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  • Articles  (164)
  • Animals  (89)
  • Organic Chemistry  (51)
  • Aircraft Stability and Control
  • GENERAL
  • Inorganic Chemistry
  • 1990-1994  (143)
  • 1960-1964  (21)
  • 1955-1959
  • 1993  (143)
  • 1961  (21)
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  • 1990-1994  (143)
  • 1960-1964  (21)
  • 1955-1959
Year
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  • 1
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    Interspecific and intraspecific horizontal transfer of Wolbachia in Drosophila (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: Cytoplasmic incompatibility (CI) in Drosophila simulans is related to infection of the germ line by a rickettsial endosymbiont (genus Wolbachia). Wolbachia were transferred by microinjection of egg cytoplasm into uninfected eggs of both D. simulans and D. melanogaster to generate infected populations. Transinfected strains of D. melanogaster with lower densities of Wolbachia than the naturally infected D. simulans strain did not express high levels of CI. However, transinfected D. melanogaster egg cytoplasm, transferred back into D. simulans, generated infected populations that expressed CI at levels near those of the naturally infected strain. A transinfected D. melanogaster line selected for increased levels of CI expression also displayed increased symbiont densities. These data suggest that a threshold level of infection is required for normal expression of CI and that host factors help determine the density of the symbiont in the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyle, L -- O'Neill, S L -- Robertson, H M -- Karr, T L -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1796-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8511587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoplasm/microbiology/physiology ; Drosophila/*microbiology/physiology ; Drosophila melanogaster/*microbiology/physiology ; Female ; Male ; Microinjections ; Microscopy ; Ovum/microbiology/physiology ; Rickettsiaceae/*physiology
    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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    Selective inhibition of ras-dependent transformation by a farnesyltransferase inhibitor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: To acquire transforming potential, the precursor of the Ras oncoprotein must undergo farnesylation of the cysteine residue located in a carboxyl-terminal tetrapeptide. Inhibitors of the enzyme that catalyzes this modification, farnesyl protein transferase (FPTase), have therefore been suggested as anticancer agents for tumors in which Ras contributes to transformation. The tetrapeptide analog L-731,735 is a potent and selective inhibitor of FPTase in vitro. A prodrug of this compound, L-731,734, inhibited Ras processing in cells transformed with v-ras. L-731,734 decreased the ability of v-ras-transformed cells to form colonies in soft agar but had no effect on the efficiency of colony formation of cells transformed by either the v-raf or v-mos oncogenes. The results demonstrate selective inhibition of ras-dependent cell transformation with a synthetic organic inhibitor of FPTase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohl, N E -- Mosser, S D -- deSolms, S J -- Giuliani, E A -- Pompliano, D L -- Graham, S L -- Smith, R L -- Scolnick, E M -- Oliff, A -- Gibbs, J B -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1934-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Research, Merck Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8316833" target="_blank"〉PubMed〈/a〉
    Keywords: *Alkyl and Aryl Transferases ; Animals ; Antineoplastic Agents/chemistry/*pharmacology ; Cell Division/drug effects ; Cell Line ; Cell Transformation, Neoplastic/*drug effects ; Dipeptides/chemistry/*pharmacology ; Drug Design ; Farnesyltranstransferase ; *Genes, ras ; Oncogene Proteins/*metabolism ; Protein Prenylation/*drug effects ; Rats ; Transferases/*antagonists & inhibitors
    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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    Induction of apoptosis by the low-affinity NGF receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: Nerve growth factor (NGF) binding to cellular receptors is required for the survival of some neural cells. In contrast to TrkA, the high-affinity NGF receptor that transduces NGF signals for survival and differentiation, the function of the low-affinity NGF receptor, p75NGFR, remains uncertain. Expression of p75NGFR induced neural cell death constitutively when p75NGFR was unbound; binding by NGF or monoclonal antibody, however, inhibited cell death induced by p75NGFR. Thus, expression of p75NGFR may explain the dependence of some neural cells on NGF for survival. These findings also suggest that p75NGFR has some functional similarities to other members of a superfamily of receptors that include tumor necrosis factor receptors, Fas (Apo-1), and CD40.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rabizadeh, S -- Oh, J -- Zhong, L T -- Yang, J -- Bitler, C M -- Butcher, L L -- Bredesen, D E -- AG10671/AG/NIA NIH HHS/ -- NS10928/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):345-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332899" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis/drug effects ; Cell Line ; Cell Survival/drug effects ; Culture Media, Serum-Free ; Nerve Growth Factors/*metabolism/pharmacology ; Neurons/*cytology/drug effects/metabolism ; PC12 Cells ; Receptors, Nerve Growth Factor/metabolism/*physiology ; Transfection
