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  • National Institutes of Health (U.S.)  (218)
  • Cells, Cultured  (175)
  • American Association for the Advancement of Science (AAAS)  (393)
  • Cell Press
  • Irkutsk : Ross. Akad. Nauk, Sibirskoe Otd., Inst. Zemnoj Kory
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • 1990-1994  (393)
  • 1965-1969
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (393)
  • Cell Press
  • Irkutsk : Ross. Akad. Nauk, Sibirskoe Otd., Inst. Zemnoj Kory
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
Years
Year
  • 1
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    Panel backs pregnant women in trials (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1216.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122099" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Clinical Trials as Topic ; Female ; Humans ; Informed Consent ; *Institute of Medicine (U.S.) ; National Institutes of Health (U.S.) ; *Pregnancy ; *Pregnant Women ; Research Subjects ; United States ; *Women's Health
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Delocalization of Vg1 mRNA from the vegetal cortex in Xenopus oocytes after destruction of Xlsirt RNA (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: The Xlsirts are a family of transcribed repeat sequence genes that do not code for protein. Xlsirt RNAs become localized to the vegetal cortex of Xenopus oocytes early in oogenesis, before the localization of the messenger RNA Vg1, which encodes a transforming growth factor-beta-like molecule involved in mesoderm formation, and coincident with the localization of Xcat2 transcripts, which encode a nanos-like molecule. Destruction of the localized Xlsirts by injection of antisense oligodeoxynucleotides into stage 4 oocytes resulted in the release of Vg1 transcripts but not Xcat2 transcripts from the vegetal cortex. Xlsirt RNAs, which may be a structural component of the vegetal cortex, are a crucial part of a genetic pathway necessary for the proper localization of Vg1 that leads to subsequent normal pattern formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kloc, M -- Etkin, L D -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1101-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7520603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Glycoproteins/*genetics ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Oogenesis ; RNA/*genetics ; RNA, Messenger/genetics/*metabolism ; RNA-Binding Proteins/genetics ; Repetitive Sequences, Nucleic Acid ; Transforming Growth Factor beta/genetics ; Xenopus ; *Xenopus Proteins ; Zinc Fingers
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Functional participation of the IL-2 receptor gamma chain in IL-7 receptor complexes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The gamma chain of the interleukin-2 (IL-2) receptor is shared with the functional IL-4 receptor and is causatively related to X-linked severe combined immunodeficiency (XSCID), which is ascribed to a profound T cell defect. Studies with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells. Participation of the gamma subunit in more than one receptor may enable the elucidation of the mechanisms of XSCID development and lymphocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, M -- Takeshita, T -- Higuchi, M -- Nakamura, M -- Sudo, T -- Nishikawa, S -- Sugamura, K -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1453-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128231" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Female ; Genetic Linkage ; Interleukin-7/*metabolism/pharmacology ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin/*metabolism ; Receptors, Interleukin-2/genetics/immunology/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/*immunology ; X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    GDNF: a potent survival factor for motoneurons present in peripheral nerve and muscle (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: For survival, embryonic motoneurons in vertebrates depend on as yet undefined neurotrophic factors present in the limb bud. Members of the neurotrophin family are currently the best candidates for such neurotrophic factors, but inactivation of their receptor genes leads to only partial loss of motoneurons, which suggests that other factors are involved. Glial cell line-derived neurotrophic factor (GDNF), originally identified as a trophic factor specific for dopaminergic neurons, was found to be 75-fold more potent than the neurotrophins in supporting the survival of purified embryonic rat motoneurons in culture. GDNF messenger RNA was found in the immediate vicinity of motoneurons during the period of cell death in development. In vivo, GDNF rescues and prevents the atrophy of facial motoneurons that have been deprived of target-derived survival factors by axotomy. GDNF may therefore be a physiological trophic factor for spinal motoneurons. Its potency and specificity in vitro and in vivo also make it a good candidate for treatment of motoneuron disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, C E -- Phillips, H S -- Pollock, R A -- Davies, A M -- Lemeulle, C -- Armanini, M -- Simmons, L -- Moffet, B -- Vandlen, R A -- Simpson LC corrected to Simmons, L -- Koliatsos, V E -- Rosenthal, A -- NS 10580/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1062-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U.382, IBDM, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor ; Cell Death ; Cell Survival/drug effects ; Cells, Cultured ; Ciliary Neurotrophic Factor ; Face/innervation ; Glial Cell Line-Derived Neurotrophic Factor ; Growth Inhibitors/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Molecular Sequence Data ; Motor Neurons/*cytology/drug effects ; Muscle Fibers, Skeletal/*metabolism ; Nerve Growth Factors/analysis/biosynthesis/genetics/*pharmacology ; Nerve Tissue Proteins/*analysis/biosynthesis/genetics/*pharmacology ; Neurons, Afferent/cytology/drug effects ; Peripheral Nerves/*metabolism ; RNA, Messenger/analysis/genetics ; Rats ; Schwann Cells/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Embryo research guidelines (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, H -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1345.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073266" target="_blank"〉PubMed〈/a〉
    Keywords: *Embryo, Mammalian ; *Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; *Research ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Potential role of human cytomegalovirus and p53 interaction in coronary restenosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-15
    Description: A subset of patients who have undergone coronary angioplasty develop restenosis, a vessel renarrowing characterized by excessive proliferation of smooth muscle cells (SMCs). Of 60 human restenosis lesions examined, 23 (38 percent) were found to have accumulated high amounts of the tumor suppressor protein p53, and this correlated with the presence of human cytomegalovirus (HCMV) in the lesions. SMCs grown from the lesions expressed HCMV protein IE84 and high amounts of p53. HCMV infection of cultured SMCs enhanced p53 accumulation, which correlated temporally with IE84 expression. IE84 also bound to p53 and abolished its ability to transcriptionally activate a reporter gene. Thus, HCMV, and IE84-mediated inhibition of p53 function, may contribute to the development of restenosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Speir, E -- Modali, R -- Huang, E S -- Leon, M B -- Shawl, F -- Finkel, T -- Epstein, S E -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023160" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; *Angioplasty, Balloon ; Antigens, Viral/*metabolism ; Atherectomy, Coronary ; Base Sequence ; Cells, Cultured ; Coronary Disease/*etiology/pathology/therapy ; Coronary Vessels/cytology/metabolism/microbiology ; Cytomegalovirus/*physiology ; Genes, p53 ; Humans ; Immediate-Early Proteins/*metabolism ; Middle Aged ; Molecular Sequence Data ; Muscle, Smooth, Vascular/cytology/metabolism/microbiology ; Recurrence ; Transcriptional Activation ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Fostering young investigators (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fochtmann, L J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):953.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973669" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; National Institutes of Health (U.S.) ; *Research ; Research Personnel/*economics ; *Research Support as Topic ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Bumps on the vaccine road (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1371-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073270" target="_blank"〉PubMed〈/a〉
    Keywords: Centers for Disease Control and Prevention (U.S.) ; Drug Approval ; Drug Industry ; Humans ; Institute of Medicine (U.S.) ; National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States ; *Vaccines ; World Health Organization
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    New fight over fetal tissue grafts (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):600-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303261" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Control Groups ; Double-Blind Method ; Federal Government ; *Fetal Research ; *Fetal Tissue Transplantation ; Financing, Government ; Humans ; National Institutes of Health (U.S.) ; Parkinson Disease/*surgery ; Peer Review, Research ; Research Subjects ; Research Support as Topic ; Risk Assessment ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Cell suicide: by ICE, not fire (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):754-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303290" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caenorhabditis elegans/genetics ; Caspase 1 ; Cells, Cultured ; Free Radicals/metabolism ; Metalloendopeptidases/*genetics/metabolism ; Mice ; Mice, Knockout ; Neurons/cytology ; Oxygen/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; bcl-2-Associated X Protein ; bcl-X Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    A molecular determinant for submillisecond desensitization in glutamate receptors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: The decay of excitatory postsynaptic currents in central neurons mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors is likely to be shaped either by receptor desensitization or by offset after removal of glutamate from the synaptic cleft. Native AMPA receptors show desensitization time constants of 1 to about 10 milliseconds, but the underlying molecular determinants of these large differences are unknown. Cloned AMPA receptors carrying the "flop" splice variants of glutamate receptor subtype C (GluR-C) and GluR-D are shown to have desensitization time constants of around 1 millisecond, whereas those with the "flip" variants are about four times slower. Cerebellar granule cells switch their expression of GluR-D splice variants from mostly flip forms in early stages to predominantly flop forms in the adult rat brain. These findings suggest that rapid desensitization of AMPA receptors can be regulated by the expression and alternative splicing of GluR-D gene transcripts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosbacher, J -- Schoepfer, R -- Monyer, H -- Burnashev, N -- Seeburg, P H -- Ruppersberg, J P -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1059-62.〈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/7973663" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cloning, Molecular ; Glutamic Acid/*pharmacology ; In Situ Hybridization ; Oocytes ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/drug effects/genetics/*physiology ; Recombinant Proteins ; Synaptic Transmission ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, 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/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
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  • 13
