol (0.1 or 0.5 milligrams per kilogram). These results, combined with a growing body of biochemical evidence, suggest that ascorbic acid plays an important role in modulating the behavioral effects of haloperidol and related antipsychotic drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rebec, G V -- Centore, J M -- White, L K -- Alloway, K D -- DA 02451/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):438-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4038426" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ascorbic Acid/*pharmacology ; Behavior, Animal/*drug effects ; Catalepsy/chemically induced ; Dextroamphetamine/pharmacology ; Drug Synergism ; Haloperidol/*pharmacology ; Humans ; Male ; Motor Activity/drug effects ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/metabolism
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  • 55
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    Glucocorticoids potentiate ischemic injury to neurons: therapeutic implications (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-27
    Description: Sustained exposure to glucocorticoids, the adrenocortical stress hormones, is toxic to neurons, and such toxicity appears to play a role in neuron loss during aging. Previous work has shown that glucocorticoids compromise the capacity of neurons to survive a variety of metabolic insults. This report extends those observations by showing that ischemic injury to neurons in rat brain is also potentiated by exposure to high physiological titers of glucocorticoids and is attenuated by adrenalectomy. The synergy between ischemic and glucocorticoid brain injury was seen even when glucocorticoid levels were manipulated after the ischemic insult. Pharmacological interventions that diminish the adrenocortical stress response may improve neurological outcome from stroke or cardiac arrest.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R M -- Pulsinelli, W A -- NS-03346/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 27;229(4720):1397-400.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4035356" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Brain/cytology/drug effects ; Brain Ischemia/metabolism/*physiopathology ; Cerebral Cortex/drug effects ; Cerebrovascular Disorders/physiopathology ; Corpus Striatum/drug effects ; Glucocorticoids/*pharmacology ; Heart Arrest/physiopathology ; Hippocampus/drug effects ; Humans ; Male ; Neurons/*drug effects ; Rats ; Rats, Inbred Strains
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    Molecular cloning of the complementary DNA for human tumor necrosis factor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-12
    Description: Tumor necrosis factor (TNF) is a soluble protein that causes damage to tumor cells but has no effect on normal cells. Human TNF was purified to apparent homogeneity as a 17.3-kilodalton protein from HL-60 leukemia cells and showed cytotoxic and cytostatic activities against various human tumor cell lines. The amino acid sequence was determined for the amino terminal end of the purified protein, and oligodeoxyribonucleotide probes were synthesized on the basis of this sequence. Complementary DNA (cDNA) encoding human TNF was cloned from induced HL-60 messenger RNA and was confirmed by hybrid-selection assay, direct expression in COS-7 cells, and nucleotide sequence analysis. The human TNF cDNA is 1585 base pairs in length and encodes a protein of 233 amino acids. The mature protein begins at residue 77, leaving a long leader sequence of 76 amino acids. Expression of high levels of human TNF in Escherichia coli was accomplished under control of the bacteriophage lambda PL promoter and gene N ribosome binding site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, A M -- Creasey, A A -- Ladner, M B -- Lin, L S -- Strickler, J -- Van Arsdell, J N -- Yamamoto, R -- Mark, D F -- New York, N.Y. -- Science. 1985 Apr 12;228(4696):149-54.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cells, Cultured ; *Cloning, Molecular ; DNA/*genetics ; DNA, Recombinant/metabolism ; Glycoproteins/*genetics/isolation & purification/pharmacology ; Humans ; Leukemia, Myeloid/metabolism ; Mice ; Mice, Nude ; Neoplasms, Experimental/drug therapy ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Rabbits ; Rats ; Tumor Necrosis Factor-alpha ; Xenopus
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    Bovine leukemia virus long terminal repeat: a cell type-specific promoter (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-18
    Description: The functional activity of the promoter unit contained within the long terminal repeat (LTR) of bovine leukemia virus (BLV) was examined by monitoring transient expression of a heterologous gene placed under its control. Various cell lines were transfected with recombinant plasmids carrying the bacterial chloramphenicol acetyltransferase (CAT) gene coupled to the BLV LTR (pBL-cat). Transient expression of CAT activity directed by the BLV LTR was observed only in the established BLV-producer cell lines derived from fetal lamb kidney (FLK) cells and bat lung cells. The amount of CAT activity transiently expressed in FLK-BLV cells was decreased approximately tenfold by deletion of LTR sequences located within a region 100 to 170 nucleotides upstream of the RNA start site. Surprisingly, removal of the region 50 base pairs downstream of the RNA initiation site to the 3'-end of the LTR reduced the expression of CAT activity by 87 percent. The BLV LTR thus appears to be an unusual promoter unit, functioning in a cell type-specific manner and possessing sequences on both the 5' and 3' sides of the RNA start site that influence gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derse, D -- Caradonna, S J -- Casey, J W -- CA07392/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 18;227(4684):317-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2981431" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; Chiroptera ; DNA, Recombinant/metabolism ; Deltaretrovirus/genetics ; Genes, Regulator ; Haplorhini ; Humans ; Leukemia Virus, Bovine/*genetics ; *Promoter Regions, Genetic ; RNA, Viral/*genetics ; *Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics ; Sheep ; Transcription, Genetic
