Browsing by Author "Inouye, Brian M"
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Item Open Access Buccal reharvest for urethroplasty after graft site closure is safe and does not affect long-term oral health(Urology, 2022-01) Inouye, Brian M; Nosé, Brent D; Krughoff, Kevin; Boysen, William R; Peterson, Andrew CItem Open Access Extirpative cultures reveal infectious pubic bone osteomyelitis in prostate cancer survivors with urinary-pubic symphysis fistulae (UPF).(Urology, 2020-05-07) Nosé, Brent D; Boysen, William R; Kahokehr, Arman A; Inouye, Brian M; Eward, William C; Hendershot, Edward F; Peterson, Andrew COBJECTIVE:To examine the infectious features of patients with urinary pubic symphysis fistula (UPF) and their association with osteomyelitis. METHODS:We conducted a review of our quality improvement database for 36 patients with UPF undergoing bone resection and extirpative surgery from October 2012 to January 2019. An assessment of bone and urine cultures was carried out along with surgical, radiologic and demographic data. We analyzed descriptive statistics and used Fisher Exact Tests and unpaired Welch t-tests to assess for associations with positive bone cultures. RESULTS:In our cohort, 33 patients (91.7%) had positive bone cultures with the three most common organisms being candida (22.0%), enterococcus (18.0%) and pseudomonas (10.0%). There was a correlation between positive pre-operative urine culture and positive bone culture (p< 0.01), with 63.0% of those with positive urine cultures growing the same organism on bone culture. CONCLUSIONS:In this series, 91.7% of patients undergoing extirpative surgery for UPF at our institution have positive bone cultures at time of pubic bone debridement. Additionally, we demonstrate a statistically significant correlation between positive urine cultures and positive bone cultures in these patients. This supports the need for a multidisciplinary approach including infectious disease, orthopedic surgery and reconstructive urology in order to address this complex clinical condition.Item Open Access NLRP3/IL-1β mediates denervation during bladder outlet obstruction in rats.(Neurourology and urodynamics, 2018-03) Lütolf, Robin; Hughes, Francis M; Inouye, Brian M; Jin, Huixia; McMains, Jennifer C; Pak, Elena S; Hannan, Johanna L; Purves, J ToddDenervation of the bladder is a detrimental consequence of bladder outlet obstruction (BOO). We have previously shown that, during BOO, inflammation triggered by the NLRP3 inflammasome in the urothelia mediates physiological bladder dysfunction and downstream fibrosis in rats. The aim of this study was to assess the effect of NLRP3-mediated inflammation on bladder denervation during BOO.There were five groups of rats: (i) Control (no surgery); (ii) Sham-operated; (iii) BOO rats given vehicle; (iv) BOO rats given the NLRP3 inhibitor glyburide; and (v) BOO rats given the IL-1 receptor antagonist anakinra. BOO was constructed by ligating the urethra over a 1 mm catheter and removing the catheter. Medications were given prior to surgery and once daily for 12 days. Bladder sections were stained for PGP9.5, a pan-neuronal marker. Whole transverse sections were used to identify and count nerves while assessing cross-sectional area. For in vitro studies, pelvic ganglion neurons were isolated and treated with IL-1β. After a 48 h incubation apoptosis, neurite length and branching were assessed.In obstructed bladders, the number of nerves decreased while total area increased, indicating a loss of cell number and/or branching. The decrease in nerve density was blocked by glyburide or anakinra, clearly implicating the NLRP3 pathway in denervation. In vitro analysis demonstrated that IL-1β, a product of the inflammasome, induced apoptosis in pelvic ganglion neurons, suggesting one mechanism of BOO-induced denervation is NLRP3/IL-1β triggered apoptosis.The NLRP3/IL-1β-mediated inflammation pathway plays a significant role in denervation during BOO.Item Open Access The Emerging Role of Inflammasomes as Central Mediators in Inflammatory Bladder Pathology.(Current urology, 2018-02) Inouye, Brian M; Hughes, Francis M; Sexton, Stephanie J; Purves, J ToddIrritative voiding symptoms (e.g. increased frequency and urgency) occur in many common pathologic conditions such as urinary tract infections and bladder outlet obstruction, and these conditions are well-established to have underlying inflammation that directly triggers these symptoms. However, it remains unclear as to how such diverse stimuli individually generate a common inflammatory process. Jürg Tschopp provided substantial insight into this conundrum when, working with extracts from THP-1 cells, he reported the existence of the inflammasome. He described it as a structure that senses multiple diverse signals from intracellular/extracellular sources and pathogens and triggers inflammation by the maturation and release of the pro-inflammatory cytokines interleukin-1β and interleukin-18. Recently, many of these sensors were found in the bladder and the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3, has been shown to be a central mediator of inflammation in several urological diseases. In this review, we introduce the nucleotide-binding domain, leucine-rich-containing family, pyrin domaincontaining-3 inflammasome, highlight its emerging role in several common urologic conditions, and speculate on the potential involvement of other inflammasomes in bladder pathology.