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    Visualization of quantal synaptic transmission by dendritic calcium imaging (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: As changes in synaptic strength are thought to be critical for learning and memory, it would be useful to monitor the activity of individual identified synapses on mammalian central neurons. Calcium imaging of cortical neurons grown in primary culture was used to visualize the activation of individual postsynaptic elements by miniature excitatory synaptic currents elicited by spontaneous quantal release. This approach revealed that the probability of spontaneous activity differed among synapses on the same dendrite. Furthermore, synapses that undergo changes in activity induced by glutamate or phorbol ester treatment were identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, T H -- Baraban, J M -- Wier, W G -- Blatter, L A -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):529-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, 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/7904774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Cerebral Cortex ; Dendrites/*metabolism ; Glutamates/pharmacology ; Glutamic Acid ; Kinetics ; Microelectrodes ; Neuronal Plasticity ; Neurons/*physiology ; Phorbol Esters/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology ; *Synaptic Transmission ; Tetrodotoxin/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Direct signaling from astrocytes to neurons in cultures of mammalian brain cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: Although astrocytes have been considered to be supportive, rather than transmissive, in the adult nervous system, recent studies have challenged this assumption by demonstrating that astrocytes possess functional neurotransmitter receptors. Astrocytes are now shown to directly modulate the free cytosolic calcium, and hence transmission characteristics, of neighboring neurons. When a focal electric field potential was applied to single astrocytes in mixed cultures of rat forebrain astrocytes and neurons, a prompt elevation of calcium occurred in the target cell. This in turn triggered a wave of calcium increase, which propagated from astrocyte to astrocyte. Neurons resting on these astrocytes responded with large increases in their concentration of cytosolic calcium. The gap junction blocker octanol attenuated the neuronal response, which suggests that the astrocytic-neuronal signaling is mediated through intercellular connections rather than synaptically. This neuronal response to local astrocytic stimulation may mediate local intercellular communication within the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedergaard, M -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, 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/8134839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/drug effects/*metabolism ; Calcium/*metabolism ; Cell Communication ; Cells, Cultured ; Electric Stimulation ; Excitatory Amino Acid Antagonists ; Gap Junctions/physiology ; Kynurenic Acid/pharmacology ; Neurons/drug effects/*metabolism ; Nifedipine/pharmacology ; Octanols/pharmacology ; Prosencephalon/*cytology/embryology ; Rats ; *Signal Transduction ; Synapses/metabolism ; Tetrodotoxin/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-22
    Description: Two molecular mechanisms of T cell-mediated cytotoxicity, one perforin-based, the other Fas-based, have been demonstrated. To determine the extent of their contribution to T cell-mediated cytotoxicity, a range of effector cells from normal control or perforin-deficient mice were tested against a panel of target cells with various levels of Fas expression. All cytotoxicity observed was due to either of these mechanisms, and no third mechanism was detected. Thus, the perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagi, D -- Vignaux, F -- Ledermann, B -- Burki, K -- Depraetere, V -- Nagata, S -- Hengartner, H -- Golstein, P -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518614" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD95 ; Antigens, Surface/*immunology ; Cells, Cultured ; Concanavalin A/pharmacology ; *Cytotoxicity, Immunologic ; Ionomycin/pharmacology ; Leukemia L1210 ; Lymphocyte Culture Test, Mixed ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A National Institute for the Environment (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saundry, P D -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):185.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146642" target="_blank"〉PubMed〈/a〉
    Keywords: *Environment ; *Government Agencies ; National Institutes of Health (U.S.) ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Modulation of epithelial cell growth by intraepithelial gamma delta T cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: The role played in immune surveillance by gamma delta T cells residing in various epithelia has not been clear. It is shown here that activated gamma delta T cells obtained from skin and intestine express the epithelial cell mitogen keratinocyte growth factor (KGF). In contrast, intraepithelial alpha beta T cells, as well as all lymphoid alpha beta and gamma delta T cell populations tested, did not produce KGF or promote the growth of cultured epithelial cells. These results suggest that intraepithelial gamma delta T cells function in surveillance and in repair of damaged epithelial tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1253-5.〈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/7973709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Dendritic Cells/*physiology ; Epithelial Cells ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors ; Growth Substances/*biosynthesis/genetics ; Keratinocytes/*cytology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; *Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocyte Subsets/immunology/metabolism/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Regulation of melanin biosynthesis in the human epidermis by tetrahydrobiopterin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The participation of (6R) 5,6,7,8-tetrahydrobiopterin (6-BH4) in regulating the tyrosine supply for melanin biosynthesis was investigated by the examination of human keratinocytes, melanocytes, and epidermal suction blisters from normal human skin and from patients with the depigmentation disorder vitiligo. Cells, as well as total epidermis, contained high phenylalanine hydroxylase activities and also displayed the capacity to synthesize and recycle 6-BH4, the essential cofactor for this enzyme. In vitiligo, 4a-hydroxy-BH4 dehydratase activity was extremely low or absent, yielding an accumulation of the nonenzymatic by-product 7-tetrahydrobiopterin (7-BH4) at concentrations up to 8 x 10(-6) M in the epidermis. This by-product is a potent competitive inhibitor in the phenylalanine hydroxylase reaction with an inhibition constant of 10(-6) M. Thus, 6-BH4 seems to control melanin biosynthesis in the human epidermis, whereas 7-BH4 may initiate depigmentation in patients with vitiligo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schallreuter, K U -- Wood, J M -- Pittelkow, M R -- Gutlich, M -- Lemke, K R -- Rodl, W -- Swanson, N N -- Hitzemann, K -- Ziegler, I -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1444-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128228" target="_blank"〉PubMed〈/a〉
    Keywords: Biopterin/*analogs & derivatives/biosynthesis/metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Epidermis/*metabolism ; GTP Cyclohydrolase/metabolism ; Humans ; Keratinocytes/metabolism ; Melanins/*biosynthesis ; Melanocytes/metabolism ; Phenylalanine Hydroxylase/antagonists & inhibitors/metabolism ; Tyrosine/biosynthesis ; Vitiligo/*metabolism
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    Padlock probes: circularizing oligonucleotides for localized DNA detection (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: Nucleotide sequence information derived from DNA segments of the human and other genomes is accumulating rapidly. However, it frequently proves difficult to use such short DNA segments to identify clones in genomic libraries or fragments in blots of the whole genome or for in situ analysis of chromosomes. Oligonucleotide probes, consisting of two target-complementary segments, connected by a linker sequence, were designed. Upon recognition of the specific nucleic acid molecule the ends of the probes were joined through the action of a ligase, creating circular DNA molecules catenated to the target sequence. These probes thus provide highly specific detection with minimal background.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nilsson, M -- Malmgren, H -- Samiotaki, M -- Kwiatkowski, M -- Chowdhary, B P -- Landegren, U -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2085-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beijer Laboratory, Department of Medical Genetics, Biomedical Center, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522346" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cells, Cultured ; Chromosomes, Human, Pair 12 ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA/*analysis ; DNA, Circular/*analysis ; Genetic Vectors ; Humans ; In Situ Hybridization ; Lymphocytes ; Membrane Proteins/genetics ; Models, Molecular ; Molecular Sequence Data ; Nucleic Acid Conformation ; *Oligonucleotide Probes/chemistry ; Repetitive Sequences, Nucleic Acid ; Templates, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Cloning of a T cell growth factor that interacts with the beta chain of the interleukin-2 receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: A cytokine was identified that stimulated the proliferation of T lymphocytes, and a complementary DNA clone encoding this new T cell growth factor was isolated. The cytokine, designated interleukin-15 (IL-15), is produced by a wide variety of cells and tissues and shares many biological properties with IL-2. Monoclonal antibodies to the beta chain of the IL-2 receptor inhibited the biological activity of IL-15, and IL-15 competed for binding with IL-2, indicating that IL-15 uses components of the IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grabstein, K H -- Eisenman, J -- Shanebeck, K -- Rauch, C -- Srinivasan, S -- Fung, V -- Beers, C -- Richardson, J -- Schoenborn, M A -- Ahdieh, M -- New York, N.Y. -- Science. 1994 May 13;264(5161):965-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Research and Development Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; *Cloning, Molecular ; Haplorhini ; Humans ; Interleukin-15 ; Interleukin-2/immunology/metabolism/pharmacology ; Interleukins/chemistry/*genetics/metabolism/pharmacology ; Killer Cells, Lymphokine-Activated/immunology ; Leukocytes, Mononuclear/immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Molecular Sequence Data ; Protein Structure, Secondary ; Receptors, Interleukin-2/immunology/*metabolism ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology
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    T cells and suppression in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, B -- Kaye, J -- Lo, D -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):464-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; *Clonal Anergy ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; T-Lymphocytes, Regulatory/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Noradrenergic regulation of cholinergic differentiation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: When the sympathetic nerves that innervate rat sweat glands reach their targets, they are induced to switch from using norepinephrine as their neurotransmitter to acetylcholine. Catecholamines (such as norepinephrine) released by nerves growing to the sweat gland induce this phenotypic conversion by stimulating production of a cholinergic differentiation factor [sweat gland factor (SGF)] by gland cells. Here, culture of gland cells with sympathetic, but not sensory, neurons induced SGF production. Blockage of alpha 1- or beta-adrenergic receptors prevented acquisition of the cholinergic phenotype in sympathetic neurons co-cultured with sweat glands, and sweat glands from sympathectomized animals lacked SGF. Thus, reciprocal instructive interactions, mediated in part by small molecule neurotransmitters, direct the development of this synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habecker, B A -- Landis, S C -- NS-023678/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1602-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106-4975.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202714" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Base Sequence ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Glycoproteins/*biosynthesis ; Molecular Sequence Data ; Neuregulins ; Neurons/cytology/physiology ; Neurons, Afferent/cytology/physiology ; Parasympathetic Nervous System/cytology/*physiology ; Phenotype ; Rats ; Receptors, Adrenergic/*physiology ; Sweat Glands/cytology/*innervation/metabolism ; Sympathectomy ; Sympathetic Nervous System/cytology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Glia: the brain's other cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):970-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973679" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/physiology ; Brain/*cytology/physiology ; Calcium/metabolism ; Cell Communication ; Cells, Cultured ; Humans ; Nerve Growth Factors/biosynthesis ; Neuroglia/*physiology ; Neurons/physiology ; Neurotransmitter Agents/metabolism ; Synapses/metabolism
