collating intraoperative data and early functional outcome.
RESULTSThe mean surgical time for LRP and RAP was 235 and 202 min ( P > 0.05) and mean (95% confidence interval) blood loss 299 (40) and 206 (63) mL ( P = 0.014), with no transfusions in either group. The positive margin rate did not differ significantly (14% LRP and 12% RAP) and there was no biochemical recurrence in either group. Early functional outcomes were similar.
CONCLUSIONSBoth LRP and RAP are technically demanding, but feasible, with the patient clearly benefiting. There were no major surgical differences between the techniques, but RAP is more costly.
The extraperitoneal approach offers the advantages of improved dexterity and visualization of the robot, while avoiding the abdominal cavity and potential associated morbidity. As surgeons gain more experience with this new technology, the extraperitoneal approach simulating the standard open retropubic technique is likely to gain popularity.
Although a large prostate volume is associated with a slight increase in short-term urinary complications postoperatively, it should not be considered a contraindication for the experienced surgeon. This higher risk raises the question of a possible need for longer catheterization in this subset of patients.
Males develop kidney stones far more frequently than females with a ratio of 2–3:1, suggesting that androgen receptor (AR) signaling might play a key role in the development of nephrolithiasis. Using the cre-loxP system to selectively knock out AR in glyoxylate-induced calcium oxalate (CaOx) crystal mouse models, we found that the mice lacking hepatic AR had less oxalate biosynthesis, which might lead to lower CaOx crystal formation, and that the mice lacking kidney proximal or distal epithelial AR also had lower CaOx crystal formation. We found that AR could directly up-regulate hepatic glycolate oxidase and kidney epithelial NADPH oxidase subunit p22-PHOX at the transcriptional level. This up-regulation might then increase oxalate biosynthesis and oxidative stress that resulted in induction of kidney tubular injury. Targeting AR with the AR degradation enhancer ASC-J9 led to suppression of CaOx crystal formation via modulation of oxalate biosynthesis and oxidative stress in both in vitro and in vivo studies. Taken together, these results established the roles of AR in CaOx crystal formation.
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