You have accessJournal of UrologyPodium, Wednesday, May 25, 2005, 10:00 am - 12:00 pm1 Apr 20051582: 3-D-Ultrasound Spectroscopy During ESWL Correlates with Stone Disintegration Marc R. Witkowski, Dominik Pernkopf, Eugen Plas, and Heinz Pflüger Marc R. WitkowskiMarc R. Witkowski More articles by this author , Dominik PernkopfDominik Pernkopf More articles by this author , Eugen PlasEugen Plas More articles by this author , and Heinz PflügerHeinz Pflüger More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)35716-1AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "1582: 3-D-Ultrasound Spectroscopy During ESWL Correlates with Stone Disintegration." The Journal of Urology, 173(4S), pp. 428–429 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 173Issue 4SApril 2005Page: 428-429 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Marc R. Witkowski More articles by this author Dominik Pernkopf More articles by this author Eugen Plas More articles by this author Heinz Pflüger More articles by this author Expand All Advertisement PDF downloadLoading ...

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.

Next to the sex steroid hormone T, PRL has been shown to influence prostatic function and development. Transgenic mice overexpressing the rat PRL gene develop dramatic enlargements of the prostate gland. Proliferation and secretory activities of epithelial cells are stimulated by PRL in rodents and men. Low concentrations of human PRL (hPRL) and hPRL receptors have been observed in human prostatic epithelial cells (ECs). The aim of this study was to compare regulation of the in vitro hPRL secretion in prostatic ECs and stromal smooth muscle cells (SMCs) after stimulation with seminal plasma (SMP), containing a variety of prostatic factors. SMCs released up to 1 ng hPRL/ml (i.e., approximately 500-fold more than unstimulated SMCs and ECs). Quantification of PRL mRNA by highly sensitive quantitative RT-PCR revealed that hPRL gene expression increased 5-fold within 24 h of SMP incubation. Sex steroids (dihydrotestosterone, progesterone, 17beta-estradiol), prostaglandins (PGE-1, PGE-2), and cAMP-stimulating substances (forskolin) were not responsible for induction of hPRL. Compared with endometrial SMCs, regulation of prostatic hPRL secretion was independent of progesterone and cAMP. HPLC analysis of human SMP revealed that the common action of at least two different proteins and a low molecular cofactor is required. We concluded that prostatic ECs secrete proteins acting synergistically with low-molecular-weight cofactors to induce differentiation and hPRL release in SMCs. Age-related increases in SMC-derived hPRL might contribute to the development of benign hyperplasia of the prostate.

Prostate epithelial cells contain the highest levels of zinc among all organs and tissues in the human body. Zinc is accumulated primarily in the mitochondria, where it is responsible for inhibition of mitochondrial aconitase activity, thereby increasing citrate production. The present study was designed to clarify the role of zinc for human prostate epithelial cell growth and apoptosis. Apoptosis of in vitro cultivated human prostate epithelial cells exposed to ZnCl2 was analyzed by determination of phospholipid membrane asymmetry, nuclear fragmentation, DNA strand breaks, changes of mitochondrial potential and cellular pro/antiapoptotic proteins. Zinc induced apoptosis without involvement of p53 by decreasing mitochondrial transmembrane potential (ΔΨm) and Bcl-2 protein levels in proliferating epithelial cells. Thus, the high local concentrations of zinc ions in the prostatic lumen seem to be necessary to regulate proliferative activities and to enforce epithelial differentiation processes.