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  • Animals  (2,269)
  • Inorganic Chemistry
  • LUNAR AND PLANETARY EXPLORATION
  • Polymer and Materials Science
  • American Association for the Advancement of Science (AAAS)  (2,269)
  • 1990-1994  (2,269)
  • 1970-1974
  • 1965-1969
  • 1955-1959
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  • American Association for the Advancement of Science (AAAS)  (2,269)
  • Wiley-Blackwell  (58,710)
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Year
  • 201
    Publication Date: 1994-08-05
    Description: Accumulation of vascular smooth muscle cells as a consequence of arterial injury is a major feature of vascular proliferative disorders. Molecular approaches to the inhibition of smooth muscle cell proliferation in these settings could potentially limit intimal expansion. This problem was approached by introducing adenoviral vectors encoding the herpesvirus thymidine kinase (tk) into porcine arteries that had been injured by a balloon on a catheter. These smooth muscle cells were shown to be infectable with adenoviral vectors, and introduction of the tk gene rendered them sensitive to the nucleoside analog ganciclovir. When this vector was introduced into porcine arteries immediately after a balloon injury, intimal hyperplasia decreased after a course of ganciclovir treatment. No major local or systemic toxicities were observed. These data suggest that transient expression of an enzyme that catalyzes the formation of a cytotoxic drug locally may limit smooth muscle cell proliferation in response to balloon injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohno, T -- Gordon, D -- San, H -- Pompili, V J -- Imperiale, M J -- Nabel, G J -- Nabel, E G -- AI33355/AI/NIAID NIH HHS/ -- HL43507/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):781-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047883" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Angioplasty, Balloon ; Animals ; Arteries/*injuries ; Arteriosclerosis/etiology/pathology/*therapy ; Cell Division ; Cell Survival/drug effects ; Ganciclovir/metabolism/therapeutic use ; *Genetic Therapy ; Genetic Vectors ; Herpesviridae/enzymology ; Hyperplasia ; Muscle, Smooth, Vascular/*cytology ; Recurrence ; Swine ; Thymidine Kinase/genetics/metabolism
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  • 202
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Epstein, P R -- Chikwenhere, G P -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1510-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079160" target="_blank"〉PubMed〈/a〉
    Keywords: Africa, Southern ; Animals ; Climate ; *Disease Vectors ; *Pest Control
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  • 203
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, L -- Murphy, M -- Gallagher, R B -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):181-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Trinity College, Dublin, Ireland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7506843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Humans ; *Mental Processes ; *Origin of Life ; *Rna
    Print ISSN: 0036-8075
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  • 204
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maruyama, Y -- Fontanesi, J -- Porter, A T -- Wierzbicki, J G -- Gaspar, L -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):714-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Boron Neutron Capture Therapy ; Brain Neoplasms/*radiotherapy ; Californium/*therapeutic use ; Humans ; Neutron Capture Therapy/*methods ; Rats
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  • 205
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Capron, M -- Capron, A -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1876-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie et de Biologie Parasitaire, INSERM U 167, Institut Pasteur, Lille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody-Dependent Cell Cytotoxicity ; Cytokines/immunology ; Granulocytes/immunology ; Humans ; Immunoglobulin E/*immunology ; Receptors, IgE/immunology ; Schistosoma haematobium/immunology ; Schistosoma mansoni/immunology ; Schistosomiasis haematobia/*immunology ; Schistosomiasis mansoni/*immunology ; T-Lymphocytes, Helper-Inducer/*immunology
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  • 206
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1321-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973719" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics/metabolism ; DNA Damage ; *DNA Repair/genetics ; DNA-Binding Proteins/metabolism ; *Drosophila Proteins ; *Genes, p53 ; Humans ; Intracellular Signaling Peptides and Proteins ; Proliferating Cell Nuclear Antigen/physiology ; Proteins/*genetics/physiology ; Tumor Suppressor Protein p53/*metabolism
    Print ISSN: 0036-8075
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  • 207
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-05
    Description: Mammalian cells respond to endotoxic lipopolysaccharide (LPS) by activation of protein kinase cascades that lead to new gene expression. A protein kinase, p38, that was tyrosine phosphorylated in response to LPS, was cloned. The p38 enzyme and the product of the Saccharomyces cerevisiae HOG1 gene, which are both members of the mitogen-activated protein (MAP) kinase family, have sequences at and adjacent to critical phosphorylation sites that distinguish these proteins from most other MAP kinase family members. Both HOG1 and p38 are tyrosine phosphorylated after extracellular changes in osmolarity. These findings link a signaling pathway in mammalian cells with a pathway in yeast that is responsive to physiological stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, J -- Lee, J D -- Bibbs, L -- Ulevitch, R J -- AI15136/AI/NIAID NIH HHS/ -- GM28485/GM/NIGMS NIH HHS/ -- GM37696/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):808-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7914033" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*chemistry/genetics ; Cell Line ; Endotoxins/*pharmacology ; Genetic Complementation Test ; Lipopolysaccharides/pharmacology ; Macrophages, Peritoneal/enzymology ; Mice ; Mice, Inbred C3H ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Osmotic Pressure ; Paclitaxel/pharmacology ; Saccharomyces cerevisiae/genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Homology, Amino Acid ; Water-Electrolyte Balance/*physiology ; p38 Mitogen-Activated Protein Kinases
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  • 208
    Publication Date: 1994-08-26
    Description: Proteasomes degrade endogenous proteins. Two subunits, LMP-2 and LMP-7, are encoded in a region of the major histocompatibility complex (MHC) that is critical for class I-restricted antigen presentation. Mice with a targeted deletion of the gene encoding LMP-7 have reduced levels of MHC class I cell-surface expression and present the endogenous antigen HY inefficiently; addition of peptides to splenocytes deficient in LMP-7 restores wild-type class I expression levels. This demonstrates the involvement of LMP-7 in the MHC class I presentation pathway and suggests that LMP-7 functions as an integral part of the peptide supply machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fehling, H J -- Swat, W -- Laplace, C -- Kuhn, R -- Rajewsky, K -- Muller, U -- von Boehmer, H -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1234-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066463" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Amino Acid Sequence ; Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Base Sequence ; Carrier Proteins/genetics ; *Cysteine Endopeptidases ; Female ; Gene Deletion ; H-2 Antigens/*biosynthesis/immunology ; H-Y Antigen/immunology ; Lymphocytes/immunology ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; *Multienzyme Complexes ; Proteasome Endopeptidase Complex ; Proteins/genetics/*physiology
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  • 209
    Publication Date: 1994-12-02
    Description: The pathway of male sexual development in mammals is initiated by SRY, a gene on the short arm of the Y chromosome. Its expression in the differentiating gonadal ridge directs testicular morphogenesis, characterized by elaboration of Mullerian inhibiting substance (MIS) and testosterone. SRY and MIS each belong to conserved gene families that function in the control of growth and differentiation. Structural and biochemical studies of the DNA binding domain of SRY (the HMG box) revealed a protein-DNA interaction consisting of partial side chain intercalation into a widened minor groove. Functional studies of SRY in a cell line from embryonic gonadal ridge demonstrated activation of a gene-regulatory pathway leading to expression of MIS. SRY molecules containing mutations associated with human sex reversal have altered structural interactions with DNA and failed to induce transcription of MIS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haqq, C M -- King, C Y -- Ukiyama, E -- Falsafi, S -- Haqq, T N -- Donahoe, P K -- Weiss, M A -- GM51558/GM/NIGMS NIH HHS/ -- HD30812/HD/NICHD NIH HHS/ -- P30HD28138/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1494-500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pediatric Surgical Research Laboratory, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985018" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Mullerian Hormone ; Base Sequence ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Female ; *Gene Expression Regulation, Developmental ; Genitalia, Male/*embryology ; *Glycoproteins ; Growth Inhibitors/biosynthesis/*genetics ; Humans ; Male ; Models, Biological ; Models, Molecular ; Molecular Sequence Data ; Mullerian Ducts ; *Nuclear Proteins ; Sex Differentiation/*genetics ; Sex-Determining Region Y Protein ; Testicular Hormones/biosynthesis/*genetics ; Transcription Factors/chemistry/*genetics/metabolism
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  • 210
    Publication Date: 1994-07-22
    Description: To carry out its transformation function, the middle tumor antigen (MT) of murine polyomavirus associates with a number of cellular proteins involved in regulation of cell proliferation, including pp60c-Src, phosphatidylinositol 3-kinase, protein phosphatase 2A, Src homologous and collagen protein and growth factor receptor-binding protein 2. Here, two additional MT-associated proteins were identified as members of the 14-3-3 family of proteins. Yeast homologs of 14-3-3 proteins have recently been shown to play a role in the timing of mitosis. Thus, regulation of 14-3-3 protein function by MT may contribute to the development of neoplasia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pallas, D C -- Fu, H -- Haehnel, L C -- Weller, W -- Collier, R J -- Roberts, T M -- CA30002/CA/NCI NIH HHS/ -- CA45285/CA/NCI NIH HHS/ -- CA50661/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):535-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036498" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; 3T3 Cells ; Adenosine Diphosphate Ribose/metabolism ; Amino Acid Sequence ; Animals ; Antigens, Polyomavirus Transforming/immunology/*metabolism ; *Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Humans ; Immune Sera ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/isolation & purification/*metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Precipitin Tests ; *Tyrosine 3-Monooxygenase
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  • 211
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):319-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278804" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Cycle ; Cell Differentiation ; Cell Transformation, Neoplastic ; Cyclin D1 ; Cyclin-Dependent Kinase 4 ; *Cyclin-Dependent Kinases ; Cyclins/genetics/*metabolism ; G1 Phase ; Genes, Tumor Suppressor ; Humans ; Neoplasms/*etiology ; Oncogene Proteins/genetics/*metabolism ; *Oncogenes ; Protein Kinases/genetics/metabolism ; *Proto-Oncogene Proteins
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  • 212
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 May 6;264(5160):766.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology/*economics ; Financing, Government ; Genetic Techniques ; Genetic Testing/*economics ; Government Agencies/*economics ; Human Genome Project ; Humans ; *Research Support as Topic ; United States
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  • 213
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1663-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209242" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/enzymology/*genetics ; Animals ; *Disease Models, Animal ; Mice ; *Mice, Transgenic ; Mutation ; Superoxide Dismutase/*genetics/metabolism
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  • 214
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fetz, E E -- Shupe, L E -- NS17413/NS/NINDS NIH HHS/ -- PSMH48185/PS/NCHHSTP CDC HHS/ -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1295-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122116" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Motor Cortex/*physiology ; Neural Networks (Computer) ; Neurons/*physiology ; Synapses/*physiology ; Synaptic Transmission
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  • 215
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-28