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    Monitoring the time course of cerebral deoxyglucose metabolism by 31P nuclear magnetic resonance spectroscopy (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-14
    Description: The phosphorylation of 2-deoxyglucose by the mammalian brain is used as an index of the brain's energy metabolism. The results of phosphorus-31 nuclear magnetic resonance (31P NMR) monitoring of conscious animals in vivo showed rapid phosphorylation of 2-deoxyglucose by brain tissue. The rate of phosphorylation as determined by 31P NMR was consistent with results achieved by tracer methods using carbon-14-labeled 2-deoxyglucose. However, the disappearance of 2-deoxyglucose-6-phosphate was shown to be faster than that reported by tracer studies and occurred without alterations of intracellular pH and energy homeostasis. These results were confirmed by gas chromatography and mass spectroscopy. It is postulated that 2-deoxyglucose may be metabolized in several ways, including dephosphorylation by a hexose phosphatase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deuel, R K -- Yue, G M -- Sherman, W R -- Schickner, D J -- Ackerman, J J -- AM-20579/AM/NIADDK NIH HHS/ -- GM-30331/GM/NIGMS NIH HHS/ -- RR 00954/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jun 14;228(4705):1329-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4001946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Deoxy Sugars/*metabolism ; Deoxyglucose/*metabolism ; Kinetics ; Magnetic Resonance Spectroscopy ; Phosphorylation ; Rats ; Rats, Inbred Strains
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    Individual tumors of multifocal EB virus-induced malignant lymphomas in tamarins arise from different B-cell clones (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-10
    Description: Cotton-top tamarins were inoculated with sufficient Epstein-Barr virus to induce multiple tumors in each animal within 14 to 21 days. The tumors consisted of large-cell lymphomas that contained multiple copies of the Epstein-Barr virus genome and generated Epstein-Barr virus-carrying cell lines showing no detectable consistent chromosomal abnormality. Hybridization of tumor DNA with immunoglobulin gene probes revealed that each lymphoma was oligo- or monoclonal in origin and that individual tumors from the same animal arose from different B-cell clones. Thus the virus induced multiple transformation events in tamarins in vivo to cause malignant tumors resembling the Epstein-Barr virus-associated lymphomas of patients with organ transplants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cleary, M L -- Epstein, M A -- Finerty, S -- Dorfman, R F -- Bornkamm, G W -- Kirkwood, J K -- Morgan, A J -- Sklar, J -- CA 34233/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 10;228(4700):722-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2986287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*microbiology ; Burkitt Lymphoma/genetics/*microbiology ; Cell Line ; DNA, Neoplasm/genetics ; Heart Transplantation ; Herpesvirus 4, Human ; Humans ; Neoplasms, Experimental/genetics/microbiology ; Nucleic Acid Hybridization ; Saguinus
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    Regional brain dopamine metabolism: a marker for the speed, direction, and posture of moving animals (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-05
    Description: Brain dopamine is necessary for normal movement. To determine whether there is a precise relation between the intensity of movement and changes in brain dopamine metabolism, the investigators ran rats on straight and circular treadmills at different speeds and with different body postures. Concentrations of dopamine and its metabolite 3,4-dihydroxyphenylacetic acid increased in the caudate and accumbens nuclei in direct relation to the speed and angular posture of the animals. Dopamine metabolism in the nucleus accumbens was more strongly linked to the speed and direction of movement, while in the caudate nucleus dopamine and 3,4-dihydroxyphenylacetic acid were affected most by posture and direction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freed, C R -- Yamamoto, B K -- K04-HL 00782/HL/NHLBI NIH HHS/ -- P50 NS 09199/NS/NINDS NIH HHS/ -- R01 NS 18639/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):62-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012312" target="_blank"〉PubMed〈/a〉
    Keywords: 3,4-Dihydroxyphenylacetic Acid/metabolism ; Animals ; Brain/*metabolism ; Caudate Nucleus/metabolism ; Dopamine/*metabolism ; Male ; *Motor Activity ; Nucleus Accumbens/metabolism ; *Posture ; Rats ; Rats, Inbred Strains
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    Gene transfer and expression of human phenylalanine hydroxylase (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-05
    Description: Phenylketonuria (PKU) is caused by a genetic deficiency of the enzyme phenylalanine hydroxylase (PAH). A full-length complementary DNA clone of human PAH was inserted into a eukaryotic expression vector and transferred into mouse NIH3T3 cells which do not normally express PAH. The transformed mouse cells expressed PAH messenger RNA, immunoreactive protein, and enzymatic activity that are characteristic of the normal human liver products, demonstrating that a single gene contains all of the necessary genetic information to code for functional PAH. These results support the use of the human PAH probe in prenatal diagnosis and detection of carriers, to provide new opportunities for the biochemical characterization of normal and mutant enzymes, and in the investigation of alternative genetic therapies for PKU.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledley, F D -- Grenett, H E -- DiLella, A G -- Kwok, S C -- Woo, S L -- HD-06495/HD/NICHD NIH HHS/ -- HD-17711/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):77-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856322" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Molecular ; DNA, Recombinant/metabolism ; *Genetic Engineering ; Humans ; Mice ; Nucleic Acid Hybridization ; Phenylalanine Hydroxylase/*genetics ; Phenylketonurias/diagnosis/genetics ; Prenatal Diagnosis ; Rats