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    Peer review. Congress finds little bias in system (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):863.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052838" target="_blank"〉PubMed〈/a〉
    Keywords: *Government Agencies ; National Institutes of Health (U.S.) ; *Peer Review, Research ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 25
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    Hepatitis study. Drug trial deaths deemed unavoidable (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1530.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202706" target="_blank"〉PubMed〈/a〉
    Keywords: Antiviral Agents/*adverse effects/therapeutic use ; Arabinofuranosyluracil/adverse effects/*analogs & derivatives/therapeutic use ; Clinical Trials as Topic/*standards ; Drug-Induced Liver Injury ; Federal Government ; Government Regulation ; Hepatitis B/*drug therapy ; Humans ; National Institutes of Health (U.S.) ; Pancreatic Diseases/chemically induced ; *Research Subjects ; 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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    Scripps to get less from Sandoz (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 May 20;264(5162):1077.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178164" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/economics ; *Biotechnology ; *Drug Industry/economics ; Financing, Government ; National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States
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  • 27
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    Genetic engineering. Safety concerns halt U.K. study (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kingman, S -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):748.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303287" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Advisory Committees ; Cells, Cultured ; *Containment of Biohazards ; *Genetic Engineering ; *Government Regulation ; Great Britain ; Humans ; *Oncogenes ; Simian virus 40/*genetics
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  • 28
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    Minnesota drug sales (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasselmo, N -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):453.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290944" target="_blank"〉PubMed〈/a〉
    Keywords: *Antilymphocyte Serum/therapeutic use ; *Drugs, Investigational ; Humans ; Minnesota ; National Institutes of Health (U.S.) ; Research/*standards ; Research Support as Topic ; *Schools, Medical ; United States
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  • 29
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    Activity-dependent changes in the intrinsic properties of cultured neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 30
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    AIDS vaccine research. U.S. panel votes to delay real-world vaccine trials (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 31
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    Weighing HIV vaccine trials (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Aug 5;265(5173):735.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047878" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; *Clinical Trials as Topic ; Humans ; National Institutes of Health (U.S.) ; United States ; World Health Organization
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Prevention of vertebrate neuronal death by the crmA gene (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Stimulation of human gamma delta T cells by nonpeptidic mycobacterial ligands (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: Most human peripheral blood gamma delta T lymphocytes respond to hitherto unidentified mycobacterial antigens. Four ligands from Mycobacterium tuberculosis strain H37Rv that stimulated proliferation of a major human gamma delta T cell subset were isolated and partially characterized. One of these ligands, TUBag4, is a 5' triphosphorylated thymidine-containing compound, to which the three other stimulatory molecules are structurally related. These findings support the hypothesis that some gamma delta T cells recognize nonpeptidic ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constant, P -- Davodeau, F -- Peyrat, M A -- Poquet, Y -- Puzo, G -- Bonneville, M -- Fournie, J J -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):267-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department III, Laboratoire de Pharmacologie et de Toxicologie Fondamentales du CNRS, Toulouse, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146660" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Bacterial/chemistry/*immunology/isolation & purification ; Cells, Cultured ; Chromatography, Ion Exchange ; Humans ; Ligands ; *Lymphocyte Activation ; Magnetic Resonance Spectroscopy ; Mycobacterium tuberculosis/*immunology ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*immunology ; Thymine Nucleotides/analysis/chemistry/*immunology/isolation & purification
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    DNA repair rates mapped along the human PGK1 gene at nucleotide resolution (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The repair of cyclobutane pyrimidine dimers (CPDs), DNA lesions induced by ultraviolet light, was studied at nucleotide resolution. Human fibroblasts were irradiated with ultraviolet light and allowed to repair. The DNA was enzymatically cleaved at the CPDs, and the induced breaks along the promoter and exon 1 of the PGK1 gene were mapped by ligation-mediated polymerase chain reaction. Repair rates within the nontranscribed strand varied as much as 15-fold, depending on nucleotide position. Preferential repair of the transcribed strand began just downstream of the transcription start site but was most pronounced beginning at nucleotide +140 in exon 1. The promoter contained two slowly repaired regions that coincided with two transcription factor binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, S -- Drouin, R -- Holmquist, G P -- CA54773/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1438-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beckman Research Institute of the City of Hope, Department of Biology, Duarte, CA 91010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128226" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cells, Cultured ; *DNA Repair ; Exons ; *Genes ; HeLa Cells ; Humans ; Kinetics ; Phosphoglycerate Kinase/*genetics ; Promoter Regions, Genetic ; Pyrimidine Dimers/*metabolism ; Skin/metabolism/*radiation effects ; Transcription Factors/metabolism ; Transcription, Genetic ; Ultraviolet Rays
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    T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Requirement for BDNF in activity-dependent survival of cortical neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Problems in clinical trials go far beyond misconduct (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1538-41.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202708" target="_blank"〉PubMed〈/a〉
    Keywords: Biomarkers ; Editorial Policies ; Education, Medical, Continuing ; Federal Government ; Female ; Government Regulation ; Humans ; Male ; Meta-Analysis as Topic ; National Institutes of Health (U.S.) ; Random Allocation ; Randomized Controlled Trials as Topic/*standards/statistics & numerical data ; Scientific Misconduct ; United States ; United States Food and Drug Administration
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    The company that genome researchers love to hate (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1800-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997873" target="_blank"〉PubMed〈/a〉
    Keywords: *Biotechnology ; Chromosome Mapping ; DNA Repair ; DNA, Complementary/*genetics ; *Databases, Factual ; Gene Expression ; *Genome, Human ; Human Genome Project ; Humans ; National Institutes of Health (U.S.) ; Private Sector ; Public Sector ; Sequence Analysis, DNA ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Tamoxifen: hanging in the balance (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1524, 1526-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202702" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Neoplasms/*prevention & control ; *Clinical Trials as Topic ; Coronary Disease/prevention & control ; Endometrial Neoplasms/chemically induced ; Female ; Humans ; Informed Consent ; Lipids/blood ; Middle Aged ; National Institutes of Health (U.S.) ; Risk Factors ; Tamoxifen/adverse effects/*therapeutic use ; United States
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    Academic medicine's stake in health care reform (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1081.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108723" target="_blank"〉PubMed〈/a〉
    Keywords: Academic Medical Centers/*economics ; Education, Medical, Graduate/economics ; Financing, Government ; *Health Care Reform ; Humans ; National Institutes of Health (U.S.) ; Preventive Medicine/economics ; *Research Support as Topic ; Schools, Medical ; United States
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  • 41
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    Involvement of the IRF-1 transcription factor in antiviral responses to interferons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: The mechanisms underlying interferon (IFN)-induced antiviral states are not well understood. Interferon regulatory factor-1 (IRF-1) is an IFN-inducible transcriptional activator, whereas IRF-2 suppresses IRF-1 action. The inhibition of encephalomyocarditis virus (EMCV) replication by IFN-alpha and especially by IFN-gamma was impaired in cells from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice). The IRF-1-/- mice were less resistant than normal mice to EMCV infection, as revealed by accelerated mortality and a larger virus titer in target organs. The absence of IRF-1 did not clearly affect replication of two other types of viruses. Thus, IRF-1 is necessary for the antiviral action of IFNs against some viruses, but IFNs activate multiple activation pathways through diverse target genes to induce the antiviral state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimura, T -- Nakayama, K -- Penninger, J -- Kitagawa, M -- Harada, H -- Matsuyama, T -- Tanaka, N -- Kamijo, R -- Vilcek, J -- Mak, T W -- R35CA49731/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1921-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009222" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiovirus Infections/*immunology/microbiology ; Cells, Cultured ; DNA-Binding Proteins/genetics/*physiology ; Encephalomyocarditis virus/physiology ; Gene Expression Regulation ; Interferon Regulatory Factor-1 ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Mice ; Mutation ; Phosphoproteins/genetics/*physiology ; Simplexvirus/physiology ; Transcription Factors/genetics/*physiology ; Vesicular stomatitis Indiana virus/physiology ; *Virus Replication
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    Ahead of schedule and on budget (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):199.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939646" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Financing, Government ; Government Agencies ; Health Care Reform ; *Human Genome Project/economics/organization & administration ; Humans ; National Institutes of Health (U.S.) ; United States