    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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    The prevention of thymic lymphomas in transgenic mice by human O6-alkylguanine-DNA alkyltransferase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: Nitrosoureas form O6-alkylguanine-DNA adducts that are converted to G to A transitions, the mutation found in the activated ras oncogenes of nitrosourea-induced mouse lymphomas and rat mammary tumors. These adducts are removed by the DNA repair protein O6-alkylguanine-DNA alkyltransferase. Transgenic mice that express the human homolog of this protein in the thymus were found to be protected from developing thymic lymphomas after exposure to N-methyl-N-nitrosourea. Thus, transgenic expression of a single human DNA repair gene is sufficient to block chemical carcinogenesis. The transduction of DNA repair genes in vivo may unravel mechanisms of carcinogenesis and provide therapeutic protection from known carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dumenco, L L -- Allay, E -- Norton, K -- Gerson, S L -- P01CA51183/CA/NCI NIH HHS/ -- P30CA43703/CA/NCI NIH HHS/ -- R01ES06288/ES/NIEHS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):219-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University Hospitals of Cleveland, OH.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8421782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Repair/genetics ; Gene Expression ; Humans ; Lymphoma, T-Cell/chemically induced/*prevention & control ; Methylnitrosourea ; Methyltransferases/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; O(6)-Methylguanine-DNA Methyltransferase ; RNA, Messenger/analysis ; Thymus Neoplasms/chemically induced/*prevention & control
    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
    Electronic Resource
    Electronic Resource
    Muricatetrocins A and B and Gigantetrocin B: Three New Cytotoxic Monotetrahydrofuran-Ring Acetogenins from Annona muricata (1993)
    New York, NY : Wiley-Blackwell
    Helvetica Chimica Acta 76 (1993), S. 2433-2444 
    Details
    ISSN: 0018-019X
    Keywords: Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Extracts from the seeds of Annona muricata yielded three new Annonaceous acetogenins: muricatetrocin A (= (5S)-3-{(2R)-2-hydroxy-9-{(2R,5S)-tetrahydro-5-[(1S,4S,5S)-1,4,5-trihydroxyheptadecyl]furan-2-yl}nonyl}-5-methylfuran-2(5H)-one; 1), muricatetrocin B (= (5S)-{(2R)-2-hydroxy-9-{(2S,5S)-tetrahydro-5-[(1S,4S,5S)-1,4,5-trihydroxyheptadecyl]furan-2-yl}nonyl}-5-methylfuran-2(5H)-one; 2), and gigantetrocin B (= (5S)-3-{(2R)-2-hydroxy-7-{(2S,5S)-tetrahydro-5-[(1S,4R,5R)-1,4,5-trihydroxynonadecyl]furan-2-yl}heptyl}-5-methyl-furan-2(5H)-one; 3). Their C-skeletons were deduced by mass spectrometry. Configurations were determined by 1H-NMR of ketal derivatives and 2D-NMR experiments utilizing Mosher esters. A previously described compound, gigantetrocin A (= (5S)-3-{(2R)-2-hydroxy-7-{(2S,5S)-tetrahydro-5-[(1S,4S,5S)-1,4,5-trihydroxynonadecyl]furan-2-yl}heptyl}-5-methylfuran-2-(5H)one; 4), was also isolated and is new to this species. Compounds 1-4 were all selectively cytotoxic for the HT-29 human colon-tumor cell line with potencies at least 10 times that of adriamycin.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/hlca.19930760703
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  • 6
    Electronic Resource
    Electronic Resource
    Homoaromaticity of decamethyl[5]pericyclyne (1993)
    Chichester : Wiley-Blackwell
    Journal of Physical Organic Chemistry 6 (1993), S. 316-318 
    Details
    ISSN: 0894-3230
    Keywords: Organic Chemistry ; Physical Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Physics
    Notes: It is shown that a theoretical computation of the Dewar resonance energy of decamethyl [5] pericyclyne should give the same value for the homoaromaticity of this compound as that calculated earlier from heat of hydrogenation measurements. Both methods show this quantity to be small, but the accuracy of the methods appears insufficient for more exact agreement.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/poc.610060510
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  • 7
    Electronic Resource
    Electronic Resource
    3-Methylcarboxy-1H-indazole. Theoretical study of its formation via intramolecular aliphatic diazonium coupling and x-ray crystal structure (1993)
    Chichester : Wiley-Blackwell
    Journal of Physical Organic Chemistry 6 (1993), S. 201-214 
    Details
    ISSN: 0894-3230
    Keywords: Organic Chemistry ; Physical Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Physics
    Notes: The methyl ester of 1H-indazole-3-carboxylic acid (2-Me) is formed in the diazotization of o-aminophenylacetic acid to o-diazoniumphenylacetic acid (1) in an intramolecular aliphatic diazonium coupling. 2-Me was identified and characterized by single-crystal x-ray diffraction and found to crystallize as hydrogen-bonded trimers of crystallographically independent molecules. The methylcarboxy groups are rotated slightly out of the best plane of the trimer resulting in only a pseudo-threefold axis. The crystal structure of 2-Me is compared with other indazoles and pyrazole. Regioselective electrophilic diazonium ion addition to the enol tautomer of 1 and subsequent hyrazone-azo tautomerization are proposed as a possible mechanism for indazole formation under acidic conditions. The tautomerization equilibrium between acetic acid and its enol 1,2-dihydroxyethene was studied and the effects of phenyl and o-diazoniumphenyl substitution on this equilibrium were explored with semi-empirical quantum mechanical methods. The performance of the semi-empirical method was assessed by comparison with ab initio and/or experimental data. It was found that the enol of o-diazoniumphenylacetic acid is stabilized greatly owing to extended conjugation and push-pull interactions in the enol form. These results suggest that the enol tautomer might be a viable reactive intermediate that warrants considerations in discussions of reaction mechanisms.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/poc.610060403