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    Evidence that the v-sis gene product transforms by interaction with the receptor for platelet-derived growth factor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-18
    Description: A scheme for partial purification of biologically active v-sis-coded protein from cells transformed with simian sarcoma virus (SSV) has made possible a functional comparison of the transforming protein with platelet-derived growth factor (PDGF). The SSV-transforming gene product is capable of specifically binding PDGF receptors, stimulating tyrosine phosphorylation of PDGF receptors, and inducing DNA synthesis in quiescent fibroblasts. Each of these activities was specifically inhibited by antibodies to different regions of the v-sis gene product. Moreover, viral infection of a variety of cell types revealed a strict correlation between those cells possessing PDGF receptors and those susceptible to transformation by SSV. These findings provide evidence that SSV-transforming activity is mediated by the interaction of a virus-coded mitogen with PDGF receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leal, F -- Williams, L T -- Robbins, K C -- Aaronson, S A -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):327-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996133" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/metabolism ; Cattle ; Cell Line ; *Cell Transformation, Viral ; Cells, Cultured ; Fibroblasts/metabolism ; *Genes ; *Genes, Viral ; Humans ; Kinetics ; Mink ; Molecular Weight ; Muscle, Smooth/metabolism ; Muscle, Smooth, Vascular/metabolism ; Platelet-Derived Growth Factor/*metabolism ; Receptors, Cell Surface/isolation & purification/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Retroviridae/*genetics ; Sarcoma Virus, Woolly Monkey/*genetics ; Viral Proteins/genetics/*metabolism
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    Localization of the gene encoding the human interleukin-2 receptor on chromosome 10 (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-28
    Description: The human interleukin-2 receptor is an inducible growth factor receptor present on the surface of activated T lymphocytes. The receptor is required for a normal T-cell immune response. High-resolution fluorescence-activated chromosome sorting and DNA spot-blot analysis with complementary DNA's for the interleukin-2 receptor indicated that the receptor gene was located on chromosome 9, 10, 11, or 12. In situ hybridization studies showed that the interleukin-2 receptor gene is on the short arm of chromosome 10, p14----15.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leonard, W J -- Donlon, T A -- Lebo, R V -- Greene, W C -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1547-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3925551" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Chromosomes, Human, 6-12 and X ; DNA/analysis ; Humans ; Lymphocyte Activation ; Male ; Nucleic Acid Hybridization ; Phytohemagglutinins/pharmacology ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-2 ; T-Lymphocytes/analysis/immunology
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    Molecular cloning of a gene sequence regulated by nerve growth factor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-26
    Description: Nerve growth factor (NGF) is essential for the development and differentiation of sympathetic or sensory neurons. A complementary DNA was cloned that corresponds to a gene sequence induced more than 50-fold in a cultured target cell line of pheochromocytoma cells (PC12 cells) 5 hours after the addition of NGF. The induced messenger RNA encodes a 90,000-dalton polypeptide that may represent one of the primary events in NGF-induced differentiation of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levi, A -- Eldridge, J D -- Paterson, B M -- New York, N.Y. -- Science. 1985 Jul 26;229(4711):393-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3839317" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Adrenal Gland Neoplasms/genetics ; Animals ; Base Sequence ; Cell Line ; Chickens ; *Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; *Genes ; Nerve Growth Factors/*physiology ; Nucleic Acid Hybridization ; Pheochromocytoma/genetics ; RNA, Messenger/genetics ; Rabbits ; Rats
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    A specific 37,000-dalton protein that accumulates in regenerating but not in nonregenerating mammalian nerves (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-26
    Description: A 37-kilodalton protein is synthesized at higher rates in the peripheral and central nervous system of newborn rats than in adult animals. As a specific response to denervation, the synthesis of the 37-kilodalton protein is increased in the mature peripheral and central nervous system; however, this protein accumulates only in the peripheral nervous system. The differences in accumulation of the protein correlate with the apparent differences in the ability of peripheral and central axons to regenerate. The synthesis of the 37-kilodalton protein is inhibited when proper innervation or reinnervation is established.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, H W -- Gebicke-Harter, P J -- Hangen, D H -- Shooter, E M -- NS 04270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):499-501.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3983637" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn/physiology ; Axons/physiology ; Brain/physiology ; Central Nervous System/metabolism/*physiology ; Molecular Weight ; *Nerve Regeneration ; Nerve Tissue Proteins/*biosynthesis ; Optic Nerve/physiology ; Peripheral Nerves/metabolism/*physiology ; Photofluorography ; Rats ; Rats, Inbred Strains ; Sciatic Nerve/physiology ; Spinal Cord/physiology