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    Malaria vaccine research (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: In our report "Activation of Raf as a result of recruitment to the plasma membrane" (3 June, p. 1463) (1), panels E and F of figure 1 on page 1464 were incorrect. The correct photographs appear below. In addition, the [See figure in the PDF file] second sentence of the legend to figure 1 should have read, "The Raf constructs were tagged at the COOH-terminus with a Glu-Glu epitope (MEYMPME) (24) for c-Raf, or at the NH(2)-terminus with both the Glu-Glu and the Myc (MEQKLISEEDL) (23) epitopes for RafCAAX"; the next-to-the-last sentence of the legend to figure 1 should have read, "The c-Raf constructs in (A through D) are Glu-Glu-tagged and were detected by using an anti Glu-Glu antibody, and the RafCAAX and Raf6QCAAX constructs used in E and F were detected by using the antibody to Raf COOH-terminal peptide"; and the third sentence of note 26 should have read, "After blocking with 5% milk in phosphate-buffered saline (M-PBS), cells were incubated with a mouse monoclonal antibody to Glu-Glu or a rabbit polyclonal antibody to a 20-amino acid COOH-terminal peptide of Raf-1 (Santa Cruz Biotechnology, Santa Cruz, California), washed, and incubated with donkey antibodies to mouse or rabbit IgG combined with Texas Red (Jackson) in M-PBS, washed, and mounted in FITC-Guard (Testog)."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ballou, W R -- Diggs, C L -- Landry, S -- Hall, B F -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1792.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7864993" target="_blank"〉PubMed〈/a〉
    Keywords: Government Agencies ; Humans ; International Cooperation ; *Malaria Vaccines ; National Institutes of Health (U.S.) ; *Research ; United States ; World Health Organization
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    AIDS research. U.S.-French patent dispute heads for a showdown (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):23-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016652" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Serodiagnosis/*legislation & jurisprudence ; France ; HIV/isolation & purification ; Humans ; National Institutes of Health (U.S.) ; *Patents as Topic ; Scientific Misconduct ; United States
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    Science in the national interest (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mikulski, B A -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):221-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146650" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; *Financing, Government ; National Institutes of Health (U.S.) ; *Research Support as Topic ; Science/*economics ; United States
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    The hand on your purse strings (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mikulski, B -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):192-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146645" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; *Financing, Government ; Government Agencies/*economics ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States ; United States Food and Drug Administration
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    NIH neural transplantation funding (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Widner, H -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):737.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303281" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; *Fetal Tissue Transplantation ; Humans ; National Institutes of Health (U.S.) ; Nerve Tissue/embryology/*transplantation ; Parkinson Disease/*surgery ; Research Support as Topic ; United States
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    MicroGeneSys. Peer review triumphs over lobbying (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):463.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290949" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/therapeutic use ; Acquired Immunodeficiency Syndrome/*therapy ; Clinical Trials as Topic ; Government Agencies ; Humans ; National Institutes of Health (U.S.) ; Peer Review, Research ; Recombinant Proteins/therapeutic use ; *Research Support as Topic ; United States ; Vaccines, Synthetic
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    AIDS blood-test royalties. NIH-Pasteur: a final rapprochement? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- Marshall, E -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023149" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Serodiagnosis/*economics ; France ; HIV/isolation & purification ; Humans ; International Cooperation ; National Institutes of Health (U.S.) ; *Patents as Topic ; United States
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    NIH to study "germ-line" therapy (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1631.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11644652" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Federal Government ; Fetal Diseases/*therapy ; *Fetal Research ; *Genetic Therapy ; *Germ Cells ; Government ; Humans ; National Institutes of Health (U.S.) ; *Public Policy ; *Research ; United States
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    Control of topographic retinal axon branching by inhibitory membrane-bound molecules (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-05
    Description: Retinotopic map development in nonmammalian vertebrates appears to be controlled by molecules that guide or restrict retinal axons to correct locations in their targets. However, the retinotopic map in the superior colliculus (SC) of the rat is developed instead by a topographic bias in collateral branching and arborization. Temporal retinal axons extending across alternating membranes from the topographically correct rostral SC or the incorrect caudal SC of embryonic rats preferentially branch on rostral membranes. Branching preference is due to an inhibitory phosphatidylinositol-linked molecule in the caudal SC. Thus, position-encoding membrane-bound molecules may establish retinotopic maps in mammals by regulating axon branching, not by directing axon growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roskies, A L -- O'Leary, D D -- NEI RO1 EY07025/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):799-803.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, Salk Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Carbocyanines ; Cells, Cultured ; Embryonic and Fetal Development/physiology ; Fluorescent Dyes ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoric Diester Hydrolases ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/*physiology ; Superior Colliculi/embryology
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    Embryo cloners jumped the gun (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Dec 23;266(5193):1949.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11644654" target="_blank"〉PubMed〈/a〉
    Keywords: *Cloning, Organism ; Deception ; *Embryo Research ; Embryo, Mammalian ; Ethical Review ; Ethics ; Ethics Committees ; Ethics Committees, Research ; Federal Government ; Government ; Government Regulation ; Humans ; National Institutes of Health (U.S.) ; Organizational Policy ; *Research ; Research Personnel ; *Scientific Misconduct ; Social Control, Formal ; United States ; Universities
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    Anergic T cells as suppressor cells in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: T cell-mediated suppression is an established phenomenon, but its underlying mechanisms are obscure. An in vitro system was used to test the possibility that anergic T cells can act as specific suppressor cells. Anergic human T cells caused inhibition of antigen-specific and allospecific T cell proliferation. In order for the inhibition to occur, the anergic T cells had to be specific for the same antigen-presenting cells (APCs) as the T cells that were suppressed. The mechanism of this suppression appears to be competition for the APC surface and for locally produced interleukin-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lombardi, G -- Sidhu, S -- Batchelor, R -- Lechler, R -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1587-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Royal Postgraduate Medical School, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202711" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Cell Line ; Cells, Cultured ; *Clonal Anergy ; Humans ; Interleukin-10/immunology ; Interleukin-2/immunology/secretion ; Interleukin-4/immunology ; Lymphocyte Activation ; Recombinant Proteins/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Transforming Growth Factor beta/immunology
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    Generation of lymphohematopoietic cells from embryonic stem cells in culture (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: An efficient system was developed that induced the differentiation of embryonic stem (ES) cells into blood cells of erythroid, myeloid, and B cell lineages by coculture with the stromal cell line OP9. This cell line does not express functional macrophage colony-stimulating factor (M-CSF). The presence of M-CSF had inhibitory effects on the differentiation of ES cells to blood cells other than macrophages. Embryoid body formation or addition of exogenous growth factors was not required, and differentiation was highly reproducible even after the selection of ES cells with the antibiotic G418. Combined with the ability to genetically manipulate ES cells, this system will facilitate the study of molecular mechanisms involved in development and differentiation of hematopoietic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, T -- Kodama, H -- Honjo, T -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Faculty of Medicine, Kyoto University Yoshida, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/cytology ; Base Sequence ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Culture Media ; Erythrocytes/cytology ; Erythropoiesis ; Gene Rearrangement ; *Hematopoiesis ; Hematopoietic Stem Cells/*cytology ; Lymphocytes/*cytology ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/cytology ; Mesoderm/cytology ; Mice ; Molecular Sequence Data ; Recombinant Proteins/pharmacology ; Stromal Cells/cytology
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    Funding crunch hobbles antibiotic resistance research (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culotta, E -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):362-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153617" target="_blank"〉PubMed〈/a〉
    Keywords: *Anti-Bacterial Agents/pharmacology/therapeutic use ; Centers for Disease Control and Prevention (U.S.) ; Drug Approval ; *Drug Resistance, Microbial ; Financing, Government ; Humans ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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    Differential effects of apolipoproteins E3 and E4 on neuronal growth in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-06
    Description: Apolipoprotein E4 (apoE4), one of the three common isoforms of apoE, has been implicated in Alzheimer's disease. The effects of apoE on neuronal growth were determined in cultures of dorsal root ganglion neurons. In the presence of beta-migrating very low density lipoproteins (beta-VLDL), apoE3 increased neurite outgrowth, whereas apoE4 decreased outgrowth. The effects of apoE3 or apoE4 in the presence of beta-VLDL were prevented by incubation with a monoclonal antibody to apoE or by reductive methylation of apoE, both of which block the ability of apoE to interact with lipoprotein receptors. The data suggest that receptor-mediated binding or internalization (or both) of apoE-enriched beta-VLDL leads to isoform-specific differences in interactions with cellular proteins that affect neurite outgrowth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathan, B P -- Bellosta, S -- Sanan, D A -- Weisgraber, K H -- Mahley, R W -- Pitas, R E -- HL 41633/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 May 6;264(5160):850-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Cardiovascular Disease, University of California, San Francisco 94141-9100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171342" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein E3 ; Apolipoprotein E4 ; Apolipoproteins E/metabolism/*pharmacology ; Cells, Cultured ; Culture Media, Serum-Free ; Fetus ; Ganglia, Spinal ; Lipoproteins, VLDL/pharmacology ; Neurites/*drug effects/ultrastructure ; Neurons/cytology/*drug effects ; Rabbits ; Receptors, LDL/metabolism
