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This study evaluates the durability of a novel tissue engineered blood vessel (TEBV) created by seeding a natural vascular tissue scaffold (decellularized human saphenous vein allograft) with autologous adipose-derived stem cells (ASC) differentiated into endothelial-like cells. Previous work with this model revealed the graft to be thrombogenic, likely due to inadequate endothelial differentiation as evidenced by minimal production of nitric oxide (NO). To evaluate the importance of NO expression by the seeded cells, we created TEBV using autologous ASC transfected with the endothelial nitric oxide synthase (eNOS) gene to produce NO. We found that transfected ASC produced NO at levels similar to endothelial cell (EC) controls in vitro and capable of causing vasorelaxation of aortic specimens ex vivo. TEBV (n=5) created with NO-producing ASC and implanted as interposition grafts within the aorta of rabbits remained patent for two months and demonstrated a non-thrombogenic surface compared to unseeded controls (n=5). Despite the xenograft nature of the scaffold, TEBV structure remained well-preserved in seeded grafts. In sum, this study demonstrates that up-regulation of NO expression within adult stem cells differentiated towards an endothelial-like cell imparts a non-thrombogenic phenotype and highlights the importance of NO production by cells to be used as endothelial cell substitutes in vascular tissue engineering applications.

A low overall rate of ureteral access failure in unstented patients is shown. Young female patients and proximal ureteral stones were less likely to be accessed primarily. This study provides information that will help urologists counsel their patients preoperatively regarding their likelihood of failing primary URS necessitating a second procedure. This will also help the patient to make an informed decision during the consent process and may guide urologists on selective prestenting in higher risk patients.

Objectives To evaluate the feasibility of performing robot‐assisted laparoscopic prostatectomy (RALP) at an ultra‐low pressure of 6 mmHg and to assess the potential impact on its clinical outcomes, as compared to those of a historical cohort of patients in which RALP was performed at a pressure of 15 mmHg. Patients and Methods We evaluated 600 consecutive RALP procedures, performed by a single surgeon, including 300 procedures performed at 6 mmHg and the previous 300 performed at 15 mmHg. We compared preoperative patient characteristics and outcomes including pain scores, morphine equivalents, length of stay (LOS) and complications. After implementing the adjustment to 6 mmHg, we began allowing same‐day discharge in patients meeting established criteria. Results All 300 consecutive RALP procedures were completed at 6 mmHg with no pressure adjustments for the entirety of the case. There were no significant differences in patient or pathological features between groups. Body mass index was 19.5–44.3 kg/m2 in the 6 mmHg group. The mean operating time was 10.5‐min longer and mean estimated blood loss 20‐mL higher at 6 mmHg, with no blood transfusions in either group. The mean LOS was shorter in the 6‐mmHg group (0.57 vs 1.00 days; P < 0.001), with 43.3% of patients in the 6‐mmHg group discharged home the day of surgery. There were no differences in morphine equivalents or maximum pain scores in the first 4 h after surgery, but there was a small improvement (18%) in pain scores at 5–12 h postoperatively (3.2 vs 3.9; P < 0.001). The 30‐day complication rate was 8.7% vs 4.0%, with 30‐day hospital readmissions of 5.7% vs 1.0% for the 15 vs 6 mmHg groups. Conclusion Robot‐assisted laparoscopic prostatectomy at a pneumoperitoneum pressure of 6 mmHg was uniformly feasible without increasing complications. Ultra‐low pneumoperitoneum may confer a pain benefit, which may contribute to safe same‐day discharge.