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    The product of the c-fms proto-oncogene: a glycoprotein with associated tyrosine kinase activity (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-04-19
    Description: The c-fms proto-oncogene is a member of a gene family that has been implicated in tumorigenesis. Glycoproteins encoded by c-fms were identified in cat spleen cells by means of an immune-complex kinase assay performed with monoclonal antibodies to v-fms-coded epitopes. The major form of the normal cellular glycoprotein has an apparent molecular weight of 170,000 and, like the product of the viral oncogene, serves as a substrate for an associated tyrosine-specific protein kinase activity in vitro. The results suggest that the transforming glycoprotein specified by v-fms is a truncated form of a c-fms-coded growth factor receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rettenmier, C W -- Chen, J H -- Roussel, M F -- Sherr, C J -- 1 RO1 CA 38187/CA/NCI NIH HHS/ -- RR-05584-20/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):320-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2580348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Cats ; Glycoproteins/immunology/*metabolism ; Humans ; Mice ; Molecular Weight ; Neoplasm Proteins/immunology/*metabolism ; *Oncogenes ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Tyrosine Kinases ; RNA/metabolism ; Rats
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  • 67
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    Patterns of growth hormone-releasing factor and somatostatin secretion into the hypophysial-portal circulation of the rat (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-25
    Description: The interrelation between the secretion of two hypophysiotropic peptides, growth hormone-releasing factor (GRF) and somatostatin (SRIF), in the generation of episodic growth hormone (GH) secretion was inferred from direct measurements of immunoreactive GRF and immunoreactive SRIF concentrations in the hypophysial-portal plasma of the rat. Secretion of immunoreactive GRF was found to be episodic, with maximal concentrations present during periods of expected GH secretory episodes. Secretion of immunoreactive GRF was accompanied by a moderate reduction in portal plasma levels of immunoreactive SRIF. Passive immunoneutralization of SRIF was associated with increased concentrations of immunoreactive GRF in hypophysial-portal plasma. On the basis of these observations, it appears that each GH secretory episode is initiated by pulsatile secretion of immunoreactive GRF into the portal circulation, which is preceded by or is concurrent with a moderate reduction of inhibitory tone provided by portal immunoreactive SRIF. These experiments provide direct insights into central and adenohypophysial mechanisms by which GRF and SRIF interact to generate episodic secretion of GH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plotsky, P M -- Vale, W -- AM26741/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):461-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2864742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Growth Hormone/blood/physiology/secretion ; Growth Hormone-Releasing Hormone/blood/physiology/*secretion ; Immune Sera/immunology ; Male ; Pituitary Gland/blood supply/*physiology ; Pituitary Gland, Anterior/secretion ; Radioimmunoassay ; Rats ; Rats, Inbred Strains ; Sheep/immunology ; Somatostatin/blood/physiology/*secretion
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    Vasopressin-stimulated release of atriopeptin: endocrine antagonists in fluid homeostasis (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-26
    Description: Administration of pharmacological doses of arginine-vasopressin, related peptides, and other pressor agents induced a profound release of atriopeptin immunoreactivity into the circulation. The stimulated release of atriopeptin apparently was related to increased arterial blood pressure. Neither the nonpressor vasopressin analog 1-deamino-D-Arg8-vasopressin nor arginine-vasopressin in the presence of a specific pressor antagonist caused atriopeptin to be released into the circulation. Urine output was correlated with the level of atriopeptin released. Physiological levels of arginine-vasopressin suppress diuresis and produced vasoconstriction. Pharmacological levels of the hormone stimulated the cardiac endocrine system to release atriopeptin, which may cause diuresis and vasodilation to physiologically antagonize the effects of vasopressin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manning, P T -- Schwartz, D -- Katsube, N C -- Holmberg, S W -- Needleman, P -- New York, N.Y. -- Science. 1985 Jul 26;229(4711):395-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990050" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/pharmacology ; Angiotensin II/pharmacology ; Animals ; Arginine Vasopressin/*pharmacology ; *Atrial Function ; Blood Pressure/drug effects ; Deamino Arginine Vasopressin/pharmacology ; Dose-Response Relationship, Drug ; Male ; Muscle Proteins/*secretion ; Oxytocin/pharmacology ; Phenylephrine/pharmacology ; Rats ; Rats, Inbred Strains ; Urodynamics/drug effects ; Water-Electrolyte Balance/*drug effects
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    Loss of M2 muscarine receptors in the cerebral cortex in Alzheimer's disease and experimental cholinergic denervation (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-31
