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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 43 (1987), S. 1039-1039 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1617-4623
    Keywords: Key wordsStreptomyces lividans ; recA ; Recombination ; Gene disruption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Temperature-sensitive integration plasmids carrying internal fragments of the Streptomyces lividans TK24 recA gene were constructed and used to inactivate the chromosomal recA gene of S. lividans by gene disruption and gene replacement. Integration of these plasmids resulted in recA mutants expressing C-terminally truncated RecA proteins, as deduced from Southern hybridization experiments. Mutants FRECD2 in which the last 42 amino acids, comprising the variable part of bacterial RecA proteins, had been deleted retained the wild-type phenotype. The S. lividans recA mutant FRECD3 produced a RecA protein lacking 87 amino acids probably including the interfilament contact site. FRECD3 was more sensitive to UV and MMS than the wild-type. Its ability to undergo homologous recombination was impaired, but not completely abolished. Integration of the disruption plasmid pFRECD3 in S. coelicolor“Müller” caused the same mutant phenotype as S. lividans FRECD3. In spite of many attempts no S. lividans recA mutants with deletions of 165 C-terminal amino acids or more were isolated. Furthermore, the recA gene could not be replaced by a kanamycin resistance cassette. These experiments indicate a crucial role of the recA gene in ensuring viability of Streptomyces.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 43 (1987), S. 1056-1061 
    ISSN: 1420-9071
    Keywords: Arrhythmias ; myocardial ischemia ; conduction block
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Ventricular arrhythmias occurring consequent to regional disturbances of myocardial perfusion are the most frequent cause of sudden cardiac death. They are related to marked changes of impulse propagation in the ischemic region, which consist of circulating excitation with re-entry. Mapping of the impulse during ventricular tachycardias and ventricular fibrillation shows that the circus movements change their shape and localization from beat to beat. Zones of tissue which block the impulse during one beat may conduct the impulse at a fast rate during the next beat. The main cause underlying this behavior is the depression of the ischemic action potential. This depression is caused by the partial inactivation and the prolonged recovery of the rapid sodium inward current. In addition to the decrease in resting potential, other factors, such as acidosis, contribute to the inactivation of the inward currents generating the upstroke of the action potential. An increase of coupling resistance between myocardial cells and/or an increase of extracellular resistance appear to be less important for explaining conduction disturbances in acute ischemia.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 46 (1990), S. 1162-1167 
    ISSN: 1420-9071
    Keywords: Myocardial ischemia ; ischemic depolarization ; cell-to-cell uncoupling ; mechanical failure ; ischemic contracture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Reduction or interruption of the blood supply to the myocardium leads to marked disturbances of electrical and mechanical function within a few seconds. Electrical dysfunction is characterized by an initial depolarization of the resting membrane, and a decrease of the amplitude, the upstroke velocity and the duration of the action potential. Both depolarization and depression of the action potential are closely associated with intracellular metabolic acidosis. After this initial phase, electrical cell-to-cell uncoupling develops, probably as a consequence of increased cytosolic free [Ca++]. Mechanical dysfunction is characterized by a dissociation of the initial decrease of active force development from the subsequent ischemic contracture. Active force development in acute ischemia is inhibited by the accumulation of ischemic metabolic products (H+, inorganic phosphate (Pi), Mg++) but not by a marked decrease of [ATP]. The subsequent ischemic contracture is probably initiated by release of Ca++ from intracellular stores. This release causes rapid consumption of ATP and the development of rigor within 1–2 minutes.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    General relativity and gravitation 10 (1979), S. 535-539 
    ISSN: 1572-9532
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract A static, plane-symmetric scalar field of long range is considered in general relativity, and a one-parameter class of exact solutions with cosmical time is studied in harmonic coordinates. The geodetic equations are solved. A velocity-dependent acceleration field is found, acting attractively on the component of the velocity normal to the plane of symmetry, and repulsively on the component parallel to that plane. The manifold is complete. Test particles at rest are insensitive to it.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 92 (1997), S. 111-119 
    ISSN: 1435-1803
    Keywords: Anisotropic conduction ; cell cultures ; microscopical conduction ; current-to-load mismatch
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In recent years it has become evident that myocardial tissue undergoes remodeling in diseased states such as myocardial infarction and hypertrophy which affects membrane channels, cell-to-cell coupling as well as the connective tissue matrix. Although the detailed mechanisms of ventricular arrhythmias in ventricular hypertrophy are not known, studies carried, out by computer simulations or high resolution mapping of electrical activity have suggested a complex interaction between changing ionic currents at the level of the cell membranes, altered cell-to-cell coupling and altered macroscopic structure. The present report summarises these recent developments and their potential relevance for arrhythmogenesis.
    Type of Medium: Electronic Resource
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