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 I. Publizierte
Arbeiten / Published studies:
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Riedl C.R., Witkowski M.,
Plas E., Pflüger H.:
„Heparin-Coating reduces encrustation of ureteral stent. A
preliminary report”
The present study evaluated the inhibition of ureteral
stent encrustation by heparin coating. In contrast to uncoated
polyurethane stents, heparin coated ureteral stents did not show any
organic (biofilms) or anorganic (crystals) deposits after being in
situ for up to 6 weeks and effectively inhibited the encrustation
process.
J.Antimicrobial Agents, 19, 507-510, 2002
- Rumpold H., Mascher K., Untergasser G., Plas E.,
Hermann M., Berger P.:
“Trans-differentiation
of prostatic stromal cells leads to decreased glycoprotein hormone
alpha production“
Age-related development of benign prostatic hyperplasia is an
important health issue in developed countries. The histopathogenetic
hallmark of this disease is the increase in relative and absolute
numbers of smooth muscle cells (SMC). Glycoprotein hormone
alpha-subunit (GPHalpha) is expressed in the human prostate, and,
because of its structural similarities to other cystine knot growth
factors, it has been considered to have growth regulatory functions of
its own. Primary cell cultures allowing for selective cultivation of
prostatic epithelial cells, fibroblasts, and SMC were established.
Directed trans-differentiation and cellular homogeneity was pursued by
confocal scanning laser microscopy with cell type-specific markers.
GPHalpha production by these cells was assessed by immunofluorimetric
assays. Its predominant source was young fibroblasts, whereas
replicative senescent fibroblasts, SMC, and control fibroblasts from
foreskin did not produce significant amounts. Functionally, GPHalpha
reduced growth of stromal cells at concentrations of 10 and 100 nmol/liter
as shown by cell viability assays. It is concluded that histogenetic
reorganization over the adult lifetime, guided by endocrine factors
like steroid hormones together with senescence of fibroblasts, leads
to a decreased production of growth inhibitors, such as GPHalpha,
favoring proliferation and the development of benign prostatic
hyperplasia.
J.Clin.Endocrinol.Metab, 87, 5297-5303, 2002
- Daha L., Riedl C., Engelhardt P., Plas E., Pflüger
H.:
“Incidence
of urological diseases in geriatric patients in a large community
hospital”
J.Am.Geriatr.Soc., 50, 1606-1607, 2002
- Rumpold H., Heinrich E., Untergasser G., Hermann
M., Pfister G., Plas E., Berger P.:
“Neuroendocrine
differentiation of human prostatic primary epithelial cells in vitro”
BACKGROUND: Dispersed prostatic neuroendocrine cells
are involved in growth regulation of the prostate and are considered
to play a role in the pathogenesis of prostate carcinoma and benign
prostatic hyperplasia (BPH). They are meant either to be derived from
the neural crest during embryogenesis or by direct differentiation of
the cells from locally present precursor cells. METHODS: An in vitro
model was developed for human prostatic epithelial and neuroendocrine
cell differentiation. Minced explants from radical prostatectomies
were seeded on collagen I-coated plates. RESULTS: The majority of
outgrowing cells were basal cells, positive for cytokeratin markers K
5/14 and CD 44, as determined by confocal laser scanning microscopy. A
small fraction of interdispersed single cells expressing c-kit, which
is found on pluripotent precursors, was identified by
immunofluorescence. From these basal cells, in vitro differentiation
of cells with neuroendocrine morphology could be achieved within 3
days. These were at rest, i.e., non-bromodeoxyuridine incorporating
cells and characteristically coexpressed K 5/14, K 18, and the
neuroendocrine marker chromogranin A. Luminal cells staining for K 8
or 18 were not observed. CONCLUSION: Neuroendocrine differentiation of
adult prostatic cells was achieved in vitro, favoring the hypothesis
that neuroendocrine cells are derived from peripheral precursor cells.
The acceleration of this differentiation pathway may be the reason for
the increased presence of neuroendocrine cells in areas of epithelial
hyperplasia in BPH.
Prostate, 53, 101-108, 2002
- Daha L., Riedl C., Hohlbrugger G., Engelhardt P.,
Pflüger H.:
“Is
a maximal bladder capacity of 400 cc an automatic exclusion criterion
for interstitial cystitis?”
Eur.Urol., Suppl.1, 178, 2002
J.Urol., Suppl., 66, 2002
- Untergasser H., Rumpold H., Tadic L., Plas E.,
Hermann M., Berger P.:
“Decreased
glycoprotein hormone production in trans-differentiaded prostatic
stromal cells: implications for BPH-pathogenesis”
Biogerontology, 3, Suppl.1: M175, 2002
- Heinrich E., Rumpold G., Untergasser G., Pfister
G., Plas E., Berger P.:
“An
in vitro model for neuroendocrine differentiation in BPH and prostate
cancer”
WMW, 152, Suppl.111, 35, 2002
- Untergasser G., Mascher K., Rumpold H., Plas E.,
Hermann M., Berger P.:
“Decreased
glycoprotein hormone a production in trans-differentiated prostatic
stromal cells: implication for BPH-pathogenesis”
WMW, 152, Suppl.111, 2002
- Heinrich E., Rumpold G., Untergasser G., Hermann
M., Pfister G., Plas E.,
Berger P.:
“In
vitro model for neuroendocrine differentiation in prostate cancer and
BPH”
AMA, 29, Suppl.1: P20, 35, 2002
- Tadic L., Untergasser G., Rumpold H., Plas E.,
Hermann M., Berger P.:
“Glycoprotein-hormone
α production decreases in trans-differentiated
prostatic stromal cells: implications for BPH pathogenesis”
Wi.Kli.Wo, Suppl.2, 114: 12, 2002
- Heinrich E., Rumpold H., Untergasser G., Pfister
G., Plas E., Berger P.:
“Neuroendocrine
differentiation in BPH and prostate cancer: establishment of in vitro
models”
Wi.Kli.Wo, Suppl.2, 114: 7, 2002
- Pflüger H., Plas E., Daha L.:
“Die alternde Blase: Ein medizinisches, soziales und wirtschaftliches
Problem”
Link
Der Mediziner, 5, 38-40, 2002
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