    Description: Rapid advances have been made in the understanding of the genetic basis of development and pattern formation in a variety of model systems. By examining the extent to which these developmental systems are conserved or altered between different organisms, insight can be gained into the evolutionary events that have generated the diversity of organisms around us. The molecular and genetic basis of early pattern formation in Drosophila melanogaster has been particularly well studied, and comparisons to other insects have revealed conservation of some aspects of development, as well as differences that may explain variations in early patterning events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patel, N H -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):581-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Embryology, Carnegie Institution of Washington, Baltimore, MD 21210-3399.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drosophila melanogaster/*embryology/genetics ; *Embryonic Development ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; *Genes, Insect ; Insects/embryology/genetics ; Morphogenesis ; Phylogeny ; Signal Transduction
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  • 216
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-13
    Description: Learning and memory arise through activity-dependent modifications of neural circuits. Although the activity dependence of synaptic efficacy has been studied extensively, less is known about how activity shapes the intrinsic electrical properties of neurons. Lobster stomatogastric ganglion neurons fire in bursts when receiving synaptic and modulatory input but fire tonically when pharmacologically isolated. Long-term isolation in culture changed their intrinsic activity from tonic firing to burst firing. Rhythmic stimulation reversed this transition through a mechanism that was mediated by a rise in intracellular calcium concentration. These data suggest that neurons regulate their conductances to maintain stable activity patterns and that the intrinsic properties of a neuron depend on its recent history of activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turrigiano, G -- Abbott, L F -- Marder, E -- MH46742/MH/NIMH NIH HHS/ -- NS17813/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 May 13;264(5161):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Cells, Cultured ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Electrophysiology ; Ganglia, Invertebrate/cytology ; Membrane Potentials ; Nephropidae ; Neurites/physiology ; Neurons/cytology/*physiology ; Synapses/physiology
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  • 217
    Publication Date: 1994-06-10
    Description: Protein tyrosine kinases (PTKs) play an integral role in T cell activation and differentiation. Defects in the Src-family PTKs in mice and in T cell lines have resulted in variable defects in thymic development and in T cell antigen receptor (TCR) signal transduction. Here, three siblings are described with an autosomal recessive form of severe combined immunodeficiency disease (SCID) in which ZAP-70, a non-Src PTK, is absent as a result of mutations in the ZAP-70 gene. This absence is associated with defects in TCR signal transduction, suggesting an important functional role for ZAP-70.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, A C -- Kadlecek, T A -- Elder, M E -- Filipovich, A H -- Kuo, W L -- Iwashima, M -- Parslow, T G -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1599-601.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202713" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/metabolism ; Cell Line ; Child ; Female ; Gene Deletion ; *Genes, Recessive ; Humans ; Lymphocyte Activation ; Male ; Molecular Sequence Data ; Mutation ; Point Mutation ; Protein-Tyrosine Kinases/deficiency/*genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Severe Combined Immunodeficiency/*genetics/immunology ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; ZAP-70 Protein-Tyrosine Kinase
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  • 218
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pimentel, D -- New York, N.Y. -- Science. 1994 May 13;264(5161):890.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bird Diseases/chemically induced ; Birds ; Costs and Cost Analysis ; Fish Diseases/chemically induced ; Pesticides/adverse effects/*economics ; United States
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  • 219
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simpson, L -- Maslov, D A -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1870-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Los Angeles, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Kinetoplastida/*genetics ; Phylogeny ; *RNA Editing ; RNA, Protozoan/genetics/metabolism ; Trypanosomatina/*genetics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hess, B -- Mikhailov, A -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):223-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institut fur Medizinische Forschung, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; *Cell Physiological Phenomena ; Diffusion ; Microtubules/metabolism ; Thermodynamics
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  • 221
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flam, F -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1799.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Boron Neutron Capture Therapy ; Brain Neoplasms/*radiotherapy ; Clinical Trials as Topic ; Ethics, Medical ; Female ; Glioblastoma/*radiotherapy ; Humans ; Investigational New Drug Application ; Rats ; United States ; United States Food and Drug Administration
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 222
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atlas, D -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):462-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939689" target="_blank"〉PubMed〈/a〉
    Keywords: Agmatine/*chemistry/*pharmacology ; Animals ; Brain Chemistry ; Cattle ; Clonidine/*antagonists & inhibitors/chemistry/isolation & ; purification/pharmacology ; Humans
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  • 223
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hines, P J -- Marx, J -- Parks, S -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):523.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939691" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Embryonic Development ; *Embryonic and Fetal Development ; *Growth ; Humans ; Morphogenesis
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  • 224
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Small, P L -- Ramakrishnan, L -- Falkow, S -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):637-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rocky Mountain Laboratories, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; Endocytosis ; Humans ; Hydrogen-Ion Concentration ; Lysosome-Associated Membrane Glycoproteins ; Macrophages/enzymology/*microbiology ; Membrane Glycoproteins/metabolism ; Mice ; Mycobacterium/*physiology ; Mycobacterium tuberculosis/*physiology ; Phagosomes/*microbiology ; Proton-Translocating ATPases/*metabolism ; Vacuoles/enzymology/*microbiology
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  • 225
    Publication Date: 1994-10-14
    Description: Three genetic complementation groups of rodent cells are defective for both repair of x-ray-induced double-strand breaks and V(D)J recombination. Cells from one group lack a DNA end-binding activity that is biochemically and antigenically similar to the Ku autoantigen. Transfection of complementary DNA (cDNA) that encoded the 86-kilodalton subunit of Ku rescued these mutant cells for DNA end-binding activity, x-ray resistance, and V(D)J recombination activity. These results establish a role for Ku in DNA repair and recombination. Furthermore, as a component of a DNA-dependent protein kinase, Ku may initiate a signaling pathway induced by DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smider, V -- Rathmell, W K -- Lieber, M R -- Chu, G -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):288-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University Medical Center, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Nuclear ; Cell Line ; Cell Line, Transformed ; Cell Survival/*radiation effects ; Cricetinae ; DNA/*metabolism ; *DNA Helicases ; *DNA Repair ; DNA, Complementary ; DNA-Binding Proteins/genetics/*physiology ; Gene Rearrangement ; Genetic Complementation Test ; Humans ; Nuclear Proteins/genetics/*physiology ; Radiation Tolerance ; *Recombination, Genetic ; Transfection
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  • 226
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: Studies of the development of murine intestinal intraepithelial lymphocytes (IELs) have yielded markedly different results depending on the experimental system used. In athymic radiation chimeras, IELs consist of all subsets found in euthymic mice; adult mice that were athymic at birth have only IELs that are positive for T cell receptor gamma delta and CD8 alpha alpha. These differences are resolved by the finding that administration of the neuropeptide thyrotropin-releasing hormone to adult mice thymectomized as neonates leads to the development of all IEL T cells. Thus, a neuroendocrine signal initiated by the thymus during fetal or neonatal life appears to be required for subsequent extrathymic maturation of gut alpha beta T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, J -- Klein, J R -- DK35566/DK/NIDDK NIH HHS/ -- R01 DK035566/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1860-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Science, University of Tulsa, OK 74104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091211" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD8/analysis ; Chimera ; Intestinal Mucosa/cytology/*immunology ; Mice ; Mice, Inbred Strains ; Mice, Nude ; Phenotype ; Receptors, Antigen, T-Cell, alpha-beta/analysis ; T-Lymphocyte Subsets/*cytology/immunology ; Thymectomy ; Thymus Gland/*physiology ; Thyrotropin-Releasing Hormone/*pharmacology
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  • 227
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kreil, G -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):996-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology, Austrian Academy of Sciences, Salzburg.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973683" target="_blank"〉PubMed〈/a〉
    Keywords: Agatoxins ; Amino Acid Sequence ; Amino Acids/*metabolism ; Animals ; Isomerases/*metabolism ; Molecular Sequence Data ; Oligopeptides/biosynthesis/chemistry/*metabolism/pharmacology ; *Protein Processing, Post-Translational ; Spider Venoms/metabolism ; Stereoisomerism
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  • 228
    Publication Date: 1994-09-09
    Description: The gene aquaporin-1 encodes channel-forming integral protein (CHIP), a member of a large family of water transporters found throughout nature. Three rare individuals were identified who do not express CHIP-associated Colton blood group antigens and whose red cells exhibit low osmotic water permeabilities. Genomic DNA analyses demonstrated that two individuals were homozygous for different nonsense mutations (exon deletion or frameshift), and the third had a missense mutation encoding a nonfunctioning CHIP molecule. Surprisingly, none of the three suffers any apparent clinical consequence, which raises questions about the physiological importance of CHIP and implies that other mechanisms may compensate for its absence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Preston, G M -- Smith, B L -- Zeidel, M L -- Moulds, J J -- Agre, P -- DK32753/DK/NIDDK NIH HHS/ -- HL33991/HL/NHLBI NIH HHS/ -- HL48268/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1585-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7521540" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquaporin 1 ; *Aquaporins ; Base Sequence ; Blood Group Antigens ; Cell Membrane Permeability ; Erythrocyte Membrane/chemistry/physiology ; Exons ; Female ; Homozygote ; Humans ; Ion Channels/blood/*genetics/urine ; Kidney Tubules/chemistry ; Molecular Sequence Data ; Mutation ; Oocytes ; Phenotype ; Polymerase Chain Reaction ; Xenopus
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  • 229
    Publication Date: 1994-10-21
    Description: Femtosecond pump-probe experiments reveal the impulsive production of photoproduct in the primary event in vision. The retinal chromophore of rhodopsin was excited with a 35-femtosecond pulse at 500 nanometers, and transient changes in absorption were measured with 10-femtosecond probe pulses. At probe wavelengths within the photo-product absorption band, oscillatory features with a period of 550 femtoseconds (60 wavenumbers) were observed whose phase and amplitude demonstrate that they are the result of nonstationary vibrational motion in the ground state of the photoproduct. The observation of coherent vibrational motion of the photoproduct supports the idea that the primary step in vision is a vibrationally coherent process and that the high quantum yield of the cis--〉trans isomerization in rhodopsin is a consequence of the extreme speed of the excited-state torsional motion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Q -- Schoenlein, R W -- Peteanu, L A -- Mathies, R A -- Shank, C V -- EY-02051/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):422-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Materials Sciences Division, Lawrence Berkeley Laboratory, University of California, 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Fourier Analysis ; Isomerism ; *Light ; Models, Molecular ; Photic Stimulation ; Photochemistry ; Rhodopsin/analogs & derivatives/*chemistry ; Spectrum Analysis ; Vision, Ocular/*physiology
