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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Fatigue & fracture of engineering materials & structures 15 (1992), S. 0 
    ISSN: 1460-2695
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Stress-controlled, low-cycle, push-pull fatigue tests were performed on three variants of the bearing steel SAE 52100 with slightly different compositions and heat treatments. The experiments demonstrated differences in the cyclic plastic behaviour of differently hardened steels (bainitically-hardened and martensitically-hardened, respectively), whereas the two martensitic variants, which differ in composition, behaved very similarly. Bainitically-hardened SAE 52100 steel exhibited initial hardening followed by cyclic softening above a stress amplitude level of 1200 MPa. In contrast, the martensitically-hardened variants showed a pronounced cyclic hardening. The deformation behaviour of the martensitically-hardened bearing steel in a monotonic tensile test and during the first cycles can be well understood on the basis of the transformation of retained austenite. This process leads to an onset of plastic deformation at lower stresses compared to the bainitically-hardened bearing steel. As a result of the subsequent cyclic hardening of the martensitic variants, the CSS curves are almost identical for the differently hardened conditions under investigation. Additional tests under pulsating compression documented that a high negative mean stress enhances the cyclic plasticity.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Archives of virology 141 (1996), S. 263-274 
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One of the causes of genital tract infections in humans are herpes simplex virus types 1 and 2 (HSV-1, HSV-2). Although primary and recurrent infections can be clinically apparent and in part very serious, many infections are asymptomatic and result only in temporary genital shedding of virus (recurrences). During our investigations of vaginitis, strain IES of HSV-1 produced an asymptomatic infection. Replication in the murine vaginal (vag.) epithelium as well as antibody formation after vag. infection was comparable to those of survivors after infection with highly virulent strains. Titration of liver, spleen, ovaries, adrenal glands, spinal cord, or brain after vag. IES infection revealed no virus, whereas after i.p. infection virus could be demonstrated in many organs examined. Histological examination with a DNA probe (in situ hybridisation), HSV antibodies (immunohistochemistry), and haematoxylin and eosin (HE) staining showed only small focal HSV lesions of the vaginal epithelium in early stages of the infection, never exceeding to the subepithelial tissue. Severe infiltrations and ulcerations after infection with highly virulent strains (17syn+, ER−) could never be demonstrated after IES vag. infection. Identical replication rates of both groups of HSV despite much greater areas of epithelial necrosis with the virulent strains may be explained by the large number of virus inactivating granulocytes induced by the virulent strains, thus inactivating the hypothetical higher virus load.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After vaginal infections of mice with neuroinvasive strains of herpes simplex virus type 1 and 2 (HSV-1, HSV-2) virus replicates in the epithelium of the vagina, in the paravaginal ganglia, in the spinal cord and finally in the brain and in the adrenal glands. However, viral antigens could be demonstrated only in the medulla of the adrenal glands but not in the cortex, as assessed by immunohistochemistry (IHC). HSV could not be isolated from liver, spleen, uterus, and ovaries. This contrasts to the intraperitoneal (i.p) route of infection with replication in different visceral organs including the adrenal gland's cortex.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1831
    Keywords: Key words Herpes simplex virus ; Vaginal infection ; Neurovirulence ; Recombination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vaginal infections of BALB/c Ann mice with herpes simplex virus type 1 (HSV-1) were studied. Mice were inoculated with virulent strains ANG path and 17 syn+ or low-virulent recombinant strains 27/III and 17-syn3 that differ from parental strains in their glycoprotein B (gB) gene sequences. When low-virulent strains were inoculated separately, no vaginitis/vulvitis was produced despite replication in the vagina. In contrast, after coinfection of mice with the two low-virulent strains, vaginitis/vulvitis was produced and virus could be recovered from the central nervous system (CNS). Two of the CNS isolates produced vaginitis/vulvitis, neuroinvasiveness and death of mice after vaginal infection. Restriction fragment analysis and sequencing were used to assess recombination events in the gB gene sequence of the CNS isolates. After mixed vaginal infection recombination between non-virulent HSV strains occurs, resulting in vaginitis/vulvitis and neuroinvasiveness. No correlation was detected between the syncytial phenotype and local vaginal virulence. Virulence of HSV is not solely dependent on gB function; it seems to be more probable that several genes act in concert to induce virulence and neuroivasiveness.
    Type of Medium: Electronic Resource
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