    Description: Cerebral cortex samples from patients with Alzheimer's disease and from rats after experimental cholinergic denervation of the cerebral cortex exhibited reductions in the presynaptic marker choline acetyltransferase activity and in the number of M2 muscarine receptors, with no change in the number of M1 receptors. These results are in keeping with evidence that M2 receptors function in cholinergic nerve terminals to regulate the release of acetylcholine, whereas M1 receptors are located on postsynaptic cells and facilitate cellular excitation. New M1-selective agonists and M2-selective antagonists directed at post- or presynaptic sites deserve consideration as potential agents for the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mash, D C -- Flynn, D D -- Potter, L T -- HLO-7188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1115-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992249" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Alzheimer Disease/*metabolism ; Animals ; Cerebral Cortex/*metabolism ; Choline O-Acetyltransferase/*metabolism ; Cholinergic Fibers/physiology ; Denervation ; Humans ; Male ; Oxotremorine ; Quinuclidinyl Benzilate ; Rats ; Rats, Inbred Strains ; Receptors, Muscarinic/*metabolism ; Synaptic Membranes/*metabolism
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    Involvement of the bcl-2 gene in human follicular lymphoma (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-21
    Description: Recombinant DNA probes were cloned for the areas flanking the breakpoint on chromosome 18 in cells from a patient with acute lymphocytic leukemia of the B-cell type; cells of this line carry the t(14;18) chromosomal translocation. Two of the probes detected DNA rearrangements in approximately 60 percent of the cases of follicular lymphoma screened. In follicular lymphoma, most of the breakpoints in band q21 of chromosome 18 were clustered within a short stretch of DNA, approximately 2.1 kilobases in length. Chromosome 18-specific DNA probes for the areas flanking the breakpoints also detected RNA transcripts 6 kilobases in length in various cell types. The gene coding for these transcript (the bcl-2 gene) seems to be interrupted in most cases of follicular lymphomas carrying the t(14;18) chromosomal translocation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsujimoto, Y -- Cossman, J -- Jaffe, E -- Croce, C M -- CA16685/CA/NCI NIH HHS/ -- CA36521/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 21;228(4706):1440-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3874430" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/ultrastructure ; Cell Line ; *Chromosomes, Human, 16-18 ; Cloning, Molecular ; Humans ; Leukemia, Lymphoid/genetics ; Lymphoma/*genetics ; *Oncogenes ; *Translocation, Genetic
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    Methionine and leucine enkephalin in rat neurohypophysis: different responses to osmotic stimuli and T2 toxin (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-03
    Description: Specific radioimmunoassays were used to measure the effects of hypertonic saline (salt loading), water deprivation, and trichothecene mycotoxin (T2 toxin) on the content of methionine enkephalin (ME), leucine enkephalin (LE), alpha-neoendorphin, dynorphin A, dynorphin B, vasopressin, and oxytocin in the rat posterior pituitary. Concentrations of vasopressin and oxytocin decreased in response to both osmotic stimuli and treatment with T2 toxin, but the decrease was greater with osmotic stimulations. Similarly, concentrations of LE and dynorphin-related peptides declined after salt loading and water deprivation; LE concentrations also decreased after treatment with T2 toxin. The concentration of ME decreased after water deprivation, did not change after salt loading, and increased after T2 toxin treatment. The differentiating effects of these stimuli on the content of immunoreactive LE and ME are consistent with the hypothesis that LE and ME may be localized in separate populations of nerve endings with different roles in the posterior pituitary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zamir, N -- Zamir, D -- Eiden, L E -- Palkovits, M -- Brownstein, M J -- Eskay, R L -- Weber, E -- Faden, A I -- Feuerstein, G -- New York, N.Y. -- Science. 1985 May 3;228(4699):606-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2858918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dynorphins/analogs & derivatives/analysis ; Endorphins/analysis ; Enkephalin, Leucine/*analysis ; Enkephalin, Methionine/*analysis ; Male ; Osmosis ; Oxytocin/analysis ; Pituitary Gland, Posterior/*analysis/drug effects ; Protein Precursors/analysis ; Rats ; Rats, Inbred Strains ; Saline Solution, Hypertonic ; Sesquiterpenes/*pharmacology ; T-2 Toxin/*pharmacology ; Vasopressins/analysis ; Water Deprivation
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    Prooxidant states and tumor promotion (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-25
    Description: There is convincing evidence that cellular prooxidant states--that is, increased concentrations of active oxygen and organic peroxides and radicals--can promote initiated cells to neoplastic growth. Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents. Many of these agents are promoters or complete carcinogens. They cause chromosomal damage by indirect action, but the role of this damage in carcinogenesis remains unclear. Prooxidant states can be prevented or suppressed by the enzymes of the cellular antioxidant defense and low molecular weight scavenger molecules, and many antioxidants are antipromoters and anticarcinogens. Finally, prooxidant states may modulate the expression of a family of prooxidant genes, which are related to cell growth and differentiation, by inducing alterations in DNA structure or by epigenetic mechanisms, for example, by polyadenosine diphosphate-ribosylation of chromosomal proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerutti, P A -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):375-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2981433" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antioxidants/pharmacology ; *Carcinogens/metabolism/pharmacology ; Cations/metabolism ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Membrane/physiology ; *Cell Transformation, Neoplastic ; Chromosome Aberrations ; Chromosomes/drug effects ; Cytochrome P-450 Enzyme System/metabolism ; DNA/metabolism ; Electron Transport ; Gene Expression Regulation ; Humans ; Hydrogen Peroxide/metabolism ; Hydroxides/metabolism ; Hydroxyl Radical ; Lipid Peroxides/metabolism ; Microbodies/metabolism ; Mutation ; Neoplasms/*chemically induced ; Oxidation-Reduction ; Oxygen/*metabolism/physiology ; Poly Adenosine Diphosphate Ribose/metabolism ; Singlet Oxygen ; Sulfhydryl Compounds/physiology ; Superoxides/metabolism ; Ultraviolet Rays