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  • 230
    Publication Date: 1994-11-18
    Description: In April and May 1979, an unusual anthrax epidemic occurred in Sverdlovsk, Union of Soviet Socialist Republics. Soviet officials attributed it to consumption of contaminated meat. U.S. agencies attributed it to inhalation of spores accidentally released at a military microbiology facility in the city. Epidemiological data show that most victims worked or lived in a narrow zone extending from the military facility to the southern city limit. Farther south, livestock died of anthrax along the zone's extended axis. The zone paralleled the northerly wind that prevailed shortly before the outbreak. It is concluded that the escape of an aerosol of anthrax pathogen at the military facility caused the outbreak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meselson, M -- Guillemin, J -- Hugh-Jones, M -- Langmuir, A -- Popova, I -- Shelokov, A -- Yampolskaya, O -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1202-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973702" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aerosols ; Aged ; *Air Microbiology ; Animals ; Animals, Domestic ; Anthrax/*epidemiology/history/microbiology/transmission/veterinary ; *Bacillus anthracis/immunology ; Bacterial Vaccines ; Biological Warfare ; *Disease Outbreaks/veterinary ; Female ; History, 20th Century ; Humans ; Male ; Meteorological Concepts ; Middle Aged ; Retrospective Studies ; Spores, Bacterial ; USSR/epidemiology ; Wind
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  • 231
    Publication Date: 1994-12-09
    Description: The association between quantitative genetic variation in bristle number and molecular variation at a candidate neurogenic locus, scabrous, was examined in Drosophila melanogaster. Approximately 32 percent of the genetic variation in abdominal bristle number (21 percent for sternopleural bristle number) among 47 second chromosomes from a natural population was correlated with DNA sequence polymorphisms at this locus. Several polymorphic sites associated with large phenotypic effects occurred at intermediate frequency. Quantitative genetic variation in natural populations caused by alleles that have large effects at a few loci and that segregate at intermediate frequencies conflicts with the classical infinitesimal model of the genetic basis of quantitative variation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lai, C -- Lyman, R F -- Long, A D -- Langley, C H -- Mackay, T F -- GM45146/GM/NIGMS NIH HHS/ -- GM45344/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1697-702.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Population Biology, University of California at Davis 95616.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992053" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; DNA/genetics ; *Drosophila Proteins ; Drosophila melanogaster/anatomy & histology/*genetics ; Female ; *Genes, Insect ; *Genetic Variation ; *Glycoproteins ; Haplotypes ; Linkage Disequilibrium ; Male ; Molecular Sequence Data ; Phenotype ; *Polymorphism, Genetic ; Proteins/*genetics ; Restriction Mapping ; Sense Organs/anatomy & histology
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  • 232
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: The development of vaccines to prevent infectious diseases has been one of the most important contributions of biomedical science. Recent advances in the basic sciences are now fueling the development of a new generation of vaccines that will be based on rational design approaches. Two factors are making this possible: an improved understanding of the microbial factors required for virulence and the nature of the immune response to infection. The status of new vaccine technologies is summarized here.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rabinovich, N R -- McInnes, P -- Klein, D L -- Hall, B F -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1401-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982-9902.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7521064" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic ; Animals ; Antigens/genetics/immunology ; Cytokines/immunology ; DNA/genetics ; Epitopes/immunology ; Humans ; ISCOMs/immunology ; Vaccination ; *Vaccines, Combined/immunology ; *Vaccines, Conjugate/immunology ; *Vaccines, Synthetic/immunology
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  • 233
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1154.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973692" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/adverse effects ; Animals ; Animals, Newborn ; Haplorhini ; Humans ; Simian Acquired Immunodeficiency Syndrome/immunology/prevention & ; control/virology ; Simian Immunodeficiency Virus/*immunology/physiology ; Vaccines, Attenuated/adverse effects ; Virus Replication
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  • 234
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Radetsky, P -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1486-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Clinical Trials as Topic ; Collagenases/analysis ; Female ; Fibronectins/analysis ; Gap Junctions/physiology ; Genital Diseases, Female/complications/drug therapy ; Humans ; Matrix Metalloproteinase 9 ; Nitric Oxide/analysis ; Obstetric Labor, Premature/etiology/*prevention & control ; Oxytocin/antagonists & inhibitors ; Pregnancy ; Pregnancy Complications, Infectious/drug therapy ; Uterine Contraction
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  • 235
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: Mitogen-activated protein kinases (MAPKs) are rapidly activated in response to stimulation of diverse receptor types. MAPKs are positively regulated by phosphorylation on threonine and tyrosine by MAP kinase or extracellular signal-regulated kinase (ERK) kinases (MEKs). MEK kinase (MEKK) is part of a family of serine-threonine protein kinases that phosphorylate and activate MEKs independently of Raf. MEKK was rapidly and persistently activated in response to stimulation of resting PC12 cells with epidermal growth factor (EGF). Nerve growth factor (NGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA) also activated MEKK, although to a lesser degree than did EGF. Activation of MEKK and B-Raf in response to EGF was inhibited by expression of dominant negative N17Ras. Expression of oncogenic Ras resulted in activation of MEKK. Stimulation of synthesis of cyclic adenosine 3',5'-monophosphate abolished activation of MEKK and B-Raf by EGF, NGF, and TPA. Thus, Ras simultaneously controls the activation of members of the Raf and MEKK families of protein kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lange-Carter, C A -- Johnson, G L -- CA58157/CA/NCI NIH HHS/ -- DK37871/DK/NIDDK NIH HHS/ -- GM30324/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1458-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073291" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/metabolism ; Enzyme Activation ; Epidermal Growth Factor/pharmacology ; *Genes, ras ; MAP Kinase Kinase 1 ; *Mitogen-Activated Protein Kinase Kinases ; Nerve Growth Factors/*pharmacology ; PC12 Cells ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Tetradecanoylphorbol Acetate/pharmacology
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  • 236
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1839.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009201" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/immunology ; Acquired Immunodeficiency Syndrome/*prevention & control ; Animals ; *Clinical Trials as Topic ; Humans ; National Institutes of Health (U.S.) ; United States
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  • 237
    Publication Date: 1994-10-21
    Description: The possibility that neurons in the basal ganglia and cerebellum innervate areas of the cerebral cortex that are involved in cognitive function has been a controversial subject. Here, retrograde transneuronal transport of herpes simplex virus type 1 (HSV1) was used to identify subcortical neurons that project via the thalamus to area 46 of the primate prefrontal cortex. This cortical area is known to be involved in spatial working memory. Many neurons in restricted regions of the dentate nucleus of the cerebellum and in the internal segment of the globus pallidus were labeled by transneuronal transport of virus from area 46. The location of these neurons was different from those labeled after HSV1 transport from motor areas of the cerebral cortex. These observations define an anatomical substrate for the involvement of basal ganglia and cerebellar output in higher cognitive function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Middleton, F A -- Strick, P L -- NS24328/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):458-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, State University of New York (SUNY) Health Science Center, Syracuse 13210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basal Ganglia/anatomy & histology/*physiology ; Brain Mapping ; Cebus ; Cerebellar Nuclei/anatomy & histology/physiology ; Cerebellum/anatomy & histology/*physiology ; *Cognition ; Globus Pallidus/anatomy & histology/physiology ; Herpesvirus 1, Human/physiology ; *Memory ; Neural Pathways ; Neurons/cytology ; Prefrontal Cortex/anatomy & histology/*physiology ; Thalamic Nuclei/anatomy & histology/physiology
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  • 238
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-28
    Description: Although objects that have just been seen may persist in memory automatically for a time and interact passively with incoming stimulation, some tasks require that the memory be actively maintained and used. To test for the existence of separate automatic and volitional mechanisms of short-term memory, recordings were made from neurons in the inferior temporal cortex of monkeys while the monkeys held a sample picture "in mind" and signaled when it was repeated in a sequence of pictures, ignoring other stimulus repetitions. Some neurons were suppressed by any picture repetition, regardless of relevance, whereas others were enhanced, but only when a picture matched the sample. Short-term memory appears to reflect the parallel operation of these two mechanisms--one being automatic and the other active.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, E K -- Desimone, R -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):520-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neuropsychology, National Institute of Mental Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290960" target="_blank"〉PubMed〈/a〉
    Keywords: Analysis of Variance ; Animals ; Macaca mulatta ; Memory, Short-Term/*physiology ; Neurons/*physiology ; Temporal Lobe/cytology/*physiology
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  • 239
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, M -- Meselson, M -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973687" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenicity Tests ; *DNA Damage ; Dose-Response Relationship, Drug ; Risk Assessment
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  • 240
    Publication Date: 1994-12-23
    Description: Hemolysin of Escherichia coli is activated by fatty acylation of the protoxin, directed by the putative acyl transferase HlyC and by acyl carrier protein (ACP). Mass spectrometry and Edman degradation of proteolytic products from mature toxin activated in vitro with tritium-labeled acylACP revealed two fatty-acylated internal lysine residues, lysine 564 and lysine 690. Resistance of the acylation to chemical treatments suggested that fatty acid was amide linked. Substitution of the two lysines confirmed that they were the only sites of acylation and showed that although each was acylated in the absence of the other, both sites were required for in vivo toxin activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stanley, P -- Packman, L C -- Koronakis, V -- Hughes, C -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):1992-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Cambridge University, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7801126" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl Carrier Protein/metabolism ; Acylation ; Acyltransferases/metabolism ; Amino Acid Sequence ; Animals ; Bacterial Proteins/chemistry/metabolism/*toxicity ; Bacterial Toxins/chemistry/metabolism/*toxicity ; *Escherichia coli ; *Escherichia coli Proteins ; Hemolysin Proteins/chemistry/metabolism/*toxicity ; Hemolysis ; Horses ; Lysine/metabolism ; Mass Spectrometry ; Molecular Sequence Data ; Protein Precursors/metabolism ; Sequence Alignment
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  • 241
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):561-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939701" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Developmental Biology/methods/trends ; *Embryonic Development ; *Embryonic and Fetal Development ; Genes ; Genes, Homeobox ; *Morphogenesis ; Signal Transduction
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  • 242
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-24
