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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Heythrop journal 4 (1963), S. 0 
    ISSN: 1468-2265
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Philosophy , Theology and Religious Studies
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Heythrop journal 6 (1965), S. 0 
    ISSN: 1468-2265
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Philosophy , Theology and Religious Studies
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    The @Journal of Steroid Biochemistry and Molecular Biology 47 (1993), S. 127-135 
    ISSN: 0960-0760
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 69 (1982), S. 340-341 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Analytical Biochemistry 152 (1986), S. 285-290 
    ISSN: 0003-2697
    Keywords: 3-aminobenzamide ; ADP-ribosyltransferase ; affinity chromatography ; enzyme purification
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 519-521 (July 2006), p. 783-788 
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Two recent methods for obtaining flow stress-strain relations up to large strains of order1.5 by channel-die compression are presented:i) for sheet metal formability tests, composite samples have been made of glued sheet layers anddeformed at room temperature in a channel-die with the compression axis directed along one of thesheet metal edge directions, i.e. RD or TD. The sheet plane is parallel to the lateral compression dieface. It is shown that, using a suitable lubricant, the sample deformation is homogeneous up tostrains of 1.5. Tests carried out on 5xxx and 6xxx alloys to evaluate the stress-strain relations showthat a generalized Voce law gives a good quantitative fit for the data.ii) for high temperature plate processing, quantitative flow stress data can be obtained up to 500°Cwith a rapid quench using a hot channel-die set-up. Some new results are presented here for highstrain hot PSC tests on Al-Mn and Al-Mg alloys together with microstructure analyses
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    World journal of urology 12 (1994), S. 99-103 
    ISSN: 1433-8726
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the prostate, androgen action affects the growth of the gland, its morphology, and regulation of protein expression. Endocrine therapy of non-organ-confined tumors is based on the androgen dependence of the vast majority of prostatic carcinomas. Although initial response rates are high, this therapy is only temporarily effective. Critical molecular changes ultimately resulting in androgen independence of tumor cells are unknown at this time. The androgen signal-transduction cascade and its central element, the androgen receptor (AR), are possible targets for such changes. Immunohistological analysis using anti-AR antibodies has revealed the presence of AR in a vast majority of therapy-responsive as well as therapy-unresponsive prostatic carcinomas, indicating that loss of AR expression is not the reason for androgen independence. On the other hand, molecular-biology studies have revealed qualitative and quantitative impairment of AR expression in prostatic tumor cell lines that represent very late stages of prostatic carcinoma development. Mutant ARs were detected in the prostatic tumor cell line LNCaP and in two specimens from primary prostatic tumors. The LNCaP mutant AR as well as mutant AR715met, one of the mutant receptors detected in tumor tissue, show a gain of function as compared with the wild-type receptor. In addition to androgens, the natural activators of the AR, the LNCaP receptor is activated also by progestagenic and estrogenic steroids and by the nonsteroidal antiandrogen flutamide. AR715met is activated by adrenal androgens and progesterone in addition to androgens. Although determination of the frequency of point mutations in late prostatic carcinoma requires further investigation, these data imply that tumor progression in an androgen-ablated environment may be accompanied by aberrant AR activation.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Urological research 28 (2000), S. 211-219 
    ISSN: 1434-0879
    Keywords: Key words Androgen receptor ; Prostate cancer ; Androgen-regulated genes ; Cell cycle ; Prostate-specific antigen ; Mutation ; Non-steroidal activation ; Anti-androgen ; Coregulatory proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Androgen receptor (AR), a key nuclear transcription factor in the prostate gland, is expressed in all histological types and stages of prostate cancer. The AR regulates proliferation of prostate cancer cells by stimulation of cyclin-dependent kinases. However, in some prostate tumors AR stimulates expression of cell cycle inhibitors, thus leading to down-regulation of cellular proliferation. Androgens, by activation of the AR, control differentiation of prostate cells and synthesis of neutral lipids. There are several mechanisms by which prostate cancer cells adapt to an environment with low androgen supply during endocrine therapy. The AR expression and activity increase in several cell lines that are used as an in vitro model for monitoring changes during long-term androgen ablation. Mutant ARs are of importance for monitoring the natural course of the disease and for determining the response to anti-androgens in metastatic lesions from prostatic carcinoma. In addition, AR activity is up-regulated by various stimulators of intracellular protein kinases. Current research efforts are focused on elucidation of function of AR coregulatory proteins, coactivators and corepressors. Their inappropriate expression and/or function might critically influence cellular events in advanced carcinoma of the prostate. It is hoped that information on these coregulatory proteins will serve as a basis for a more efficient pharmacological inhibition of the AR in advanced carcinoma of the prostate.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1434-0879
    Keywords: R3327 prostatic carcinoma ; Adrenal androgens ; Relapse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Adrenal androgens are discussed as a reason for tumor progression after androgen ablation therapy. Because of the difference in the secretion of androgens by the adrenals of humans and rats, there is no reliable tumor model to study the role of adrenal androgens in tumor progression. Therefore, the main adrenal androgens were administered to rats in order to mimic human endocrine conditions. Application of dehydroepiandrosteron-sulfate (DHEA-S) alone or a mixture of androstendione (A), 11β-hydroxyandrostendione (OHA), dehydroepiandrosterone (DHEA), and its sulfate (DHEA-S) to castrated rats caused only a slight increase of prostate and seminal vesicle weights. Contrary to these findings, growth of the R3327 prostatic carcinoma in castrated rats was greatly stimulated by these adrenal androgens up to the level of the intact control. Thus, in spite of androgen ablation, tumor progression could be induced by exogenous adrenal androgens.
    Type of Medium: Electronic Resource
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