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    Leukotrienes as mediators in tissue trauma (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-18
    Description: A significant increase in the production of cysteinyl leukotrienes was observed after mechanical or thermal trauma in the anesthesized rat. The amount of biliary N-acetyl-leukotriene E4, which represents a suitable indicator for blood plasma leukotrienes, was used as a measure of leukotriene generation. Cysteinyl leukotrienes were rapidly eliminated from blood plasma into bile where N-acetyl-leukotriene E4 was the major metabolite. Leukotrienes were at a much lower concentration in blood plasma than in bile and differed in the pattern of metabolites. The detected amounts of leukotrienes were sufficient to induce known phenomena associated with trauma, such as tissue edema and circulatory and respiratory dysfunction. Increased leukotriene generation appears to play an important role in the pathophysiology of tissue trauma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denzlinger, C -- Rapp, S -- Hagmann, W -- Keppler, D -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):330-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4048937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Abdominal/injuries ; Bile/metabolism ; Bile Ducts/surgery ; Burns/physiopathology ; Female ; Fractures, Bone/physiopathology ; Half-Life ; Kinetics ; Rats ; Rats, Inbred Strains ; SRS-A/*biosynthesis/blood ; Tritium ; Wounds and Injuries/*physiopathology
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    Growth regulation of human melanocytes: mitogenic factors in extracts of melanoma, astrocytoma, and fibroblast cell lines (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-06
    Description: Melanocytes derived from fetal or adult skin do not propagate in vitro unless cultured in the presence of factors such as 12-O-tetradecanoylphorbol 13-acetate (TPA). In a search for physiological factors regulating the growth of melanocytes, extracts of various cultured cell types were tested. Factors produced by melanoma and astrocytoma cell lines support continued proliferation of melanocytes in the absence of TPA. WI-38, a fibroblast cell line derived from human embryonic lung, was the most active source of melanocyte growth factors. No melanocyte growth-promoting activity was found in extracts of cultured neuroblastoma, renal cancer, normal keratinocytes, or renal epithelium. Nerve growth factor, epidermal growth factor, melanocyte-stimulating hormone, transforming growth factor-beta, and platelet-derived growth factor did not have growth-promoting activity for melanocytes. The presence of melanocyte growth factors and TPA together resulted in the strongest mitogenic activity for melanocytes, permitting the recovery (at 20 days) of 4 to 20 times as many cells as in growth factor or TPA alone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisinger, M -- Marko, O -- Ogata, S -- Old, L J -- 1R01 CA-32152/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 6;229(4717):984-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4023718" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytoma/physiopathology ; Cell Division/drug effects ; Cell Line ; Cholera Toxin/pharmacology ; Fibroblasts/physiology ; Growth Substances/isolation & purification/*pharmacology ; Humans ; Melanocytes/*cytology ; Melanoma/physiopathology ; Tetradecanoylphorbol Acetate/pharmacology
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    B lineage--specific interactions of an immunoglobulin enhancer with cellular factors in vivo (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-11
    Description: The mouse heavy chain immunoglobulin gene contains a tissue-specific enhancer. The enhancer and flanking sequences were studied in vivo by carrying out dimethyl sulfate protection experiments on living cells, in combination with genomic sequencing. Relative to reactions on naked DNA, there are changes (protections and enhancements) in the reactivity of guanine residues to dimethyl sulfate within the enhancer sequence in myeloma, B, and early B cells, whereas virtually no alterations appear in cells of non-B lineage. Most of the affected residues are in four clusters, in sequences homologous to the octamer 5'CAGGTGGC 3' (C, cytosine; A, adenine; G. guanine; T, thymine). The alterations in the pattern of G reactivity are consistent with the tissue-specific binding of molecules to the mouse immunoglobulin heavy chain enhancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ephrussi, A -- Church, G M -- Tonegawa, S -- Gilbert, W -- 2T 32 CA 09255/CA/NCI NIH HHS/ -- CA 14041/CA/NCI NIH HHS/ -- GM-09541-22/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 11;227(4683):134-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3917574" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*metabolism ; Base Sequence ; Cell Line ; *Enhancer Elements, Genetic ; *Genes, Regulator ; Guanine/metabolism ; Immunoglobulin Heavy Chains/*genetics ; Methylation ; Mice ; Multiple Myeloma/genetics ; RNA, Messenger/metabolism ; Sulfuric Acid Esters/metabolism
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    A new role for DNA virus early proteins in viral carcinogenesis (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-04