    Description: Malaria is a disease caused by repeated cycles of growth of the parasite Plasmodium in the erythrocyte. Various cellular and molecular strategies allow the parasite to evade the human immune response for many cycles of parasite multiplication. Under certain circumstances Plasmodium infection causes severe anemia or cerebral malaria; the expression of disease is influenced by both parasite and host factors, as exemplified by the exacerbation of disease during pregnancy. This article provides an overview of malaria pathogenesis, synthesizing the recent field, laboratory, and epidemiological data that will lead to the development of strategies to reduce mortality and morbidity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, L H -- Good, M F -- Milon, G -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1878-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Malaria Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009217" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia/etiology ; Animals ; Antibodies, Protozoan/immunology ; Erythrocytes/*parasitology ; Female ; Host-Parasite Interactions ; Humans ; Infant, Newborn ; Malaria/complications/immunology/*parasitology ; Malaria, Cerebral/etiology/parasitology ; Malaria, Falciparum/complications/immunology/*parasitology ; Plasmodium/growth & development/immunology/*pathogenicity ; Plasmodium falciparum/growth & development/immunology/pathogenicity ; Pregnancy ; Pregnancy Complications, Parasitic/immunology/parasitology ; Recurrence
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  • 243
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Aug 19;265(5175):1023.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066438" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; Animals ; *Computer Communication Networks ; *Databases, Factual ; Humans ; *Research
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  • 244
    Publication Date: 1994-02-04
    Description: Increased discharge activity of mesopontine cholinergic neurons participates in the production of electroencephalographic (EEG) arousal; such arousal diminishes as a function of the duration of prior wakefulness or of brain hyperthermia. Whole-cell and extracellular recordings in a brainstem slice show that mesopontine cholinergic neurons are under the tonic inhibitory control of endogenous adenosine, a neuromodulator released during brain metabolism. This inhibitory tone is mediated postsynaptically by an inwardly rectifying potassium conductance and by an inhibition of the hyperpolarization-activated current. These data provide a coupling mechanism linking neuronal control of EEG arousal with the effects of prior wakefulness, brain hyperthermia, and the use of the adenosine receptor blockers caffeine and theophylline.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612520/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612520/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rainnie, D G -- Grunze, H C -- McCarley, R W -- Greene, R W -- R01 MH039683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Harvard University, Brockton, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303279" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*physiology ; Animals ; Arousal/*physiology ; Calcium/metabolism ; Electric Conductivity ; *Electroencephalography/drug effects ; Female ; Frontal Lobe/physiology ; In Vitro Techniques ; Male ; Membrane Potentials ; Neurons/*physiology ; Parasympathetic Nervous System/*physiology ; Potassium/metabolism ; Rats
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  • 245
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-21
    Description: Quality control mechanisms prevent the cell surface expression of incompletely assembled multisubunit receptors such as the T cell receptor (TCR). The molecular chaperone function of calnexin (IP90, p88), a 90-kilodalton protein that resides in the endoplasmic reticulum (ER), in the retention of representative chains of the TCR-CD3 complex in the ER was tested. Truncation mutants of calnexin, when transiently expressed in COS cells, were exported from the ER and either accumulated in the Golgi or progressed to the cell surface. CD3 epsilon chains cotransfected with the forms of calnexin that were not retained in the ER exited the ER and colocalized with calnexin. Since engineered calnexin determined the intracellular localization of the proteins associated with it, it is concluded that calnexin interacts with incompletely assembled TCR components and retains them in the ER.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajagopalan, S -- Xu, Y -- Brenner, M B -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):387-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Rheumatology and Immunology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278814" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD3/*metabolism ; Base Sequence ; Calcium-Binding Proteins/analysis/chemistry/*metabolism ; Calnexin ; Cell Line ; Cell Membrane/metabolism ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/metabolism ; Histocompatibility Antigens Class I/metabolism ; Lysosomes/metabolism ; Membrane Proteins/analysis/chemistry/*metabolism ; Molecular Sequence Data ; Nuclear Envelope/metabolism ; Receptor-CD3 Complex, Antigen, T-Cell/*metabolism ; Recombinant Proteins/metabolism ; Transfection
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  • 246
    Publication Date: 1994-11-04
    Description: The function of keratinocyte growth factor (KGF) in normal and wounded skin was assessed by expression of a dominant-negative KGF receptor transgene in basal keratinocytes. The skin of transgenic mice was characterized by epidermal atrophy, abnormalities in the hair follicles, and dermal hyperthickening. Upon skin injury, inhibition of KGF receptor signaling reduced the proliferation rate of epidermal keratinocytes at the wound edge, resulting in substantially delayed reepithelialization of the wound.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werner, S -- Smola, H -- Liao, X -- Longaker, M T -- Krieg, T -- Hofschneider, P H -- Williams, L T -- HL-43821/HL/NHLBI NIH HHS/ -- R01 HL32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):819-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Institute, University of California at San Francisco (UCSF) 94143-0130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973639" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Division ; Cell Movement ; Epidermis/pathology ; Epithelial Cells ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors ; Growth Substances/*physiology ; Hair/cytology/growth & development ; Keratinocytes/*cytology/physiology ; Mice ; Mice, Transgenic ; Phenotype ; Receptor, Fibroblast Growth Factor, Type 2 ; *Receptors, Fibroblast Growth Factor ; Receptors, Growth Factor/genetics/*physiology ; Signal Transduction ; Skin/*cytology ; Wound Healing/*physiology
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  • 247
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1800-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522343" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Line ; Central Nervous System/*cytology ; Ganglia, Spinal/cytology ; Myelin Proteins/pharmacology/*physiology ; Myelin-Associated Glycoprotein ; Nerve Regeneration/*physiology ; Neurites/physiology ; Neurons/*physiology ; Neurons, Afferent/physiology ; Rats
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  • 248
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1690-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209247" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Alcoholism/genetics ; Animals ; *Behavior, Animal ; Crosses, Genetic ; Drosophila/genetics ; Drosophila Proteins ; Genes ; Genes, Insect ; Genetic Markers ; Genetic Techniques ; *Genetics, Behavioral/methods ; Humans ; Learning ; Mice ; Nuclear Proteins/genetics ; Period Circadian Proteins ; Rats
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  • 249
    Publication Date: 1994-01-21
    Description: After injury to the cell membrane, rapid resealing of the membrane occurs with little loss of intracellular contents. This process has been studied by measurement of the rate of dye loss after membrane puncture in both the sea urchin embryo and 3T3 fibroblasts. Resealing of disrupted cell membranes requires external calcium that can be antagonized by magnesium. Block of multifunctional calcium/calmodulin kinase, which regulates exocytotic vesicle availability at synapses, and of kinesin, which is required for outward-directed transport of vesicles, inhibited membrane resealing. Resealing was also inhibited by botulinum neurotoxins B and A, suggesting that the two synaptosomal-associated proteins synaptobrevin and SNAP-25 also participate in resealing. This pattern of inhibition indicates that the calcium-dependent mechanisms for cell membrane resealing may involve vesicle delivery, docking, and fusion, similar to the exocytosis of neurotransmitters.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steinhardt, R A -- Bi, G -- Alderton, J M -- R01 AR41129/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):390-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7904084" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Botulinum Toxins/pharmacology ; Calcium/*metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Division/drug effects ; Cell Membrane/drug effects/*physiology ; Female ; Kinesin/physiology ; Magnesium/pharmacology ; Membrane Proteins/physiology ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/physiology ; Neurotransmitter Agents/*metabolism ; Oligopeptides/pharmacology ; Ovum ; R-SNARE Proteins ; Sea Urchins ; Synaptic Transmission ; Synaptosomal-Associated Protein 25 ; Zygote
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  • 250
    Publication Date: 1994-12-09
    Description: A posttranslational modification was detected in the carboxyl-terminal region of axonemal tubulin from Paramecium. Tubulin carboxyl-terminal peptides were isolated and analyzed by Edman degradation sequencing, mass spectrometry, and amino acid analysis. All of the peptides, derived from both alpha and beta tubulin subunits, were modified by polyglycylation, containing up to 34 glycyl units covalently bound to the gamma carboxyl group of glutamyl residues. This modification, present in one of the most stable microtubular systems, may influence microtubule stability or axoneme function, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Redeker, V -- Levilliers, N -- Schmitter, J M -- Le Caer, J P -- Rossier, J -- Adoutte, A -- Bre, M H -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1688-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Alfred Fessard, CNRS Unite Propre de Recherche 2212, Gif-sur-Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992051" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cilia/chemistry/*metabolism/ultrastructure ; Glutamic Acid/metabolism ; Glycine/analysis/*metabolism ; Mass Spectrometry ; Microtubules/chemistry/*metabolism/ultrastructure ; Molecular Sequence Data ; Paramecium/*metabolism/ultrastructure ; Peptides/analysis/*metabolism ; *Protein Processing, Post-Translational ; Tubulin/analysis/chemistry/*metabolism
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  • 251
    Publication Date: 1994-12-09
    Description: Growth factors activate mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs) and Jun kinases (JNKs). Although the signaling cascade from growth factor receptors to ERKs is relatively well understood, the pathway leading to JNK activation is more obscure. Activation of JNK by epidermal growth factor (EGF) or nerve growth factor (NGF) was dependent on H-Ras activation, whereas JNK activation by tumor necrosis factor alpha (TNF-alpha) was Ras-independent. Ras activates two protein kinases, Raf-1 and MEK (MAPK, or ERK, kinase) kinase (MEKK). Raf-1 contributes directly to ERK activation but not to JNK activation, whereas MEKK participated in JNK activation but caused ERK activation only after overexpression. These results demonstrate the existence of two distinct Ras-dependent MAPK cascades--one initiated by Raf-1 leading to ERK activation, and the other initiated by MEKK leading to JNK activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minden, A -- Lin, A -- McMahon, M -- Lange-Carter, C -- Derijard, B -- Davis, R J -- Johnson, G L -- Karin, M -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1719-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California at San Diego, La Jolla 92093-0636.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992057" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Enzyme Activation/drug effects ; Epidermal Growth Factor/pharmacology ; Genes, ras ; HeLa Cells ; Humans ; JNK Mitogen-Activated Protein Kinases ; *MAP Kinase Kinase Kinase 1 ; Mice ; Mitogen-Activated Protein Kinase 1 ; *Mitogen-Activated Protein Kinases ; Nerve Growth Factors/pharmacology ; PC12 Cells ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; ras Proteins/*pharmacology
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  • 252
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 May 6;264(5160):775.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171332" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Auditory Cortex/cytology/*physiology ; Cats ; Neural Networks (Computer) ; Neurons/*physiology ; Sound Localization/*physiology
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  • 253
    Publication Date: 1994-08-19
