The rapid spread of locally restricted neural and hormonal signals among the vast array of largely inexcitable corporal smooth muscle cells is an absolute prerequisite to normal erectile function. And yet the mechanism(s) responsible for this phenomenon is not well understood. As a first step toward a more integrative understanding of erectile physiology and/or dysfunction, an 8- to 12-wk period of experimental diabetes was induced in 2-mo-old male Fischer 344 rats by either intraperitoneal streptozotocin (STZ) injection (35 mg/kg; n = 22) or subtotal pancreatectomy (n = 11). Fourteen age-matched control animals received injection of vehicle only while nine others served as sham-operated control animals. Eight STZ-diabetic animals received insulin replacement. Erectile function was assessed by evaluation of penile reflexes and monitoring of intracavernous pressure responses to both electrical stimulation of the cavernous nerve and intracorporal papaverine or nitroglycerin injection. Intracavernous pressure responses to neurostimulation were significantly attenuated in both STZ-diabetic and subtotal pancreatectomy animals compared with age-matched control animals (P < 0.05). Penile reflexes were also significantly diminished (P < 0.05). Regression analysis revealed that diabetes-related decreases in neurostimulated intracavernous pressure responses were strongly correlated with diminished synaptophysin immunoreactivity in the corpora (P < 0.001; r = 0.88). However, there were no detectable diabetes-related differences in pharmacological erections induced by intracavernous papaverine or nitroglycerin injection. Northern analysis revealed a marked diabetes-related increase in the amount of connexin 43 mRNA measured in frozen corporal tissue. Insulin replacement partially restored (attenuated the loss of) synaptophysin immunoreactivity and maintained neurostimulated intracavernous pressure responses to control levels while having no effect on penile reflexes. These observations may have important implications to the understanding of erectile physiology as well as the etiology of diabetes-related erectile dysfunction.

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BACKGROUND Molecular mechanisms of chemotherapy resistance are present in prostate carcinoma, some of which increase after androgen ablation (AA) therapy. Therefore, the authors hypothesized that chemotherapy in patients with prostate specific antigen (PSA) progression after local therapy, before androgen ablation therapy, will have greater antitumor activity. METHODS Twenty‐three hormone‐naive patients with PSA progression after prostatectomy or radiation therapy were registered in this study. Twenty‐two were treated with 10 mg/m2 of mitoxantrone initially, followed by 12 mg/m2 every 3 weeks for a maximum of 8 cycles. Prostatectomy specimens were assessed, when possible, for topoisomerase II alpha, multidrug resistance protein MRP, and bcl‐2 by immunohistochemistry. RESULTS Twenty‐two patients received a total of 131 cycles of therapy. Three patients had transient Grade 3 or 4 neutropenia without fever. During treatment, 10 of 22 patients showed a decrease in PSA, without an associated decrease in testosterone. In this group of 10 patients, the mean PSA decrease was 29% at 3 months and 43% at 6 months. Overall, 4 of 22 patients had a decrease in PSA of greater than or equal to 50%. The PSA decreased in three of seven patients whose cancer overexpressed MRP and in three of seven patients who overexpressed bcl‐2. No patient with overexpression of topoisomerase II alpha (n = 4) had a decrease in PSA during the study. CONCLUSIONS To the authors' knowledge, this is the first reported study of mitoxantrone in patients with hormone‐naive prostate carcinoma and PSA progression after local therapy; mitoxantrone was safe and biochemically active, similar to prior studies in hormone refractory prostate carcinoma, suggesting that critical molecular mechanisms of chemotherapy resistance are present independent of AA. Further studies are warranted to determine whether pharmacogenomic assessment of topoisomerase II, MRP, or bcl‐2 may predict for response to mitoxantrone. Cancer 2001;92:2065–71. © 2001 American Cancer Society.

From these in-vitro studies, it is apparent that the Nitinol basket designs have the best retrieval capabilities. The ability to articulate the basket improves release of a stone once engaged.

We describe a technique to reduce the tension on the urethra while performing the urethrovesical anastomosis during a laparoscopic radical prostatectomy. A Lowsley tractor is passed through the urethral stump, and a single traction stitch is placed in the posterior bladder neck. The first anastomotic stitch is placed through the urethra and bladder neck at the 6 o'clock position but not tied. The traction stitch is then grasped with the wings of the Lowsley and retracted into the urethra, bringing the bladder neck and urethral stump into close proximity. While maintaining traction on the bladder neck, the previously placed 6 o'clock suture is tied. Before releasing the traction stitch from the Lowsley tractor and bladder neck, two additional stitches are placed at the 4 and 8 o'clock positions, completing the posterior anastomosis. Grasping the traction stitch with the Lowsley tractor relieves tension on the posterior urethra and places it on the bladder neck. This prevents urethral tears and gaps in the posterior wall. The anterior portion of the urethra and bladder neck remains open, maintaining vision. Creating a secure posterior anastomosis allows the remaining sutures to be placed under minimal tension. This technique uses an instrument readily available in the urology operating room and facilitates completion of the difficult anastomosis under minimal tension, resulting in a high-quality anastomosis with fewer gaps.

We believe that our 3 port, transabdominal laparoscopic pyeloplasty technique is an efficient one with the least number of incisions and morbidity to the patient. It has proved to be feasible in more than 75% of our cases. Additional ports can easily be added but usually they are not required.