    Description: The T antigen proteins encoded by DNA tumor virus early genes are involved in the transformation of normal cells to immortalized neoplastic cells that may or may not be tumorigenic in immunocompetent animals. Studies have been made of the tumorigenicity of DNA virus-transformed cells and the interactions of these cells in vivo and in vitro with immunologically nonspecific host effector cells such as natural killer cells and macrophages. The results imply that the T proteins determine the capacity of transformed cells to induce tumors by governing the level of susceptibility that transformed cells express to destruction by such host cellular defenses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewis, A M Jr -- Cook, J L -- CA 31732/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):15-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3843807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming ; Antigens, Viral, Tumor/*metabolism ; Cell Line ; Cell Transformation, Neoplastic/immunology/*metabolism ; *Cell Transformation, Viral ; Cricetinae ; Cytotoxicity, Immunologic ; DNA Viruses/*metabolism ; Humans ; Immunity, Cellular ; Killer Cells, Natural/immunology ; Major Histocompatibility Complex ; Mesocricetus ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental/immunology ; Rats ; Viral Proteins/*metabolism
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    Targeted modulation of acute inflammation (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-11
    Description: Localized inflammation of the lungs was induced with the neutrophil chemoattractant, N-formylmethionylleucylphenylalanine (FMLP) in combination with magnetically responsive albumin microspheres, a drug carrier that provides efficient, extremely rapid localization in tissue. Intravenous targeting to rat lungs was accomplished by means of an external thoracic magnet. This caused progressive local accumulation of neutrophils, extravascular cell migration, and acute tissue injury. Microscopic findings favored chemotaxis as the principal mechanism of cell accumulation. This system provides a new experimental model for acute alveolar damage, a rapid in vivo assay for drugs that modulate neutrophil chemotaxis, and a new therapeutic approach to focusing inflammation in patients with chemotactic defects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ranney, D F -- CA15673/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 11;227(4683):182-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3966151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemotaxis, Leukocyte ; Disease Models, Animal ; Magnetics ; Microspheres ; N-Formylmethionine Leucyl-Phenylalanine/*pharmacology ; Pneumonia/*etiology/immunology ; Pulmonary Edema/etiology/immunology ; Rats ; Rats, Inbred Strains ; Serum Albumin
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    Abrupt induction of a membrane digestive enzyme by its intraintestinal substrate (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-04
    Description: The regulation of amino-oligopeptidase (AOP), an intestinal brush border hydrolase essential for the surface digestion of peptide nutrients, was examined in rats in vivo. Short-term (30-minute) intraintestinal perfusion of a tetrapeptide substrate, Gly-Leu-Gly-Gly, or a synthetic substrate, leucyl-beta-naphthylamide, induced a doubling in the incorporation of [3H]leucine into the AOP in association with intracellular membranes. The subsequent conversion of AOP from nascent to mature enzyme and its membrane-associated transport to the brush border occurred at normal rates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reisenauer, A M -- Gray, G M -- AM 07056/AM/NIADDK NIH HHS/ -- AM 11270/AM/NIADDK NIH HHS/ -- AM 15802/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):70-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838079" target="_blank"〉PubMed〈/a〉
    Keywords: Aminopeptidases/*biosynthesis ; Animals ; *Antigens, CD13 ; Dietary Proteins/metabolism ; Digestion ; Endoplasmic Reticulum/metabolism ; Enzyme Induction ; Golgi Apparatus/metabolism ; Intestines/*enzymology ; Kinetics ; Leucine/analogs & derivatives/metabolism ; Male ; Microvilli/enzymology ; Oligopeptides/metabolism ; Rats ; Rats, Inbred Strains
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    A mammalian host-vector system that regulates expression and amplification of transfected genes by temperature induction (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-04
    Description: SV40-transformed simian cells that permit temperature-dependent regulation of vector DNA replication were isolated and characterized. These cell lines (ts COS cells) produce high levels of thermolabile large T antigen under the transcriptional control of the Rous sarcoma virus long terminal repeat. The ts COS cell lines can complement SV40 A gene mutants and support replication of SV40-origin containing vectors at 33 degrees C but not at 40 degrees C. It should now be possible to regulate the copy number of transfected plasmid DNA's and also maintain selectable vector sequences either as integrated DNA or as autonomously replicating episomes by modulating T antigen activity in ts COS cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rio, D C -- Clark, S G -- Tjian, R -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):23-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2981116" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral, Tumor/genetics ; Cell Line ; Cell Transformation, Viral ; DNA Replication ; *Gene Amplification ; *Gene Expression Regulation ; *Genetic Vectors ; Haplorhini ; Plasmids ; RNA, Messenger/metabolism ; Simian virus 40/physiology ; Temperature ; *Transfection ; Virus Replication
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    Response to ethanol reduced by past thiamine deficiency (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-15