    Description: Ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) each promote the survival and differentiation of developing motor neurons, but do so through distinct cellular signaling pathways. Administration of either factor alone has been shown to slow, but not to arrest, progression of motor neuron dysfunction in wobbler mice, an animal model of motor neuron disease. Because CNTF and BDNF are known to synergize in vitro and in ovo, the efficacy of CNTF and BDNF cotreatment was tested in the same animal mode. Subcutaneous injection of the two factors on alternate days was found to arrest disease progression in wobbler mice for 1 month, as measured by several behavioral, physiological, and histological criteria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitsumoto, H -- Ikeda, K -- Klinkosz, B -- Cedarbaum, J M -- Wong, V -- Lindsay, R M -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1107-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Cleveland Clinic Foundation, OH 44195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066451" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor ; Ciliary Neurotrophic Factor ; Drug Synergism ; Drug Therapy, Combination ; Mice ; Mice, Mutant Strains ; Motor Neuron Disease/*drug therapy/pathology/physiopathology ; Motor Neurons/drug effects ; Muscles/drug effects/pathology ; Nerve Fibers, Myelinated/drug effects ; Nerve Growth Factors/*therapeutic use ; Nerve Tissue Proteins/*therapeutic use ; Random Allocation
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  • 254
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reggiani, G M -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1829-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009200" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dioxins/*adverse effects/analysis ; Environmental Exposure ; Humans ; Neoplasms/*chemically induced ; Occupational Exposure ; Tetrachlorodibenzodioxin/adverse effects
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  • 255
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1225.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; Muscles/*innervation ; Neuromuscular Junction/*physiology ; Synapses/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 256
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sternberg, S -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1632-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7702654" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Opportunistic Infections/epidemiology ; Animals ; Antifungal Agents/adverse effects/*therapeutic use ; California/epidemiology ; Candidiasis/epidemiology ; Cross Infection/*epidemiology ; Drug Resistance, Microbial ; Fungi/drug effects ; Humans ; Immunocompromised Host ; Mycoses/drug therapy/*epidemiology/etiology ; Opportunistic Infections/*epidemiology ; Research
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 257
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Remington, S J -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):298-300.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939670" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Blood ; Crystallization ; Crystallography, X-Ray ; Hemoglobins/*chemistry ; History, Ancient ; Humans ; Paleontology/*methods ; Species Specificity
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  • 258
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-29
    Description: Simultaneous recordings were made from large ensembles of hippocampal "place cells" in three rats during spatial behavioral tasks and in slow-wave sleep preceding and following these behaviors. Cells that fired together when the animal occupied particular locations in the environment exhibited an increased tendency to fire together during subsequent sleep, in comparison to sleep episodes preceding the behavioral tasks. Cells that were inactive during behavior, or that were active but had non-overlapping spatial firing, did not show this increase. This effect, which declined gradually during each post-behavior sleep session, may result from synaptic modification during waking experience. Information acquired during active behavior is thus re-expressed in hippocampal circuits during sleep, as postulated by some theories of memory consolidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, M A -- McNaughton, B L -- MH46823/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):676-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neural Systems, Memory, and Aging, University of Arizona, Tucson 85724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036517" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Hippocampus/*physiology ; Male ; Memory/*physiology ; Models, Neurological ; Motor Activity/physiology ; Nerve Net/physiology ; Neurons/*physiology ; Pyramidal Cells/physiology ; Rats ; Rats, Inbred F344 ; Reaction Time/physiology ; Sleep/*physiology ; Spatial Behavior/physiology
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  • 259
    Publication Date: 1994-02-04
    Description: The mechanism by which western equine encephalomyelitis (WEE) virus and other mosquito-borne alphaviruses (Togaviridae) survive during periods of vector inactivity is unknown. Recently, three strains of WEE virus were isolated from adult Aedes dorsalis collected as larvae from a salt marsh in a coastal region of California. This provides evidence of vertical transmission of WEE virus in mosquitoes in nature. Vertical transmission in Ae. dorsalis and closely related mosquito species may be an important mechanism for the maintenance of WEE virus in temperate regions in North America where horizontal transmission of the virus is seasonal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fulhorst, C F -- Hardy, J L -- Eldridge, B F -- Presser, S B -- Reeves, W C -- AI-03028/AI/NIAID NIH HHS/ -- AI-26154/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):676-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303276" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*microbiology ; Animals ; California ; Encephalitis Virus, Western Equine/isolation & purification/*physiology ; Encephalomyelitis, Equine/transmission ; Female ; Insect Vectors/*microbiology ; Larva/microbiology ; Male ; Seasons
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  • 260
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-28
    Description: Six baboons (Papio cynocephalus) were intravenously inoculated with the human immunodeficiency virus-type 2 (HIV-2) strain HIV-2UC2. All seroconverted within 6 weeks after inoculation; five animals became persistently infected. Four developed lymphadenopathy, and three of the animals had CD4+ T cell loss within 18 to 24 months after inoculation. One of these baboons, showing severe clinical symptoms, showed at necropsy widespread dissemination of virus with follicular depletion in the lymph nodes, extensive fibromatosis involving lymphoid and nonlymphoid tissues, and lymphocytic interstitial pneumonitis. Another animal is cachectic and exhibited lymphoid follicular lysis and fibrous skin lesions. Other baboons inoculated with a second strain, HIV-2UC14, have shown evidence of persistent infection. HIV-2 infection of baboons provides a valuable animal model for studying HIV persistence and pathogenesis and for evaluating approaches to antiviral therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnett, S W -- Murthy, K K -- Herndier, B G -- Levy, J A -- U01-AI26471/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):642-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, School of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939718" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome/immunology/pathology/virology ; Animals ; CD4 Lymphocyte Count ; CD4-CD8 Ratio ; *Disease Models, Animal ; *HIV-2/isolation & purification/physiology ; Leukocytes, Mononuclear/virology ; Lung Diseases, Interstitial/complications ; Lymph Nodes/immunology/pathology/virology ; Lymphoid Tissue/pathology/virology ; *Papio/virology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 261
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moffat, A S -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1090-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108725" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/prevention & control/*transmission ; Animals ; Birds ; *Ecology ; Ecosystem ; Humans ; Models, Biological
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  • 262
    Publication Date: 1994-12-02
    Description: Extracellular signaling proteins encoded by the hedgehog (hh) multigene family are responsible for the patterning of a variety of embryonic structures in vertebrates and invertebrates. The Drosophila hh gene has now been shown to generate two predominant protein species that are derived by an internal autoproteolytic cleavage of a larger precursor. Mutations that reduced the efficiency of autoproteolysis in vitro diminished precursor cleavage in vivo and also impaired the signaling and patterning activities of the HH protein. The two HH protein species exhibited distinctive biochemical properties and tissue distribution, and these differences suggest a mechanism that could account for the long- and short-range signaling activities of HH in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, J J -- Ekker, S C -- von Kessler, D P -- Porter, J A -- Sun, B I -- Beachy, P A -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1528-37.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, Johns Hopkins School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985023" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Drosophila/embryology/genetics/*metabolism ; *Drosophila Proteins ; Embryo, Nonmammalian/*metabolism ; Embryonic Induction ; Gene Expression Regulation, Developmental ; Genes, Insect ; Hedgehog Proteins ; Models, Biological ; Molecular Sequence Data ; Mutation ; Protein Precursors/chemistry/genetics/metabolism ; *Protein Processing, Post-Translational ; Proteins/chemistry/genetics/*metabolism ; Serine Endopeptidases/chemistry ; *Signal Transduction
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  • 263
    Publication Date: 1994-07-08
    Description: A tendency for exons to correspond to discrete units of protein structure in protein-coding genes of ancient origin would provide clear evidence in favor of the exon theory of genes, which proposes that split genes arose not by insertion of introns into unsplit genes, but from combinations of primordial mini-genes (exons) separated by spacers (introns). Although putative examples of such correspondence have strongly influenced previous debate on the origin of introns, a general correspondence has not been rigorously proved. Objective methods for detecting correspondences were developed and applied to four examples that have been cited previously as evidence of the exon theory of genes. No significant correspondence between exons and units of protein structure was detected, suggesting that the putative correspondence does not exist and that the exon theory of genes is untenable.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stoltzfus, A -- Spencer, D F -- Zuker, M -- Logsdon, J M Jr -- Doolittle, W F -- GM-35087/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):202-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Dalhousie University, Halifax, Nova Scotia, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023140" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Dehydrogenase/chemistry/genetics ; Animals ; Biological Evolution ; *Exons ; *Genes ; Globins/chemistry/genetics ; *Introns ; *Protein Conformation ; Protein Structure, Secondary ; Pyruvate Kinase/chemistry/genetics ; Triose-Phosphate Isomerase/chemistry/genetics
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  • 264
    Publication Date: 1994-10-07
    Description: The effect of the number of cystic fibrosis (CF) alleles on cholera toxin (CT)-induced intestinal secretion was examined in the CF mouse model. CF mice that expressed no CF transmembrane conductance regulator (CFTR) protein did not secrete fluid in response to CT. Heterozygotes expressed 50 percent of the normal amount of CFTR protein in the intestinal epithelium and secreted 50 percent of the normal fluid and chloride ion in intestinal epithelium and secreted 50 percent of the normal fluid and chloride ion and fluid secretion suggests that CF heterozygotes might possess a selective advantage of resistance to cholera.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gabriel, S E -- Brigman, K N -- Koller, B H -- Boucher, R C -- Stutts, M J -- DK46003/DK/NIDDK NIH HHS/ -- HL34322/HL/NHLBI NIH HHS/ -- HL42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):107-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7524148" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Body Fluids/*secretion ; Chloride Channels/metabolism ; Chlorides/*metabolism ; Cholera Toxin/*toxicity ; Crosses, Genetic ; Cyclic AMP/metabolism ; Cystic Fibrosis/*genetics/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Female ; Heterozygote ; Intestinal Mucosa/*secretion ; Intestine, Small/secretion ; Male ; Membrane Proteins/*genetics/metabolism ; Mice
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  • 265
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolffe, A P -- New York, N.Y. -- Science. 1994 May 20;264(5162):1100-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Embryology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; DNA/chemistry/*metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; High Mobility Group Proteins/chemistry ; Histones/chemistry/metabolism ; *Nucleic Acid Conformation ; Nucleosomes ; *Pol1 Transcription Initiation Complex Proteins ; Transcription Factors/chemistry/*metabolism ; *Transcription, Genetic
