SUMMARY
Although the ureter is functionally simply a tube to transport urine, ureteric surgery requires detailed anatomical knowledge and advanced surgical skills, because the ureter has a delicate blood supply. Therefore, the urological surgeon must have distinct strategies available to bridge ureteric defects of various sites and lengths. Furthermore, handling during and after surgery should be individualized to the patient's pre‐ and intraoperative situation. In this review, the indications for reconstruction of a specific ureteric defect, the required techniques and postoperative recommendations are discussed.
BACKGROUND AND PURPOSE α1‐Adrenoceptor‐induced contraction of prostate smooth muscle is mediated by calcium‐ and Rho kinase‐dependent mechanisms. In addition, other mechanisms, such as activation of c‐jun N‐terminal kinase (JNK) may be involved. Here, we investigated whether JNK participates in α1‐adrenoceptor‐induced contraction of human prostate smooth muscle.
EXPERIMENTAL APPROACH Prostate tissue was obtained from patients undergoing radical prostatectomy. Effects of the JNK inhibitors SP600125 (50 µM) and BI‐78D3 (30 µM) on contractions induced by phenylephrine, noradrenaline and electric field stimulation (EFS) were studied in myographic measurements. JNK activation by noradrenaline (30 µM) and phenylephrine (10 µM), and the effects of JNK inhibitors of c‐Jun phosphorylation were assessed by Western blot analyses with phospho‐specific antibodies. Expression of JNK was studied by immunohistochemistry and fluorescence double staining.
KEY RESULTS The JNK inhibitors SP600125 and BI‐78D3 reduced phenylephrine‐ and noradrenaline‐induced contractions of human prostate strips. In addition, SP600125 reduced EFS‐induced contraction of prostate strips. Stimulation of prostate tissue with noradrenaline or phenylephrine in vitro resulted in activation of JNK. Incubation of prostate tissue with SP600125 or BI‐78D3 reduced the phosphorylation state of c‐Jun. Immunohistochemical staining demonstrated the expression of JNK in smooth muscle cells of human prostate tissue. Fluorescence staining showed that α1A‐adrenoceptors and JNK are expressed in the same cells.
CONCLUSIONS AND IMPLICATIONS Activation of JNK is involved in α1‐adrenoceptor‐induced prostate smooth muscle contraction. Models of α1‐adrenoceptor‐mediated prostate smooth muscle contraction should include this JNK‐dependent mechanism.
Prostate cancer is one of the most frequent malignant diseases in men. Despite constant progress achieved in imaging procedures, prostate biopsy is the gold standard for diagnosing prostate cancer. For the assessment of lymph node status, only staging lymphadenectomy provides valid information. The aim of this work is to analyze the imaging procedures available in Germany and their value in primary and lymph node staging as well as biochemical recurrence.
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