    Description: Ethanol-induced intoxication and hypothermia were studied in rats approximately 7 months after severe thiamine deficiency, when treated rats appeared to have recovered their physical health. Previously induced thiamine deficiency without prior ethanol exposure significantly decreased the area under the curve plotted for the concentration of ethanol in blood and also decreased behavioral impairment and hypothermia due to ethanol exposure. Pathophysiologic changes resulting from thiamine deficiency may contribute to both the pharmacodynamic and pharmacokinetic tolerance to ethanol in chronic alcoholics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, P R -- Majchrowicz, E -- Tamborska, E -- Marietta, C -- Mukherjee, A B -- Eckardt, M J -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1365-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975622" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Amnestic Disorder/pathology ; Alcoholic Intoxication/physiopathology ; Animals ; Behavior, Animal/drug effects ; Body Temperature/drug effects ; Brain/pathology ; Ethanol/*pharmacology ; Female ; Humans ; Hypothermia/chemically induced ; Male ; Rats ; Rats, Inbred Strains ; Thiamine Deficiency/*physiopathology ; Wernicke Encephalopathy/pathology
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    Antigenic and genetic properties of viruses linked to hemorrhagic fever with renal syndrome (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-01
    Description: Hemorrhagic fever with renal syndrome (HFRS) comprises a variety of clinically similar diseases of viral etiology that are endemic to and sporadically epidemic throughout the Eurasian continent and Japan. Although HFRS has not been reported in North America, viruses that are antigenically similar to HFRS agents were recently isolated from rodents in the United States. Examination and comparison of eight representative isolates from endemic disease areas and from regions with no known associated HFRS indicate that these viruses represent a new and unique group that constitutes a separate genus in the Bunyaviridae family of animal viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmaljohn, C S -- Hasty, S E -- Dalrymple, J M -- LeDuc, J W -- Lee, H W -- von Bonsdorff, C H -- Brummer-Korvenkontio, M -- Vaheri, A -- Tsai, T F -- Regnery, H L -- New York, N.Y. -- Science. 1985 Mar 1;227(4690):1041-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2858126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral/immunology ; Arvicolinae ; Base Sequence ; Bunyaviridae/genetics ; Hantavirus/genetics/*immunology ; Hemorrhagic Fever with Renal Syndrome/genetics/immunology/*microbiology ; Humans ; Korea ; Mice ; Muridae ; Neutralization Tests ; RNA Viruses/*immunology ; Radioimmunoassay ; Rats ; Rats, Inbred Strains ; United States
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    A macrophage factor inhibits adipocyte gene expression: an in vitro model of cachexia (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-08-30
    Description: Certain infections and malignancies in mammals cause the development of a condition known as cachexia in which the animal continues to lose weight, often while consuming an adequate diet. When macrophages are stimulated with an endotoxin, they produce a factor or factors, termed cachectin, that inhibits the activity of fat-producing (lipogenic) enzymes in cultured adipocytes. This effect may reflect one of the physiological bases for cachexia. In the present study, clones of complementary DNA from genes whose expression is increased during the differentiation of adipocytes were used to study the molecular basis of cachectin's actions. In the presence of cachectin, the expression of the corresponding genes was reversibly and specifically inhibited. Furthermore, when mature adipocytes were exposed to cachectin, the messenger RNA's of those genes diminished and rapidly approached the levels present before differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torti, F M -- Dieckmann, B -- Beutler, B -- Cerami, A -- Ringold, G M -- AM0131401/AM/NIADDK NIH HHS/ -- GM25821/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 30;229(4716):867-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3839597" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Adipose Tissue/cytology/*enzymology ; Animals ; Cachexia/*etiology ; Cell Differentiation ; Cell Division/drug effects ; Cell Line ; Cell Survival/drug effects ; Dna ; Endotoxins/pharmacology ; Gene Expression Regulation/drug effects ; Glycerolphosphate Dehydrogenase/genetics ; Lipids/*biosynthesis ; Macrophages/*metabolism ; Models, Biological ; Proteins/*pharmacology ; RNA, Messenger/genetics ; Tumor Necrosis Factor-alpha
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    Cyclic AMP regulation of eukaryotic gene transcription by two discrete molecular mechanisms (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-19
    Description: In experiments designed to study the mechanism by which peptide hormones binding to their plasma membrane receptors stimulate the expression of specific genes, the transcription of two neuroendocrine genes, prolactin and growth hormone, was analyzed in a rat pituitary cell line. The results showed that cyclic adenosine monophosphate (cyclic AMP) stimulates the transcription of discrete subsets of eukaryotic genes by at least two independent molecular mechanisms. Cyclic AMP stimulated growth hormone gene transcription and phosphorylation of a 19,000-dalton nuclear protein; this appears to reflect direct nuclear actions of the cyclic AMP-dependent protein kinase. In contrast, the stimulation by cyclic AMP of prolactin gene transcription appears to reflect activation of a discrete calcium-dependent event.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waterman, M -- Murdoch, G H -- Evans, R M -- Rosenfeld, M G -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):267-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/metabolism ; Cobalt/pharmacology ; Colforsin ; Cyclic AMP/*physiology ; Diterpenes/pharmacology ; Growth Hormone/biosynthesis/genetics ; Phosphorylation ; Pituitary Gland/cytology ; Prolactin/biosynthesis/genetics ; Protein Kinases/physiology ; Rats ; Thyrotropin-Releasing Hormone/pharmacology ; *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
    Published by American Association for the Advancement of Science (AAAS)
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