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  • 266
    Publication Date: 1994-02-11
    Description: Interleukin-1 beta converting enzyme (ICE) is a mammalian homolog of CED-3, a protein required for programmed cell death in the nematode Caenorhabditis elegans. The activity of ICE can be specifically inhibited by the product of crmA, a cytokine response modifier gene encoded by cowpox virus. Microinjection of the crmA gene into chicken dorsal root ganglion neurons was found to prevent cell death induced by deprivation of nerve growth factor. Thus, ICE is likely to participate in neuronal death in vertebrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gagliardini, V -- Fernandez, P A -- Lee, R K -- Drexler, H C -- Rotello, R J -- Fishman, M C -- Yuan, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):826-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 1 ; Cells, Cultured ; Chickens ; Ganglia, Spinal ; Gene Expression ; Metalloendopeptidases/*genetics/physiology ; Microinjections ; Nerve Growth Factors/pharmacology ; Neurons, Afferent/*cytology/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Serpins/*genetics/physiology ; *Viral Proteins
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  • 267
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-11
    Description: The low-affinity neurotrophin receptor p75 binds all neurotrophins with similar affinity. For elucidation of its function, mice bearing a null mutation in the p75 locus were generated. Examination of sympathetic innervation of target tissues revealed that pineal glands lacked innervation and sweat gland innervation was absent or reduced in particular footpads. The absence of adult innervation reflects the failure of axons to reach these targets during development rather than a target deficit. These results indicate that p75 facilitates development of specific populations of sympathetic neurons, for which it may support axon growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K F -- Bachman, K -- Landis, S -- Jaenisch, R -- 5 R35 CA44339/CA/NCI NIH HHS/ -- NS 023678/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1447-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128229" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Fibers/*physiology/ultrastructure ; Animals ; Axons/physiology/ultrastructure ; Mice ; Mutation ; Pilocarpine/pharmacology ; Pineal Gland/*innervation ; Receptors, Nerve Growth Factor/genetics/*physiology ; Sweat Glands/chemistry/drug effects/*innervation/physiology ; Sweating ; Vasoactive Intestinal Peptide/analysis
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  • 268
    Publication Date: 1994-09-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ringwald, M -- Baldock, R -- Bard, J -- Kaufman, M -- Eppig, J T -- Richardson, J E -- Nadeau, J H -- Davidson, D -- MC_U127527203/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2033-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, Bar Harbor, ME 04609.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091224" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Computer Communication Networks ; *Databases, Factual ; Embryonic and Fetal Development ; *Gene Expression ; Mice/embryology/*genetics
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  • 269
    Publication Date: 1994-08-12
    Description: The critical discriminatory event in the activation of T lymphocytes bearing alpha beta T cell receptors (TCRs) is their interaction with a molecular complex consisting of a peptide bound to a major histocompatibility complex (MHC)-encoded class I or class II molecule on the surface of an antigen-presenting cell. The kinetics of binding were measured of a purified TCR to molecular complexes of a purified soluble analog of the murine MHC class I molecule H-2Ld (sH-2Ld) and a synthetic octamer peptide p2CL in a direct, real-time assay based on surface plasmon resonance. The kinetic dissociation rate of the MHC-peptide complex from the TCR was rapid (2.6 x 10(-2) second-1, corresponding to a half-time for dissociation of approximately 27 seconds), and the kinetic association rate was 2.1 x 10(5) M-1 second-1. The equilibrium constant for dissociation was approximately 10(-7) M. These values indicate that TCRs must interact with a multivalent array of MHC-peptide complexes to trigger T cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corr, M -- Slanetz, A E -- Boyd, L F -- Jelonek, M T -- Khilko, S -- al-Ramadi, B K -- Kim, Y S -- Maher, S E -- Bothwell, A L -- Margulies, D H -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Section, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biosensing Techniques ; H-2 Antigens/*metabolism ; Histocompatibility Antigen H-2D ; Kinetics ; *Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Receptors, Antigen, T-Cell, alpha-beta/*metabolism ; Solubility
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  • 270
    Publication Date: 1994-06-24
    Description: Maternal sources of transforming growth factor-beta 1 (TGF-beta 1) are shown here to contribute to the normal appearance and perinatal survival of TGF-beta 1 null newborn mice. Labeled TGF-beta 1 crossed the placenta and was recovered intact from various tissues after oral administration to mouse pups. TGF beta-1 protein was also detected in cells recovered from breast milk. In immunohistochemical analyses, TGF-beta 1 null embryos and null newborn pups born to TGF-beta 1 heterozygotes stained positive for TGF-beta 1, whereas those born to a null female were negative and had severe cardiac abnormalities. These results suggest an important role for maternal sources of TGF-beta 1 during development and, more generally, provide evidence for maternal rescue of targeted gene disruption in the fetus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letterio, J J -- Geiser, A G -- Kulkarni, A B -- Roche, N S -- Sporn, M B -- Roberts, A B -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1936-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009224" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Embryonic and Fetal Development ; Female ; Fetus/*metabolism ; Heart Defects, Congenital/etiology ; Heterozygote ; Homozygote ; *Maternal-Fetal Exchange ; Mice ; Milk/chemistry ; Pregnancy ; Transforming Growth Factor beta/analysis/biosynthesis/*metabolism
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  • 271
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1661.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Mitochondrial/genetics ; Electron Transport Complex IV/genetics ; *Genetic Variation ; Gorilla gorilla/classification/*genetics ; Hominidae/genetics ; Humans ; Pan troglodytes/classification/genetics
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  • 272
    Publication Date: 1994-02-18
    Description: Clonidine, an antihypertensive drug, binds to alpha 2-adrenergic and imidazoline receptors. The endogenous ligand for imidazoline receptors may be a clonidine-displacing substance, a small molecule isolated from bovine brain. This clonidine-displacing substance was purified and determined by mass spectroscopy to be agmatine (decarboxylated arginine), heretofore not detected in brain. Agmatine binds to alpha 2-adrenergic and imidazoline receptors and stimulates release of catecholamines from adrenal chromaffin cells. Its biosynthetic enzyme, arginine decarboxylase, is present in brain. Agmatine, locally synthesized, is an endogenous agonist at imidazoline receptors, a noncatecholamine ligand at alpha 2-adrenergic receptors and may act as a neurotransmitter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, G -- Regunathan, S -- Barrow, C J -- Eshraghi, J -- Cooper, R -- Reis, D J -- HL18974/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 18;263(5149):966-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7906055" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/drug effects/metabolism ; Agmatine/chemistry/isolation & purification/*metabolism/pharmacology ; Animals ; Binding Sites ; Brain/enzymology/metabolism ; *Brain Chemistry ; Carboxy-Lyases/metabolism ; Cattle ; Cerebral Cortex/metabolism ; Clonidine/analogs & derivatives/metabolism ; Epinephrine/metabolism ; Imidazoline Receptors ; Neurotransmitter Agents/metabolism ; Norepinephrine/metabolism ; Rats ; Receptors, Adrenergic, alpha/metabolism ; Receptors, Drug/metabolism
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  • 273
    Publication Date: 1994-05-20
    Description: Xenopus UBF (xUBF) interacts with DNA by way of multiple HMG-box domains. When xUBF binds to the ribosomal promoter, the carboxyl-terminal acidic tail and amino-terminal HMG-box interact. Binding also leads to negative DNA supercoiling and the formation of a disk-like structure, the enhancesome. Within the enhancesome, an xUBF dimer makes a low-density protein core around which DNA is looped into a single 180-base pair turn, probably by in-phase bending. The enhancesome structure suggests a mechanism for xUBF-dependent recruitment of the TATA box-binding protein complex without direct interaction between the two factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bazett-Jones, D P -- Leblanc, B -- Herfort, M -- Moss, T -- New York, N.Y. -- Science. 1994 May 20;264(5162):1134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry and Anatomy, Faculty of Medicine, Health Sciences Center, University of Calgary, Alberta, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; DNA/chemistry/*metabolism ; DNA, Superhelical/chemistry/metabolism ; Enhancer Elements, Genetic ; High Mobility Group Proteins/chemistry/*metabolism ; Models, Genetic ; Nucleic Acid Conformation ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/chemistry/metabolism ; Transcription Factors/chemistry/*metabolism ; Xenopus Proteins ; Xenopus laevis
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  • 274
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-18
    Description: Although signals for retention in the endoplasmic reticulum (ER) have been identified in the cytoplasmic domain of various ER-resident type I transmembrane proteins, the mechanisms responsible for ER retention are still unknown. Yeast and mammalian ER retention motifs interacted specifically in cell lysates with the coatomer, a polypeptide complex implicated in membrane traffic. Mutations that affect the ER retention capacity of the motifs also abolished binding of the coatomer. These results suggest a role for the coatomer in the retrieval of transmembrane proteins to the ER in both yeast and mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cosson, P -- Letourneur, F -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1629-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128252" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Cell Line ; Coatomer Protein ; Endoplasmic Reticulum/*metabolism ; Fungal Proteins/chemistry/*metabolism ; Golgi Apparatus/metabolism ; *Hexosyltransferases ; Lysine/chemistry/*metabolism ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Recombinant Fusion Proteins/chemistry/metabolism ; Transferases/chemistry/*metabolism
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  • 275
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1664.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209243" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/blood ; Antigens, Viral/analysis ; Disease Outbreaks/*veterinary ; Distemper/diagnosis/*epidemiology/microbiology ; Distemper Virus, Canine/immunology ; Inclusion Bodies, Viral ; Lions/*microbiology ; Tanzania/epidemiology
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  • 276
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-25
    Description: To complete their maturation, most immature thymocytes depend on the simultaneous engagement of their antigen receptor [alpha beta T cell receptor (TCR)] and their CD4 or CD8 coreceptors with major histocompatibility complex class II or I ligands, respectively. However, a normal subset of mature alpha beta TCR+ thymocytes did not follow these rules. These thymocytes expressed NK1.1 and a restricted set of alpha beta TCRs that are intrinsically class I-reactive because their positive selection was class I-dependent but CD8-independent. These cells were CD4+ and CD4-8- but never CD8+, because the presence of CD8 caused negative selection. Thus, neither CD4 nor CD8 contributes signals that direct their maturation into the CD4+ and CD4-8- lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bendelac, A -- Killeen, N -- Littman, D R -- Schwartz, R H -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1774-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7907820" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Antigens, Ly ; Antigens, Surface ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Female ; Histocompatibility Antigens Class I/*physiology ; Lectins, C-Type ; Ligands ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; NK Cell Lectin-Like Receptor Subfamily B ; Phenotype ; Proteins/analysis ; Receptors, Antigen, T-Cell, alpha-beta/analysis/*physiology ; T-Lymphocyte Subsets/cytology/*immunology
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  • 277
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, R -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):308-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023147" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Wild/physiology ; Environmental Pollutants/*adverse effects/metabolism/toxicity ; Estrogens/*adverse effects/metabolism/toxicity ; Female ; Humans ; Male ; Pregnancy ; Prenatal Exposure Delayed Effects ; Reproduction/*drug effects ; Sperm Count/drug effects ; Testicular Neoplasms/epidemiology/etiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 278