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    Control of angiogenesis in fibroblasts by p53 regulation of thrombospondin-1 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-09
    Description: As normal cells progress toward malignancy, they must switch to an angiogenic phenotype to attract the nourishing vasculature that they depend on for their growth. In cultured fibroblasts from Li-Fraumeni patients, this switch was found to coincide with loss of the wild-type allele of the p53 tumor suppressor gene and to be the result of reduced expression of thrombospondin-1 (TSP-1), a potent inhibitor of angiogenesis. Transfection assays revealed that p53 can stimulate the endogenous TSP-1 gene and positively regulate TSP-1 promoter sequences. These data indicate that, in fibroblasts, wild-type p53 inhibits angiogenesis through regulation of TSP-1 synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dameron, K M -- Volpert, O V -- Tainsky, M A -- Bouck, N -- CA52750/CA/NCI NIH HHS/ -- CA64239/CA/NCI NIH HHS/ -- P01 CA34936/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1582-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7521539" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cells, Cultured ; Fibroblasts/*metabolism ; *Gene Expression Regulation ; *Genes, p53 ; Humans ; Li-Fraumeni Syndrome ; Membrane Glycoproteins/biosynthesis/*genetics/physiology ; *Neovascularization, Pathologic ; Phenotype ; Promoter Regions, Genetic ; Thrombospondins ; Transfection
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    Ability of HIV to promote a TH1 to TH0 shift and to replicate preferentially in TH2 and TH0 cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: Both interferon gamma (IFN-gamma) produced by T helper 1 (TH1) lymphocytes and interleukin-4 (IL-4) produced by TH2 lymphocytes were reduced in either bulk circulating mononuclear cells or mitogen-induced CD4+ T cell clones from the peripheral blood of individuals infected with human immunodeficiency virus (HIV). There was a preferential reduction in clones producing IL-4 and IL-5 in the advanced phases of infection. However, enhanced proportions of CD4+ T cell clones producing both TH1-type and TH2-type cytokines (TH0 clones) were generated from either skin-infiltrating T cells that had been activated in vivo or peripheral blood T cells stimulated by antigen in vitro when cells were isolated from HIV-infected individuals. All TH2 and most TH0 clones supported viral replication, although viral replication was not detected in any of the TH1 clones infected in vitro with HIV. These results suggest that HIV (i) does not induce a definite TH1 to TH2 switch, but can favor a shift to the TH0 phenotype in response to recall antigens, and (ii) preferentially replicates in CD4+ T cells producing TH2-type cytokines (TH2 and TH0).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maggi, E -- Mazzetti, M -- Ravina, A -- Annunziato, F -- de Carli, M -- Piccinni, M P -- Manetti, R -- Carbonari, M -- Pesce, A M -- del Prete, G -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):244-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Clinical Immunology and Allergy, University of Florence, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023142" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Cell Line ; Cells, Cultured ; HIV/*physiology ; HIV Infections/*immunology/microbiology ; HIV Seropositivity/immunology ; Humans ; Immunologic Memory ; Interferon-gamma/*biosynthesis ; Interleukin-4/biosynthesis ; Interleukin-5/biosynthesis ; Interleukins/*biosynthesis ; Lymphocyte Activation ; Phenotype ; T-Lymphocytes, Helper-Inducer/*immunology/microbiology ; Virus Replication
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    c-Fos: a key regulator of osteoclast-macrophage lineage determination and bone remodeling (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-21
    Description: Mice lacking the proto-oncogene c-fos develop the bone disease osteopetrosis. Fos mutant mice were found to have a block in the differentiation of bone-resorbing osteoclasts that was intrinsic to hematopoietic cells. Bone marrow transplantation rescued the osteopetrosis, and ectopic c-fos expression overcame this differentiation block. The lack of Fos also caused a lineage shift between osteoclasts and macrophages that resulted in increased numbers of bone marrow macrophages. These results identify Fos as a key regulator of osteoclast-macrophage lineage determination in vivo and provide insights into the molecular mechanisms underlying metabolic bone diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grigoriadis, A E -- Wang, Z Q -- Cecchini, M G -- Hofstetter, W -- Felix, R -- Fleisch, H A -- Wagner, E F -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):443-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Transplantation ; Bone Remodeling/*physiology ; Cell Differentiation ; Cells, Cultured ; Genes, fos ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology ; Macrophages/*cytology ; Mice ; Mice, Mutant Strains ; Osteoclasts/*cytology ; Osteogenesis ; Osteopetrosis/metabolism/pathology ; Proto-Oncogene Proteins c-fos/genetics/*physiology
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    Human embryo research. Clinton rules out some studies (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1634-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992040" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Embryo Research ; *Embryo, Mammalian ; Federal Government ; Financing, Government ; *Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; *Research ; *Research Embryo Creation ; Research Support as Topic ; United States
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    Molecular medicine. One less hoop for gene therapy (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036507" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Clinical Protocols ; Ethical Review ; Federal Government ; Genetic Therapy/*legislation & jurisprudence ; *Government Regulation ; Humans ; National Institutes of Health (U.S.) ; United States ; United States Food and Drug Administration
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    Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-11
    Description: Ultraviolet light has been linked with the development of human skin cancers. Such cancers often exhibit mutations in the p53 tumor suppressor gene. Ligation-mediated polymerase chain reaction was used to analyze at nucleotide resolution the repair of cyclobutane pyrimidine dimers along the p53 gene in ultraviolet-irradiated human fibroblasts. Repair rates at individual nucleotides were highly variable and sequence-dependent. Slow repair was seen at seven of eight positions frequently mutated in skin cancer, suggesting that repair efficiency may strongly contribute to the mutation spectrum in a cancer-associated gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tornaletti, S -- Pfeifer, G P -- ES06070/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1436-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beckman Rsearch Institute of the City of Hope, Department of Biology, Duarte, CA 91010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128225" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; *DNA Repair ; Exons ; *Genes, p53 ; HeLa Cells ; Humans ; Mutation ; Phosphoglycerate Kinase/genetics ; Polymerase Chain Reaction ; Pyrimidine Dimers/*metabolism ; Skin/metabolism/*radiation effects ; Skin Neoplasms/*genetics/metabolism ; Ultraviolet Rays
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  • 63
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    Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-08
    Description: Although beta-amyloid is the main constituent of neurite plaques and may play a role in the pathophysiology of Alzheimer's disease, mechanisms by which soluble beta-amyloid might produce early symptoms such as memory loss before diffuse plaque deposition have not been implicated. Treatment of fibroblasts with beta-amyloid (10 nM) induced the same potassium channel dysfunction previously shown to occur specifically in fibroblasts from patients with Alzheimer's disease--namely, the absence of a 113-picosiemen potassium channel. A tetraethylammonium-induced increase of intracellular concentrations of calcium, [Ca2+]i, a response that depends on functional 113-picosiemen potassium channels, was also eliminated or markedly reduced by 10 nM beta-amyloid. Increased [Ca2+]i induced by high concentrations of extracellular potassium and 166-picosiemen potassium channels were unaffected by 10 nM beta-amyloid. In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Etcheberrigaray, R -- Ito, E -- Kim, C S -- Alkon, D L -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146663" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism ; Amyloid beta-Peptides/*pharmacology ; Bombesin/pharmacology ; Calcium/metabolism ; Cell Line ; Cells, Cultured ; Dimethyl Sulfoxide/pharmacology ; Female ; Fibroblasts/*drug effects/metabolism ; Humans ; Male ; Phenotype ; Potassium Channel Blockers ; Potassium Channels/*drug effects/metabolism ; Potassium Chloride/pharmacology ; Solubility ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology
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    Parallel computing in biomedical research (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: Scalable parallel computer architectures provide the computational performance needed for advanced biomedical computing problems. The National Institutes of Health have developed a number of parallel algorithms and techniques useful in determining biological structure and function. These applications include processing electron micrographs to determine the three-dimensional structure of viruses, calculating the solvent-accessible surface area of proteins to help predict the three-dimensional conformation of these molecules from their primary structures, and searching for homologous DNA or amino acid sequences in large biological databases. Timing results demonstrate substantial performance improvements with parallel implementations compared with conventional sequential systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martino, R L -- Johnson, C A -- Suh, E B -- Trus, B L -- Yap, T K -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):902-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computational Bioscience and Engineering Laboratory, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052847" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Capsid/ultrastructure ; *Computer Simulation ; *Computers ; Databases, Factual ; Image Processing, Computer-Assisted ; National Institutes of Health (U.S.) ; Protein Conformation ; Protein Folding ; *Research ; Sequence Homology, Nucleic Acid ; Simplexvirus/ultrastructure ; Tomography, Emission-Computed ; United States