This study examined the role of the brain stem in inhibition of bladder reflexes induced by tibial nerve stimulation (TNS) in ␣-chloralose-anesthetized decerebrate cats. Repeated cystometrograms (CMGs) were performed by infusing saline or 0.25% acetic acid (AA) to elicit normal or overactive bladder reflexes, respectively. TNS (5 or 30 Hz) at three times the threshold (3T) intensity for inducing toe movement was applied for 30 min between CMGs to induce post-TNS inhibition or applied during the CMGs to induce acute TNS inhibition. Inhibition was evident as an increase in bladder capacity without a change in amplitude of bladder contractions. TNS applied for 30 min between saline CMGs elicited prolonged (Ͼ2 h) poststimulation inhibition that significantly (P Ͻ 0.05) increased bladder capacity to 30 -60% above control; however, TNS did not produce this effect during AA irritation. TNS applied during CMGs at 5 Hz but not 30 Hz significantly (P Ͻ 0.01) increased bladder capacity to 127.3 Ϯ 6.1% of saline control or 187.6 Ϯ 5.0% of AA control. During AA irritation, naloxone (an opioid receptor antagonist) administered intravenously (1 mg/kg) or directly to the surface of the rostral brain stem (300 -900 g) eliminated acute TNS inhibition and significantly (P Ͻ 0.05) reduced bladder capacity to 62.8 Ϯ 22.6% (intravenously) or 47.6 Ϯ 25.5% (brain stem application). Results of this and previous studies indicate 1) forebrain circuitry rostral to the pons is not essential for TNS inhibition; and 2) opioid receptors in the brain stem have a critical role in TNS inhibition of overactive bladder reflexes but are not involved in inhibition of normal bladder reflexes. neuromodulation; brain stem; opioid; tibial; cat TIBIAL NEUROMODULATION, a Food and Drug Administration (FDA)-approved therapy for overactive bladder (OAB) symptoms, including urgency, frequency, and incontinence (7,19,20,29), is often used to treat patients whose symptoms are not completely controlled by drugs or who have unacceptable drug side effects (1,2,8,18). However, the mechanisms underlying tibial neuromodulation therapy are uncertain. Understanding the site of action and neurotransmitters involved in the inhibition of bladder reflexes by tibial nerve stimulation (TNS) is important for developing new OAB treatments by combining drug therapies with tibial neuromodulation to achieve a higher efficacy with fewer side effects (14,33).Previous studies in cats have demonstrated the inhibitory effect of TNS on bladder reflexes elicited during non-nociceptive saline distention as well as nociceptive acetic acid (AA) irritation (23,27). The failure of TNS to inhibit reflex bladder contractions during AA irritation in animals with acute spinal cord transection at the T9/T10 level (32) indicates that supraspinal neural circuits are necessary for TNS inhibition. However, it is unknown whether these supraspinal circuits are located in the forebrain or in the brain stem.A major clinical benefit of TNS is the long-lasting poststimulation inhibitory effect, which allows...

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In a-chloralose anesthetized cats, we examined the role of opioid receptor (OR) subtypes (m, k, and d) in tibial nerve stimulation (TNS)-induced inhibition of bladder overactivity elicited by intravesical infusion of 0.25% acetic acid (AA). The sensitivity of TNS inhibition to cumulative i.v. doses of selective OR antagonists (cyprodime for m, nor-binaltorphimine for k, or naltrindole for d ORs) was tested. Naloxone (1 mg/kg, i.v., an antagonist for m, k, and d ORs) was administered at the end of each experiment. AA caused bladder overactivity and significantly (P , 0.01) reduced bladder capacity to 21.1% 6 2.6% of the saline control. TNS at 2 or 4 times threshold (T) intensity for inducing toe movement significantly (P , 0.01) restored bladder capacity to 52.9% 6 3.6% or 57.4% 6 4.6% of control, respectively. Cyprodime (0.3-1.0 mg/kg) completely removed TNS inhibition without changing AA control capacity. Nor-binaltorphimine (3-10 mg/kg) also completely reversed TNS inhibition and significantly (P , 0.05) increased AA control capacity. Naltrindole (1-10 mg/kg) reduced (P , 0.05) TNS inhibition but significantly (P , 0.05) increased AA control capacity. Naloxone (1 mg/kg) had no effect in cyprodime pretreated cats, but it reversed the nor-binaltorphimine-induced increase in bladder capacity and eliminated the TNS inhibition remaining in naltrindole pretreated cats. These results indicate a major role of m and k ORs in TNS inhibition, whereas d ORs play a minor role. Meanwhile, k and d ORs also have an excitatory role in irritation-induced bladder overactivity.