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):171-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/genetics ; Female ; Humans ; Male ; Mutation ; *Recombination, Genetic ; Sex Determination Analysis ; *Y Chromosome
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  • 279
    Publication Date: 1994-08-26
    Description: Hypotheses about chimpanzee social behavior, phylogeography, and evolution were evaluated by noninvasive genotyping of free-ranging individuals from 20 African sites. Degrees of relatedness among individuals in one community were inferred from allele-sharing at eight nuclear simple sequence repeat (SSR) loci. Males are related on the order of half-siblings, and homozygosity is significantly increased at several SSR loci compared to Hardy-Weinberg expectations. These data support the kin-selection hypothesis for the evolution of cooperation among males. Sequence variation patterns at two mitochondrial loci indicate historically high long-distance gene flow and clarify the relationships among three allopatric subspecies. The unexpectedly large genetic distance between the western subspecies, Pan troglodytes verus, and the other two subspecies suggests a divergence time of about 1.58 million years. This result, if confirmed at nuclear loci and supported by eco-behavioral data, implies that P. t. verus should be elevated to full species rank.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morin, P A -- Moore, J J -- Chakraborty, R -- Jin, L -- Goodall, J -- Woodruff, D S -- 1T32 HG00005-02/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1193-201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla 92093-0116.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7915048" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Alleles ; Animals ; Base Sequence ; *Biological Evolution ; DNA/analysis/genetics ; Female ; *Genetic Variation ; Hair/chemistry ; Male ; Molecular Sequence Data ; Pan troglodytes/classification/*genetics/psychology ; Phylogeny ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Repetitive Sequences, Nucleic Acid ; *Social Behavior ; Tanzania
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  • 280
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jansen, A S -- Loewy, A D -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):121-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Heart Ventricles/*innervation/microbiology ; Herpesvirus 1, Suid/*physiology ; Medulla Oblongata/*anatomy & histology/microbiology ; Neural Pathways ; Neurons/*cytology/microbiology ; Rats ; Vagus Nerve/*anatomy & histology/microbiology
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  • 281
    Publication Date: 1994-10-28
    Description: PHAS-I is a heat-stable protein (relative molecular mass approximately 12,400) found in many tissues. It is rapidly phosphorylated in rat adipocytes incubated with insulin or growth factors. Nonphosphorylated PHAS-I bound to initiation factor 4E (eIF-4E) and inhibited protein synthesis. Serine-64 in PHAS-I was rapidly phosphorylated by mitogen-activated (MAP) kinase, the major insulin-stimulated PHAS-I kinase in adipocyte extracts. Results obtained with antibodies, immobilized PHAS-I, and a messenger RNA cap affinity resin indicated that PHAS-I did not bind eIF-4E when serine-64 was phosphorylated. Thus, PHAS-I may be a key mediator of the stimulation of protein synthesis by the diverse group of agents and stimuli that activate MAP kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, T A -- Kong, X -- Haystead, T A -- Pause, A -- Belsham, G -- Sonenberg, N -- Lawrence, J C Jr -- AR41180/AR/NIAMS NIH HHS/ -- DK28312/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939721" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/metabolism ; Animals ; *Carrier Proteins ; Insulin/*pharmacology ; Mice ; Mitogen-Activated Protein Kinase 1 ; Peptide Initiation Factors/isolation & purification/*metabolism ; Phosphoproteins/*metabolism ; Phosphorylation ; *Protein Biosynthesis ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Recombinant Proteins/metabolism ; Serine/metabolism
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  • 282
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, R -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140415" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Abdominal ; Aortic Diseases/*etiology ; Arteriosclerosis/*etiology ; Chickens ; Humans ; Male ; Tobacco Smoke Pollution/*adverse effects
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  • 283
    Publication Date: 1994-02-25
    Description: Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Critchfield, J M -- Racke, M K -- Zuniga-Pflucker, J C -- Cannella, B -- Raine, C S -- Goverman, J -- Lenardo, M J -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1139-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; Apoptosis ; CD4-Positive T-Lymphocytes/*immunology ; Cell Division ; Cells, Cultured ; Cytochrome c Group/immunology ; Dose-Response Relationship, Immunologic ; Encephalomyelitis, Autoimmune, Experimental/*immunology/pathology/therapy ; *Immune Tolerance ; Immunotherapy ; Interleukin-2/immunology/pharmacology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Myelin Basic Protein/immunology ; Myelin Sheath/immunology/pathology ; Spinal Cord/pathology ; T-Lymphocytes/*immunology
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  • 284
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-18
    Description: Cultured embryonic cortical neurons from rats were used to explore mechanisms of activity-dependent neuronal survival. Cell survival was increased by the activation of voltage-sensitive calcium channels (VSCCs) but not by activation of N-methyl-D-aspartate receptors. These effects correlated with the expression of brain-derived neurotrophic factor (BDNF) induced by these two classes of calcium channels. Antibodies to BDNF (which block intracellular signaling by BDNF, but not by nerve growth factor, NT3, or NT4/5) reduced the survival of cortical neurons and reversed the VSCC-mediated increase in survival. Thus, endogenous BDNF is a trophic factor for cortical neurons whose expression is VSCC-regulated and that functions in the VSCC-dependent survival of these neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, A -- Carnahan, J -- Greenberg, M E -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1618-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7907431" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Brain-Derived Neurotrophic Factor ; Calcium Channels/*physiology ; Cell Division/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Cerebral Cortex/*cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Embryo, Mammalian ; Glutamates/pharmacology ; Glutamic Acid ; N-Methylaspartate/pharmacology ; Nerve Growth Factors/biosynthesis/genetics/immunology/*physiology ; Nerve Tissue Proteins/biosynthesis/genetics/immunology/*physiology ; Neurons/*cytology ; Phosphorylation ; Potassium Chloride/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Signal Transduction
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  • 285
    Publication Date: 1994-11-25
    Description: Although several ion channels have been reported to be directly modulated by calcium-calmodulin, they have not been conclusively shown to bind calmodulin, nor are the modulatory mechanisms understood. Study of the olfactory cyclic nucleotide-activated cation channel, which is modulated by calcium-calmodulin, indicates that calcium-calmodulin directly binds to a specific domain on the amino terminus of the channel. This binding reduces the effective affinity of the channel for cyclic nucleotides, apparently by acting on channel gating, which is tightly coupled to ligand binding. The data reveal a control mechanism that resembles those underlying the regulation of enzymes by calmodulin. The results also point to the amino-terminal part of the olfactory channel as an element for gating, which may have general significance in the operation of ion channels with similar overall structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, M -- Chen, T Y -- Ahamed, B -- Li, J -- Yau, K W -- EY 06837/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1348-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baltimore, MD.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7526466" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Calcium/*metabolism ; Calmodulin/*metabolism ; Cell Line ; Cyclic AMP/*metabolism ; Cyclic GMP/*metabolism ; Humans ; *Ion Channel Gating ; Ion Channels/chemistry/*metabolism ; Molecular Sequence Data ; Olfactory Receptor Neurons/metabolism ; Peptides/metabolism ; Protein Structure, Secondary ; Rats ; Recombinant Fusion Proteins/metabolism
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  • 286
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, M -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Parasites/*physiology ; *Parasitic Diseases ; Parasitic Diseases, Animal ; *Research
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  • 287
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):541.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939698" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; China ; Egypt ; *Fossils ; Haplorhini/anatomy & histology ; History, Ancient ; Skull/*anatomy & histology ; Strepsirhini/*anatomy & histology
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  • 288
    Publication Date: 1994-04-01
    Description: The STAT family of proteins carries out a dual function: signal transduction and activation of transcription. A new family member, Stat3, becomes activated through phosphorylation on tyrosine as a DNA binding protein in response to epidermal growth factor (EGF) and interleukin-6 (IL-6) but not interferon gamma (IFN-gamma). It is likely that this phosphoprotein forms homodimers as well as heterodimers with the first described member of the STAT family, Stat91 (renamed Stat1 alpha), which is activated by the IFNs and EGF. Differential activation of different STAT proteins in response to different ligands should help to explain specificity in nuclear signaling from the cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhong, Z -- Wen, Z -- Darnell, J E Jr -- AI32489/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):95-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140422" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/chemistry/genetics/isolation & purification/*metabolism ; Epidermal Growth Factor/*pharmacology ; Humans ; Interferon-gamma ; Interleukin-6/*pharmacology ; Mice ; Molecular Sequence Data ; Phosphorylation ; Regulatory Sequences, Nucleic Acid ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Sequence Alignment ; Trans-Activators/metabolism ; Transfection ; Tumor Cells, Cultured ; Tyrosine/metabolism
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  • 289
    Publication Date: 1994-09-16
    Description: Coaxial stacking of helical elements is a determinant of three-dimensional structure in RNA. In the catalytic center of the Tetrahymena group I intron, helices P4 and P6 are part of a tertiary structural domain that folds independently of the remainder of the intron. When P4 and P6 were fused with a phosphodiester linkage, the resulting RNA retained the detailed tertiary interactions characteristic of the native P4-P6 domain and even required lower magnesium ion concentrations for folding. These results indicate that P4 and P6 are coaxial in the P4-P6 domain and, therefore, in the native ribozyme. Helix fusion could provide a general method for identifying pairs of coaxially stacked helices in biological RNA molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, F L -- Wang, Y H -- Griffith, J D -- Cech, T R -- GM31819/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1709-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Edetic Acid ; Electrophoresis, Polyacrylamide Gel ; Ferrous Compounds ; Introns ; Magnesium/pharmacology ; Molecular Sequence Data ; *Nucleic Acid Conformation ; RNA, Catalytic/*chemistry/ultrastructure ; RNA, Protozoan/*chemistry/ultrastructure ; Tetrahymena/*genetics
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  • 290
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, B -- van Huffel, C -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):667-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas 75235-9050.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171316" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Division ; Gene Deletion ; Ligands ; Lymph Nodes/cytology/growth & development ; Lymphotoxin-alpha/genetics/*physiology ; Mice ; Mice, Knockout ; Phenotype ; Receptors, Tumor Necrosis Factor/genetics/*physiology
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  • 291
    Publication Date: 1994-09-16