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    Aberrant neurites and synaptic vesicle protein deficiency in synapsin II-depleted neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: Synapsin I and synapsin II are neuron-specific phosphoproteins that have a role in the regulation of neurotransmitter release and in the formation of nerve terminals. After depletion of synapsin II by antisense oligonucleotides, rat hippocampal neurons in culture were unable to consolidate their minor processes and did not elongate axons. These aberrant morphological changes were accompanied by an abnormal distribution of intracellular filamentous actin (F-actin). In addition, synapsin II suppression resulted in a selective decrease in the amounts of several synaptic vesicle-associated proteins. These data suggest that synapsin II participates in cytoskeletal organization during the early stages of nerve cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, A -- Kosik, K S -- Greengard, P -- Han, H Q -- New York, N.Y. -- Science. 1994 May 13;264(5161):977-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurological Diseases, 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/8178158" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Base Sequence ; *Calcium-Binding Proteins ; Cells, Cultured ; Hippocampus/cytology ; Membrane Glycoproteins/*metabolism ; Microtubule-Associated Proteins/metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/*metabolism ; Neurites/*physiology ; Neurons/*cytology/metabolism/ultrastructure ; Oligonucleotides, Antisense/pharmacology ; Rats ; Synapsins/genetics/*metabolism ; Synaptophysin/*metabolism ; Synaptotagmins ; Tubulin/metabolism ; tau Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Breast cancer. How not to publicize a misconduct finding (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1679.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134830" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*surgery ; Clinical Trials as Topic ; Federal Government ; Female ; Government Regulation ; Humans ; *Information Dissemination ; Mastectomy ; *Mastectomy, Segmental ; National Institutes of Health (U.S.) ; *Scientific Misconduct ; United States ; United States Office of Research Integrity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Role of intracellular calcium in NI-35-evoked collapse of neuronal growth cones (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: A myelin-associated protein from the central nervous system, the neurite growth inhibitor NI-35, inhibits regeneration of lesioned neuronal fiber tracts in vivo and growth of neurites in vitro. Growth cones of cultured rat dorsal root ganglion neurons arrested their growth and collapsed when exposed to liposomes containing NI-35. Before morphological changes, the concentration of free intracellular calcium ([Ca2+]i) showed a rapid and large increase in growth cones exposed to liposomes containing NI-35. Neither an increase in [Ca2+]i nor collapse of growth cones was detected in the presence of antibodies to NI-35. Dantrolene, an inhibitor of calcium release from caffeine-sensitive intracellular calcium stores, protected growth cones from collapse evoked by NI-35. Depletion of these caffeine-sensitive intracellular calcium stores prevented the increase in [Ca2+]i evoked by NI-35. The NI-35-evoked cascade of intracellular messengers that mediates collapse of growth cones includes the crucial step of calcium release from intracellular stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandtlow, C E -- Schmidt, M F -- Hassinger, T D -- Schwab, M E -- Kater, S B -- NS24683/NS/NINDS NIH HHS/ -- NS28323/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):80-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Institute, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caffeine/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; Drug Carriers ; Fura-2 ; Ganglia, Spinal/*physiology ; Growth Inhibitors/*pharmacology ; Kinetics ; Liposomes ; Nerve Fibers/drug effects/*physiology/ultrastructure ; Neurons/drug effects/*physiology/ultrastructure ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Gene therapy approval process (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Royston, I -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1678-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456290" target="_blank"〉PubMed〈/a〉
    Keywords: Genetic Therapy/*legislation & jurisprudence ; Humans ; National Institutes of Health (U.S.) ; United States
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    A 'Manhattan project' for AIDS? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1112-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8438161" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome/economics ; *Hiv ; Humans ; National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Agencies spar over vaccine trial (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):752-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430324" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/economics/*therapeutic use ; Acquired Immunodeficiency Syndrome/economics/immunology/*therapy ; Antigens, CD4/analysis ; Government Agencies ; HIV Infections/economics/immunology/*therapy ; Humans ; Military Medicine ; National Institutes of Health (U.S.) ; Research Support as Topic ; United States ; United States Food and Drug Administration
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    Human genome program. Healy and Collins strike a deal (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, L -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):22-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418490" target="_blank"〉PubMed〈/a〉
    Keywords: Government Agencies ; Human Genome Project/*organization & administration ; Humans ; National Institutes of Health (U.S.) ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A new five-year plan for the U.S. Human Genome Project (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, F -- Galas, D -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):43-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Human Genome Research, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research ; Chromosome Mapping ; Ethics, Medical ; Federal Government ; Financing, Government ; Genetic Diseases, Inborn ; Genetic Markers ; Genetic Techniques ; Government Agencies ; *Human Genome Project/economics/legislation & jurisprudence ; Humans ; Industry ; International Cooperation ; Internationality ; Mice ; National Institutes of Health (U.S.) ; Research ; Sequence Analysis, DNA ; United States
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    Altered fluid transport across airway epithelium in cystic fibrosis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-15
    Description: In cystic fibrosis (CF), absence or dysfunction of a phosphorylation-regulated chloride channel [CF transmembrane conductance regulator (CFTR)] leads to the loss or reduction of chloride secretion into the airways. Active sodium absorption is also increased in CF, and both of these ion transport changes could alter fluid transport across the airways. Under baseline conditions, cultured human airway epithelia from normal individuals absorbed fluid, and this absorption was increased in epithelia from patients with CF. In normal and CF epithelial cultures fluid absorption was inhibited by amiloride. Adenosine 3',5'-monophosphate stimulated fluid secretion in normal epithelial cultures but not in cultures from individuals with CF. In contrast, fluid secretion induced by nucleotide triphosphates (uridine triphosphate or adenosine triphosphate) was unaltered in cultures of epithelia from patients with CF, suggesting an approach to the treatment of CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, C -- Finkbeiner, W E -- Widdicombe, J H -- McCray, P B Jr -- Miller, S S -- HL 42368/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):424-7.〈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/8211164" target="_blank"〉PubMed〈/a〉
    Keywords: Absorption ; Adenosine Triphosphate/pharmacology ; Adolescent ; Adult ; Amiloride/pharmacology ; Body Fluids/*metabolism ; Cells, Cultured ; Cyclic AMP/pharmacology ; Cystic Fibrosis/*metabolism ; Epithelial Cells ; Epithelium/metabolism ; Female ; Humans ; Male ; Middle Aged ; Nasal Mucosa/cytology/*metabolism ; Sodium/metabolism ; Sodium Channels/metabolism ; Trachea/cytology/*metabolism ; Uridine Triphosphate/pharmacology
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    AIDS research. Reorganization plan draws fire at NIH (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):753-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430325" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome/economics ; Humans ; National Institutes of Health (U.S.) ; Politics ; *Research ; Research Support as Topic ; United States ; United States Dept. of Health and Human Services
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    Should dying patients receive untested genetic methods? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, L -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):452.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8424165" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Bioethics ; Brain Neoplasms/*therapy ; DNA, Recombinant ; Death ; *Ethical Review ; Federal Government ; Female ; *Genetic Therapy ; *Government Regulation ; Humans ; Middle Aged ; National Institutes of Health (U.S.) ; *Therapeutic Human Experimentation ; United States
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    GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-21
    Description: A potent neurotrophic factor that enhances survival of midbrain dopaminergic neurons was purified and cloned. Glial cell line-derived neurotrophic factor (GDNF) is a glycosylated, disulfide-bonded homodimer that is a distantly related member of the transforming growth factor-beta superfamily. In embryonic midbrain cultures, recombinant human GDNF promoted the survival and morphological differentiation of dopaminergic neurons and increased their high-affinity dopamine uptake. These effects were relatively specific; GDNF did not increase total neuron or astrocyte numbers nor did it increase transmitter uptake by gamma-aminobutyric-containing and serotonergic neurons. GDNF may have utility in the treatment of Parkinson's disease, which is marked by progressive degeneration of midbrain dopaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Doherty, D H -- Lile, J D -- Bektesh, S -- Collins, F -- New York, N.Y. -- Science. 1993 May 21;260(5111):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Astrocytes/cytology/drug effects ; Base Sequence ; Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; Cloning, Molecular ; Dopamine/*biosynthesis ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Mesencephalon/cytology/*drug effects/metabolism ; Molecular Sequence Data ; Molecular Weight ; *Nerve Growth Factors ; Nerve Tissue Proteins/chemistry/genetics/isolation & purification/*pharmacology ; Neuroglia/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Parkinson Disease/drug therapy ; Rats
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    Gene therapy. Healy approves an unproven treatment (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, L -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):172.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8421780" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Ethical Review ; Federal Government ; Female ; Genetic Therapy/*legislation & jurisprudence ; *Government Regulation ; Humans ; Interleukin-2/*genetics ; Middle Aged ; National Institutes of Health (U.S.) ; Neoplasms/*therapy ; Patient Selection ; Research Subjects ; United States
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    Space woes begin to take a toll at UCSF (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1392-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8451633" target="_blank"〉PubMed〈/a〉
    Keywords: Education, Graduate ; Faculty ; Genetics, Medical ; Humans ; National Institutes of Health (U.S.) ; *Research ; San Francisco ; United States ; *Universities
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    Death gives birth to the nervous system. But how? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):762-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/physiology ; Caenorhabditis elegans/embryology/genetics ; Cell Death/*physiology ; Cells, Cultured ; Embryo, Nonmammalian/physiology ; Nerve Growth Factors/physiology ; Nervous System/cytology/*embryology ; Neurons/cytology/*physiology ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogenes
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    Enhancement by histamine of NMDA-mediated synaptic transmission in the hippocampus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: Histamine is a neuromodulator in the brain, and the hippocampus is one of the regions of the brain that is innervated by histaminergic neurons. When applied to cultured hippocampal neurons, histamine selectively increased by up to tenfold the amplitude of the component of synaptic transmission that was mediated by N-methyl-D-aspartate (NMDA) receptors. Spontaneous miniature synaptic currents and the current elicited by applied NMDA also were enhanced, indicating that the histamine effect was expressed primarily postsynaptically. These results suggest that histamine may modulate processes involving NMDA receptors, such as the induction of long-term potentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bekkers, J M -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):104-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, John Curtin School of Medical Research, Australian National Univresity, Canberra, ACT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cells, Cultured ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Hippocampus/cytology/drug effects/*physiology ; Histamine/*pharmacology ; Ion Channel Gating/drug effects ; N-Methylaspartate/*metabolism/pharmacology ; Rats ; Receptors, Histamine/physiology ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; Synaptic Transmission/*drug effects ; Virulence Factors, Bordetella/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Interleukin-7: a cofactor for V(D)J rearrangement of the T cell receptor beta gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: The diversity of the T cell receptor repertoire is generated by rearrangement of gene elements in immature thymocytes. To identify a thymic signal that induces this rearrangement, a variety of agents were tested for their ability to induce rearrangement of the T cell receptor beta gene in suspensions of thymocytes from mouse embryos at day 14 of gestation. Of 16 agents tested, only interleukin-7 (IL-7) induced V(D)J gene rearrangement and sustained expression of the RAG-1 and RAG-2 genes, which are known to control rearrangement. These data implicate IL-7, a cytokine that is abundantly expressed in embryonic thymus, in driving gene rearrangement during early T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muegge, K -- Vila, M P -- Durum, S K -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):93-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Carcinogenesis and Development Program, Program Resources Inc./Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7686307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; *DNA-Binding Proteins ; Gene Expression ; *Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Genes, RAG-1 ; Hematopoietic Cell Growth Factors/pharmacology ; Interleukin-7/*pharmacology ; Ionomycin/pharmacology ; Mice ; Molecular Sequence Data ; Organ Culture Techniques ; Proteins/genetics ; Stem Cell Factor ; T-Lymphocytes/cytology/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/embryology/immunology ; Tumor Cells, Cultured
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    Neuroprotective effects of glutamate antagonists and extracellular acidity (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Glutamate antagonists protect neurons from hypoxic injury both in vivo and in vitro, but in vitro studies have not been done under the acidic conditions typical of hypoxia-ischemia in vivo. Consistent with glutamate receptor antagonism, extracellular acidity reduced neuronal death in murine cortical cultures that were deprived of oxygen and glucose. Under these acid conditions, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-kainate antagonists further reduced neuronal death, such that some neurons tolerated prolonged oxygen and glucose deprivation almost as well as did astrocytes. Neuroprotection induced by this combination exceeded that induced by glutamate antagonists alone, suggesting that extracellular acidity has beneficial effects beyond the attenuation of ionotropic glutamate receptor activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaku, D A -- Giffard, R G -- Choi, D W -- NS 01425/NS/NINDS NIH HHS/ -- NS 26907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1516-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8389056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cell Hypoxia/physiology ; Cells, Cultured ; Cerebral Cortex/cytology ; *Excitatory Amino Acid Antagonists ; Extracellular Space/*metabolism ; Glucose/deficiency ; *Hydrogen-Ion Concentration ; L-Lactate Dehydrogenase/metabolism ; Mice ; Nerve Degeneration/drug effects ; Neurons/*drug effects/enzymology ; Receptors, AMPA ; Receptors, Kainic Acid ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Getting organized to fight AIDS (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1993 Dec 24;262(5142):1963.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266086" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control ; Humans ; National Institutes of Health (U.S.) ; Research/organization & administration ; United States
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  • 84
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    Doctor-doctor: growing demand for M.D.-Ph.D.s (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culotta, E -- New York, N.Y. -- Science. 1993 Sep 24;261(5129):1784-5, 1787.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8378777" target="_blank"〉PubMed〈/a〉
    Keywords: Career Choice ; *Clinical Medicine/education ; *Education, Graduate ; *Education, Medical ; Education, Medical, Graduate ; Employment ; National Institutes of Health (U.S.) ; *Research ; Salaries and Fringe Benefits ; United States
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  • 85
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    Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karupiah, G -- Xie, Q W -- Buller, R M -- Nathan, C -- Duarte, C -- MacMicking, J D -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1445-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, 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/7690156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/*biosynthesis/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Cell Line ; Cells, Cultured ; Ectromelia virus/drug effects/*physiology ; Ectromelia, Infectious/microbiology ; Enzyme Induction ; Female ; Humans ; Interferon-gamma/*pharmacology ; Macrophages/*microbiology ; Mice ; Mice, Inbred C57BL ; Nitric Oxide/metabolism/pharmacology ; Nitric Oxide Synthase ; Simplexvirus/drug effects/physiology ; Transfection ; Vaccinia virus/drug effects/physiology ; *Virus Replication/drug effects ; omega-N-Methylarginine
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  • 86
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    Developmental regulation of neural response to FGF-1 and FGF-2 by heparan sulfate proteoglycan (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: Murine neural precursor cells and cell lines derived from them are stimulated by members of the heparin-binding fibroblast growth factor (FGF) family. The activity of FGF is regulated by heparan sulfate proteoglycans (HSPGs), and this interaction is an essential prerequisite for the binding of growth factor to the signal transducing receptors. Messenger RNA for FGF-2 was detectable in the neuroepithelium at embryonic day 9, and the HSPGs produced by these cells at this time preferentially bound FGF-2. However, at embryonic day 11, when messenger RNA for FGF-1 was first detectable, there was a switch in the binding specificity of the HSPG to FGF-1. Thus, a single species of HSPG undergoes a rapid, tightly controlled change in growth factor-binding specificity concomitant with the temporal expression of the FGFs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nurcombe, V -- Ford, M D -- Wildschut, J A -- Bartlett, P F -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7682010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Culture Media, Conditioned ; Epithelium/chemistry/embryology ; Fibroblast Growth Factor 1/genetics/*pharmacology ; Fibroblast Growth Factor 2/genetics/*pharmacology ; Gene Expression ; Gestational Age ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate/*pharmacology ; Mice ; Molecular Weight ; Nervous System/chemistry/*embryology/metabolism ; Neurons/cytology ; Polysaccharide-Lyases/metabolism ; Proteoglycans/*pharmacology ; RNA, Messenger/analysis ; Signal Transduction/physiology ; Stem Cells/cytology
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  • 87
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    AIDS theories (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtis, T -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418488" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/immunology/*transmission ; Animals ; Cells, Cultured ; *Hiv-1 ; Haplorhini ; Humans ; Kidney ; Male
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  • 88
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    Science and the new administration (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, J M -- Kirschner, M -- Varmus, H -- New York, N.Y. -- Science. 1993 Jan 22;259(5094):444-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Medicine, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8424162" target="_blank"〉PubMed〈/a〉
    Keywords: Government Agencies ; National Institutes of Health (U.S.) ; *Politics ; *Research ; Research Support as Topic ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    Endgame for MicroGeneSys vaccine trial? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1993 Dec 10;262(5140):1635.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8259501" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/economics/*therapeutic use ; Acquired Immunodeficiency Syndrome/therapy ; Clinical Trials as Topic ; Government Agencies ; Humans ; National Institutes of Health (U.S.) ; Recombinant Proteins/economics/therapeutic use ; United States ; United States Food and Drug Administration ; Vaccines, Synthetic/economics/therapeutic use
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    Beta-adrenergic receptor kinase-2 and beta-arrestin-2 as mediators of odorant-induced desensitization (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-05
    Description: beta-Adrenergic receptor kinase (beta ARK) and beta-arrestin function in the homologous or agonist-activated desensitization of G protein-coupled receptors. The isoforms beta ARK-2 and beta-arrestin-2 are highly enriched in and localized to the dendritic knobs and cilia of the olfactory receptor neurons where the initial events of olfactory signal transduction occur. Odorants induce a rapid and transient elevation of adenosine 3',5'-monophosphate (cAMP), which activates a nonspecific cation channel and produces membrane depolarization. Preincubation of rat olfactory cilia with antibodies raised against beta ARK-2 and beta-arrestin-2 increased the odorant-induced elevation of cAMP and attenuated desensitization. These results suggest that beta ARK-2 and beta-arrestin-2 mediate agonist-dependent desensitization in olfaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, T M -- Arriza, J L -- Jaworsky, D E -- Borisy, F F -- Attramadal, H -- Lefkowitz, R J -- Ronnett, G V -- NS 01578-01/NS/NINDS NIH HHS/ -- NS-02131/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 5;259(5096):825-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8381559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*metabolism ; *Arrestins ; Cells, Cultured ; Cyclic AMP/metabolism ; *Cyclic AMP-Dependent Protein Kinases ; Cytosol/metabolism ; Dendrites/physiology ; Eye Proteins/*metabolism ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Proteins/*metabolism ; Isoenzymes/metabolism ; Male ; Mechanoreceptors/*physiology ; Neurons/*physiology ; *Odors ; Olfactory Bulb/*physiology ; Protein Kinases/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta/*physiology ; Signal Transduction ; *Smell ; Testis/physiology ; Turbinates/*physiology ; beta-Adrenergic Receptor Kinases
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  • 91
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    Proliferation of human smooth muscle cells promoted by lipoprotein(a) (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: Elevated blood concentrations of lipoprotein(a) [Lp(a)] and its constituent, apolipoprotein(a) [apo(a)], constitute a major risk factor for atherosclerosis, but their physiological activities remain obscure. Lp(a) and purified apo(a) stimulated the growth of human smooth muscle cells in culture. This effect resulted from inhibition of plasminogen activation, and consequently the activation by plasmin of latent transforming growth factor-beta, which is an inhibitor of smooth muscle cell growth. Because smooth muscle proliferation is one of the hallmarks of atherosclerotic lesions, these results point to a plausible mechanism for the atherogenic activity of Lp(a).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grainger, D J -- Kirschenlohr, H L -- Metcalfe, J C -- Weissberg, P L -- Wade, D P -- Lawn, R M -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins/physiology ; Apoprotein(a) ; Cell Division/drug effects/physiology ; Cells, Cultured ; Fibrinolysin/physiology ; Humans ; Lipoprotein(a)/*physiology ; Muscle, Smooth, Vascular/*cytology/metabolism ; Plasminogen Activators/metabolism ; Rats ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/physiology
