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@PHDTHESIS{Siebel:62156,
      author       = {Siebel, Philip},
      othercontributors = {Hegele-Hartung, Christa},
      title        = {{D}ie {W}irkung von selektiven Östrogenrezeptor [alpha]
                      und [beta]-{A}gonisten auf {O}var und {U}terus am
                      {N}agetier},
      address      = {Aachen},
      publisher    = {Publikationsserver der RWTH Aachen University},
      reportid     = {RWTH-CONV-123746},
      pages        = {112 S. : Ill., graph. Darst.},
      year         = {2005},
      note         = {Aachen, Techn. Hochsch., Diss., 2005},
      abstract     = {Novel isotype selective estrogen receptor (ER) agonists,
                      the selective ERAlphaagonist 16Alpha-LE2 and the selective
                      ERBeta agonist 8Beta-VE2, were used in hypophysectomized
                      rats or GnRH antagonist treated immature mice as well as in
                      ovariectomized mature rats to elucidate the effect of
                      subtype selective estrogens on the physiology of ovarian
                      folliculogenesis, uterine proliferation and gene regulation,
                      respectively. In immature hypophysectomized animals, the
                      ERBeta agonist and the reference compound 17Beta-estradiol
                      caused stimulation of early folliculogenesis, a decrease in
                      follicular atresia and induction of ovarian gene expression.
                      The ERBeta agonist exhibited the same efficiency and a
                      similar high potency as 17Beta-estradiol in the respective
                      studies. In contrast, the ERAlphaagonist had little or no
                      effect on these parameters implying that direct estrogen
                      effects on ovarian follicular development and gene
                      regulation are mediated by ERBeta. In ovariectomized mature
                      rats the ERAlpha agonist and the reference compound
                      17Beta-estradiol caused stimulation of uterine weight, cell
                      proliferation and cell-compartment dependant gene
                      regulation. The ERAlpha agonist exhibited the same
                      efficiency and a similar high potency as 17Beta-estradiol in
                      the respective studies. On the other hand, the ERBeta
                      agonist did not stimulate uterine weight and cell
                      proliferation in intact female rats and had no effect on
                      gene regulation, showing that estrogen receptor Alpha is the
                      dominant receptor in the uterus and responsible for
                      mediating direct estrogen effects. This is in line with the
                      assumption that stimulation of uterine growth and other
                      known estrogen effects are mediated by ERAlpha but not by
                      ERBeta and that ovarian ERBeta dominance is responsible for
                      increased stimulation of folliculogenesis. This unique
                      endocrine profile of selective estrogen receptor agonists
                      provides new options for targeted pharmacotherapeutical
                      indications as for example tailoring classical ovarian
                      stimulation protocols by the use of ERBeta agonists or
                      inventing new contraceptive agents by inhibition via an
                      action on the hypothalamic-pituitary-ovarian axis by the use
                      of ERAlpha agonists.},
      cin          = {510000-1},
      ddc          = {610},
      cid          = {$I:(DE-82)510000-1_20140620$},
      typ          = {PUB:(DE-HGF)11},
      urn          = {urn:nbn:de:hbz:82-opus-12124},
      url          = {https://publications.rwth-aachen.de/record/62156},
}