    Description: After activation in mesoderm and neuroectoderm, expression of the Hoxb-1 gene is progressively restricted to rhombomere (r) 4 in the hindbrain. Analysis of the chick and mouse Hoxb-1 genes identified positive and negative regulatory regions that cooperate to mediate segment-restricted expression during rhombomere formation. An enhancer generates expression extending into r3 and r5, and a repressor limits this domain to r4. The repressor contains a conserved retinoic acid response element, point mutations in which allow expression to spread into adjacent rhombomeres. Retinoids and their nuclear receptors may therefore participate in sharpening segment-restricted expression of Hoxb-1 during rhombomere boundary formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Studer, M -- Popperl, H -- Marshall, H -- Kuroiwa, A -- Krumlauf, R -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1728-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lab of Developmental Neurobiology, National Institute for Medical Research, Mill Hill, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916164" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chick Embryo ; Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes, Homeobox ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Neural Crest/metabolism ; Oligonucleotides/metabolism ; Point Mutation ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Retinoic Acid/metabolism ; *Regulatory Sequences, Nucleic Acid ; Retinoid X Receptors ; Rhombencephalon/*embryology/metabolism ; *Transcription Factors ; Tretinoin/*pharmacology
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  • 292
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-04
    Description: Drug-induced lupus is a serious side effect of certain medications, but the chemical features that confer this property and the underlying pathogenesis are puzzling. Prototypes of all six therapeutic classes of lupus-inducing drugs were highly cytotoxic only in the presence of activated neutrophils. Removal of extracellular hydrogen peroxide before, but not after, exposure of the drug to activated neutrophils prevented cytotoxicity. Neutrophil-dependent cytotoxicity required the enzymatic action of myeloperoxidase, resulting in the chemical transformation of the drug to a reactive product. The capacity of drugs to serve as myeloperoxidase substrates in vitro was associated with the ability to induce lupus in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, X -- Khursigara, G -- Rubin, R L -- MO1 RR00833/RR/NCRR NIH HHS/ -- R01 AG09574/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):810-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉W. M. Keck Autoimmune Disease Center, Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973636" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Biotransformation ; Cell Death/*drug effects ; Chlorpromazine/analogs & derivatives/metabolism/toxicity ; Humans ; Hydralazine/analogs & derivatives/metabolism/toxicity ; Hydrogen Peroxide/metabolism ; Isoniazid/analogs & derivatives/metabolism/toxicity ; Lupus Erythematosus, Systemic/*chemically induced ; Mice ; *Neutrophil Activation ; Neutrophils/enzymology/*metabolism ; Peroxidase/*metabolism ; Procainamide/analogs & derivatives/metabolism/toxicity ; Propylthiouracil/analogs & derivatives/metabolism/toxicity ; Quinidine/analogs & derivatives/metabolism/toxicity ; Tumor Cells, Cultured
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  • 293
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biggin, S -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1798.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997871" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/organization & administration ; Animals ; Biotechnology ; Italy ; Mice ; *Molecular Biology
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  • 294
    Publication Date: 1994-10-14
    Description: Inbreeding is known to lead to decreased survival and reproduction in captive populations of animals. It is also important to know whether inbreeding has deleterious effects in natural habitats. An estimate was made of the effects of inbreeding in white-footed mice, Peromyscus leucopus noveboracensis, derived from a wild population. This study demonstrates that inbreeding had a significant detrimental effect on the survivorship of mice reintroduced into a natural habitat. This effect was more severe than the effect observed in laboratory studies of the population.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jimenez, J A -- Hughes, K A -- Alaks, G -- Graham, L -- Lacy, R C -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):271-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Illinois-Chicago 60680.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939661" target="_blank"〉PubMed〈/a〉
    Keywords: Analysis of Variance ; Animals ; Body Weight ; Female ; *Inbreeding ; Likelihood Functions ; Male ; Peromyscus/genetics/*physiology ; Regression Analysis ; Survival Rate
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  • 295
    Publication Date: 1994-02-04
    Description: The success of Mycobacterium species as pathogens depends on their ability to maintain an infection inside the phagocytic vacuole of the macrophage. Although the bacteria are reported to modulate maturation of their intracellular vacuoles, the nature of such modifications is unknown. In this study, vacuoles formed around Mycobacterium avium failed to acidify below pH 6.3 to 6.5. Immunoelectron microscopy of infected macrophages and immunoblotting of isolated phagosomes showed that Mycobacterium vacuoles acquire the lysosomal membrane protein LAMP-1, but not the vesicular proton-adenosine triphosphatase (ATPase) responsible for phagosomal acidification. This suggests either a selective inhibition of fusion with proton-ATPase-containing vesicles or a rapid removal of the complex from Mycobacterium phagosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sturgill-Koszycki, S -- Schlesinger, P H -- Chakraborty, P -- Haddix, P L -- Collins, H L -- Fok, A K -- Allen, R D -- Gluck, S L -- Heuser, J -- Russell, D G -- AI26889/AI/NIAID NIH HHS/ -- AI34207/AI/NIAID NIH HHS/ -- AR42370/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):678-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University Medical Center, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; Hydrogen-Ion Concentration ; Leishmania mexicana/physiology ; Lysosome-Associated Membrane Glycoproteins ; Macrophages/metabolism/*microbiology/parasitology/ultrastructure ; Membrane Fusion ; Membrane Glycoproteins/metabolism ; Mice ; Microscopy, Immunoelectron ; Mycobacterium avium/*physiology ; Mycobacterium tuberculosis/physiology ; Phagosomes/metabolism/*microbiology/parasitology/ultrastructure ; Proton-Translocating ATPases/*metabolism ; Vacuoles/metabolism/microbiology/parasitology/ultrastructure
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  • 296
    Publication Date: 1994-05-27
    Description: The transporter associated with antigen processing (TAP) delivers cytosolic peptides into the endoplasmic reticulum (ER) where they bind to nascent class 1 histocompatibility molecules. Class 1-peptide complexes are then displayed at the cell surface for recognition by cytotoxic T lymphocytes. Immunoprecipitation of either TAP or class 1 molecules revealed an association between the transporter and diverse class 1 products. TAP bound preferentially to heterodimers of the class 1 heavy chain and beta 2-microglobulin, and the complex subsequently dissociated in parallel with transport of class 1 molecules from the ER to the Golgi apparatus. The TAP-class 1 complexes could also be dissociated in vitro by the addition of class 1-binding peptides. The association of class 1 molecules with TAP likely promotes efficient capture of peptides before their exposure to the lumen of the ER.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, W K -- Cohen-Doyle, M F -- Fruh, K -- Wang, K -- Peterson, P A -- Williams, D B -- New York, N.Y. -- Science. 1994 May 27;264(5163):1322-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8191286" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Amino Acid Sequence ; Animals ; *Antigen Presentation ; Biological Transport ; Carrier Proteins/immunology/*metabolism ; Cell Line ; Endoplasmic Reticulum/metabolism ; Golgi Apparatus/metabolism ; H-2 Antigens/*metabolism ; Immune Sera ; Mice ; Molecular Sequence Data ; Precipitin Tests ; Protein Binding ; beta 2-Microglobulin/metabolism
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  • 297
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-09
    Description: Although several Plio-Pleistocene hominids are found in association with stone and bone tools, it has been generally assumed that at any one time the hominid with the largest brain was the toolmaker. Fossils recovered over the last decade suggest that early hominids subsequent to 2.5 million years ago all might have used tools and occupied "cultural" niches. A test for humanlike precision grasping (the enhanced ability to manipulate tools) is proposed and applied to australopithecines and early Homo. The results indicate that tools were likely to have been used by all early hominids at around 2.0 million years ago. The earliest australopithecines, which predate the appearance of stone tools in the archaeological record, do not show signs of advanced precision grasping.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Susman, R L -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1570-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomical Sciences, School of Medicine, State University at Stony Brook, NY 11794-8081.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomechanical Phenomena ; *Fossils ; Hand/anatomy & histology/*physiology ; History, Ancient ; Hominidae/*anatomy & histology ; Humans ; Metacarpus/*anatomy & histology ; Motor Skills ; Muscles/anatomy & histology/physiology ; Pan troglodytes/anatomy & histology ; *Thumb
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  • 298
    Publication Date: 1994-01-28
    Description: A gene encoding a protein related to the serpin family of protease inhibitors was identified as a candidate tumor suppressor gene that may play a role in human breast cancer. The gene product, called maspin, is expressed in normal mammary epithelial cells but not in most mammary carcinoma cell lines. Transfection of MDA-MB-435 mammary carcinoma cells with the maspin gene did not alter the cells' growth properties in vitro, but reduced the cells' ability to induce tumors and metastasize in nude mice and to invade through a basement membrane matrix in vitro. Analysis of human breast cancer specimens revealed that loss of maspin expression occurred most frequently in advanced cancers. These results support the hypothesis that maspin functions as a tumor suppressor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, Z -- Anisowicz, A -- Hendrix, M J -- Thor, A -- Neveu, M -- Sheng, S -- Rafidi, K -- Seftor, E -- Sager, R -- CA39814/CA/NCI NIH HHS/ -- P01 CA22427/CA/NCI NIH HHS/ -- R01 CA59702/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):526-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cancer Genetics, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290962" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Breast/*chemistry ; Breast Neoplasms/*chemistry/pathology ; Down-Regulation ; Epithelium/chemistry ; Female ; Gene Expression ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Nude ; Molecular Sequence Data ; Neoplasm Metastasis ; Neoplasm Transplantation ; Neoplasms, Experimental/pathology ; Proteins/analysis/genetics/*physiology ; Sequence Analysis ; Serpins/analysis/genetics/*physiology ; Transfection ; Tumor Cells, Cultured
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  • 299
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilmore, G L -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):264.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8093155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Immunity, Innate/genetics ; Interleukin-4/deficiency/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Murine Acquired Immunodeficiency Syndrome/genetics/*immunology ; Retroviridae/physiology ; T-Lymphocytes, Helper-Inducer/immunology
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  • 300
    Publication Date: 1994-11-18
    Description: The T cell antigen receptor (TCR) beta chain regulates early T cell development in the absence of the TCR alpha chain. The developmentally controlled gene described here encodes the pre-TCR alpha (pT alpha) chain, which covalently associates with TCR beta and with the CD3 proteins forms a pre-TCR complex that transduces signals in immature thymocytes. Unlike the lambda 5 pre-B cell receptor protein, the pT alpha chain is a type I transmembrane protein whose cytoplasmic tail contains two potential phosphorylation sites and a Src homology 3 (SH3)-domain binding sequence. Pre-TCR alpha transfection experiments indicated that surface expression of the pre-TCR is controlled by additional developmentally regulated proteins. Identification of the pT alpha gene represents an essential step in the structure-function analysis of the pre-TCR complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saint-Ruf, C -- Ungewiss, K -- Groettrup, M -- Bruno, L -- Fehling, H J -- von Boehmer, H -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1208-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM 373, Institut Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973703" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD3/metabolism ; Base Sequence ; Cell Line ; *Cloning, Molecular ; DNA, Complementary/genetics ; *Gene Expression Regulation, Developmental ; Gene Rearrangement ; Membrane Glycoproteins/chemistry/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Open Reading Frames ; Phosphorylation ; Polymerase Chain Reaction ; Rabbits ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/*genetics/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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