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  • 92
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    MSU officials criticized for mishandling data dispute (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):592-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430304" target="_blank"〉PubMed〈/a〉
    Keywords: Authorship ; Humans ; Mexico ; Michigan ; National Institutes of Health (U.S.) ; Onchocerciasis, Ocular/therapy ; *Scientific Misconduct ; Sudan ; United States ; Universities
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  • 93
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    A Ca-dependent early step in the release of catecholamines from adrenal chromaffin cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: Intense stimuli, such as trains of depolarizing pulses or the caffeine-induced release of calcium from intracellular stores, readily depress the secretory response in neuroendocrine cells. Secretory responses are restored by rest periods of minutes in duration. This recovery was accelerated when the concentration of cytosolic calcium was moderately increased and probably resulted from calcium-dependent replenishment of a pool of release-ready granules. Continuously increased concentrations of calcium led the over-filling of such a pool. Subsequently, secretory responses to stronger calcium stimuli were augmented. Hormone-induced calcium transients with a plateau phase of increased concentration of calcium may enhance the secretory response in this way.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Ruden, L -- Neher, E -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1061-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Membrane Biophysics, Max-Planck-Institut fur biophysikalische Chemie, Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235626" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/cytology/drug effects/metabolism/*secretion ; Animals ; Bradykinin/pharmacology ; Caffeine/pharmacology ; Calcium/*metabolism ; Catecholamines/metabolism/*secretion ; Cattle ; Cells, Cultured ; Chromaffin Granules/drug effects/*secretion ; Electric Conductivity ; Histamine ; Membrane Potentials ; Models, Biological ; Nystatin/pharmacology
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  • 94
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    Translocation of repetitive RNA sequences with the germ plasm in Xenopus oocytes (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: Xlsirts are a family of interspersed repeat RNAs from Xenopus laevis that contain from 3 to 13 repeat units (each 79 to 81 nucleotides long) flanked by unique sequences. They are homologous to the mammalian Xist gene that is involved in X chromosome inactivation. Xlsirt RNA appears first in the mitochondrial cloud (Balbiani body) in stage 2 oocytes and is then translocated as island-like structures to the vegetal cortex at early stage 3 coincident with the localization of the germ plasm. Exogenous Xlsirt RNA injected into oocytes translocates to the location of the endogenous RNA at that particular stage. The Xlsirt RNA repeat sequences are required for translocation and can cause the translocation of heterologous unique RNAs to the vegetal cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kloc, M -- Spohr, G -- Etkin, L D -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1712-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7505061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary ; Female ; In Situ Hybridization ; Molecular Sequence Data ; Nucleic Acid Conformation ; Oocytes/*metabolism ; Oogenesis ; RNA/chemistry/*metabolism ; *Repetitive Sequences, Nucleic Acid ; Xenopus laevis
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  • 95
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    Switch of CD8 T cells to noncytolytic CD8-CD4- cells that make TH2 cytokines and help B cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: CD8+ T cells are a major defense against viral infections and intracellular parasites. Their production of interferon-gamma (IFN-gamma) and their cytolytic activity are key elements in the immune response to these pathogens. Mature mouse CD8+ T cells that were activated in the presence of interleukin-4 (IL-4) developed into a CD8-CD4- population that was not cytolytic and did not produce IFN-gamma. However, these CD8- cells produced large amounts of IL-4, IL-5, and IL-10 and helped activate resting B cells. Thus, CD8 effector functions are potentially diverse and could be exploited by infectious agents that switch off host protective cytolytic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erard, F -- Wild, M T -- Garcia-Sanz, J A -- Le Gros, G -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Allergy/Immunology, Ciba-Geigy Ltd., Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511588" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, CD8/*analysis ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Cytotoxicity, Immunologic ; Immunophenotyping ; Interleukin-10/biosynthesis ; Interleukin-2/pharmacology ; Interleukin-4/biosynthesis/pharmacology ; Interleukin-5/biosynthesis ; Interleukins/*biosynthesis ; Ionomycin/pharmacology ; *Lymphocyte Activation ; Membrane Glycoproteins/genetics ; Mice ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Tetradecanoylphorbol Acetate/pharmacology
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  • 96
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    Scripps backs down on controversial Sandoz deal (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1872-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316826" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes ; *Biomedical Research ; Contracts ; *Drug Industry ; *Federal Government ; *Government Regulation ; Internationality ; National Institutes of Health (U.S.) ; *Research Support as Topic ; *Social Control, Formal ; Switzerland ; United States
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  • 97
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    CNTF protection of oligodendrocytes against natural and tumor necrosis factor-induced death (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: A proportion of developing oligodendrocytes undergo natural cell death by apoptosis, and mature oligodendrocytes die, either by apoptosis or necrosis, in response to injurious signals such as cytotoxic cytokines and complement. Ciliary neurotrophic factor (CNTF), a trophic factor found in astrocytes in the central nervous system (CNS), promoted the survival and maturation of cultured oligodendrocytes. This trophic factor also protected oligodendrocytes from death induced by tumor necrosis factors (apoptosis) but not against complement (necrosis). These results suggest that CNTF functions in the survival of oligodendrocytes during development and may lead to therapeutic approaches for degenerative diseases of the CNS that involve oligodendrocyte destruction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Louis, J C -- Magal, E -- Takayama, S -- Varon, S -- NS16349/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8430320" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/physiology ; Cell Death/*drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Central Nervous System/physiology ; Ciliary Neurotrophic Factor ; Dose-Response Relationship, Drug ; Humans ; Kinetics ; Lymphotoxin-alpha/*pharmacology ; Nerve Growth Factors/*pharmacology ; Nerve Tissue Proteins/*pharmacology ; Oligodendroglia/cytology/drug effects/*physiology ; Recombinant Proteins/pharmacology ; Time Factors ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 98
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    Retinal degeneration in choroideremia: deficiency of rab geranylgeranyl transferase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: Rab geranylgeranyl transferase (GG transferase) is a two-component enzyme that attaches 20-carbon isoprenoid groups to cysteine residues in Rab proteins, a family of guanosine triphosphate-binding proteins that regulate vesicular traffic. The mutant gene in human choroideremia, an X-linked form of retinal degeneration, encodes a protein that resembles component A of rat Rab GG transferase. Lymphoblasts from choroideremia subjects showed a marked deficiency in the activity of component A, but not component B, of Rab GG transferase. The deficiency was more pronounced when the substrate was Rab3A, a synaptic vesicle protein, than it was when the substrate was Rab1A, a protein of the endoplasmic reticulum. The data imply the existence of multiple component A proteins, one of which is missing in choroideremia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seabra, M C -- Brown, M S -- Goldstein, J L -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):377-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8380507" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Alkyl and Aryl Transferases ; Cell Line, Transformed ; Cells, Cultured ; Choroid/chemistry ; Choroideremia/*genetics ; Female ; GTP-Binding Proteins/analysis/*metabolism ; Gene Expression Regulation, Enzymologic ; Humans ; Lymphocyte Activation ; Male ; Middle Aged ; Mutation ; Nerve Tissue Proteins/analysis/*metabolism ; Photoreceptor Cells/chemistry ; Pigment Epithelium of Eye/chemistry ; Protein Prenylation ; Retina/chemistry ; Substrate Specificity ; Transferases/*deficiency/genetics ; rab1 GTP-Binding Proteins ; rab3 GTP-Binding Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 99
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    The skipping of constitutive exons in vivo induced by nonsense mutations (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-29
    Description: Nonsense mutations create a premature signal for the termination of translation of messenger RNA. Such mutations have been observed to cause a severe reduction in the amount of mutant allele transcript or to generate a peptide truncated at the carboxyl end. Analysis of fibrillin transcript from a patient with Marfan syndrome revealed the skipping of a constitutive exon containing a nonsense mutation. Similar results were observed for two nonsense mutations in the gene encoding ornithine delta-aminotransferase from patients with gyrate atrophy. All genomic DNA sequences flanking these exons that are known to influence RNA splicing were unaltered, which suggests that nonsense mutations can alter splice site selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dietz, H C -- Valle, D -- Francomano, C A -- Kendzior, R J Jr -- Pyeritz, R E -- Cutting, G R -- AR-41135/AR/NIAMS NIH HHS/ -- HG-00373/HG/NHGRI NIH HHS/ -- RR-00722/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 29;259(5095):680-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, 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/8430317" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cells, Cultured ; DNA/*genetics/isolation & purification ; *Exons ; Female ; Fibroblasts/physiology ; Humans ; Male ; Marfan Syndrome/*genetics ; Microfilament Proteins/*genetics ; Molecular Sequence Data ; *Mutation ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Reference Values
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 100
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    Minorities in science: the dialogue (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sherman, W V -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8438160" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans ; Humans ; *Minority Groups ; National Institutes of Health (U.S.) ; Science/*manpower ; United States ; Universities
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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