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  • 8
    Electronic Resource
    Electronic Resource
    Ethylation of methylarsenic(III) compounds by sodium tetraethylborate (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Applied Organometallic Chemistry 7 (1993), S. 577-581 
    Details
    ISSN: 0268-2605
    Keywords: Organoarsenic ; sodium tetraethylborate ; gas chromatography-atomic absorption spectrometry ; cold trap-atomic absorption spectrometry ; Chemistry ; Organic Chemistry
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: The compounds MeAsBr2 and Me2AsBr at concentrations of (1-5) × 10-3 M in acetone solution are ethylated in high yield by NaBEt4 to MeEt2As and Me2EtAs, as shown by 1H NMR spectroscopy. The extents of ethylation of MeAs2+ and Me2As+ (expressed as ions, by convention) in aqueous acid solutions [at concentrations of (5-20) × 10-6 M] were investigated using cold trap/AA and GC AA procedures. The species Me2As+ was ethylated (to give Me2EtAs) in good yield (88%); in contrast, MeAs2+ produced the volatile trialkylarsine, MeEt2As, in poor yield (30%). No volatile trialkylarsine could be obtained on treating inorganic arsenic(III) (As3+) solutions with NaBEt4.
    Additional Material: 5 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aoc.590070718
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  • 9
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    Mutations in the glucose-6-phosphatase gene that cause glycogen storage disease type 1a (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-22
    Description: Glycogen storage disease (GSD) type 1a is caused by the deficiency of D-glucose-6-phosphatase (G6Pase), the key enzyme in glucose homeostasis. Despite both a high incidence and morbidity, the molecular mechanisms underlying this deficiency have eluded characterization. In the present study, the molecular and biochemical characterization of the human G6Pase complementary DNA, its gene, and the expressed protein, which is indistinguishable from human microsomal G6Pase, are reported. Several mutations in the G6Pase gene of affected individuals that completely inactivate the enzyme have been identified. These results establish the molecular basis of this disease and open the way for future gene therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lei, K J -- Shelly, L L -- Pan, C J -- Sidbury, J B -- Chou, J Y -- New York, N.Y. -- Science. 1993 Oct 22;262(5133):580-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211187" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA, Complementary/genetics ; Exons ; Glucose-6-Phosphatase/*genetics/metabolism ; Glycogen Storage Disease Type I/enzymology/*genetics ; Glycosylation ; Humans ; Liver/enzymology ; Mice ; Molecular Sequence Data ; *Mutation ; Protein Conformation ; Transfection
    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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    Expression cloning and signaling properties of the rat glucagon receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Glucagon and the glucagon receptor are a primary source of control over blood glucose concentrations and are especially important to studies of diabetes in which the loss of control over blood glucose concentrations clinically defines the disease. A complementary DNA clone for the glucagon receptor was isolated by an expression cloning strategy, and the receptor protein was expressed in several kidney cell lines. The cloned receptor bound glucagon and caused an increase in the intracellular concentration of adenosine 3', 5'-monophosphate (cAMP). The cloned glucagon receptor also transduced a signal that led to an increased concentration of intracellular calcium. The glucagon receptor is similar to the calcitonin and parathyroid hormone receptors. It can transduce signals leading to the accumulation of two different second messengers, cAMP and calcium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jelinek, L J -- Lok, S -- Rosenberg, G B -- Smith, R A -- Grant, F J -- Biggs, S -- Bensch, P A -- Kuijper, J L -- Sheppard, P O -- Sprecher, C A -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1614-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ZymoGenetics Inc., Seattle, WA 98105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8384375" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Cell Line ; Cloning, Molecular ; Cricetinae ; Cyclic AMP/metabolism ; Glucagon/metabolism/*pharmacology ; Kidney ; Kinetics ; Liver/*metabolism ; Molecular Sequence Data ; Rats ; Receptors, Gastrointestinal Hormone/genetics/metabolism/*physiology ; Receptors, Glucagon ; *Signal Transduction ; Transfection
    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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