Cloacal Exstrophy Closure Without Osteotomy and Immobilization: A Recipe for Failure.

Background: Cloacal exstrophy (CE) remains one of the most severe birth defects compatible with life with a constellation of anomalies involving the bladder, genitalia, hindgut, and spinal cord. Pelvic osteotomy and immobilization have been utilized to facilitate bladder closure, yet their role as adjuncts remains a topic of debate. The authors sought to evaluate the outcomes of CE closure without the use of osteotomy or lower extremity (LE)/pelvic immobilization.

A Rocky Road: Bladder Stones in the Augmented Exstrophy-Epispadias Complex Patient.

Objective: To determine the rate of stone formation amongst patients of the exstrophy-epispadias complex with augmentation cystoplasty. We hypothesize that bowel segment choice influences the rate of stone formation after bladder augmentation and the rate of complications from bladder stone surgery.

Methods: An IRB-approved institutional database of 1512 exstrophy-epispadias patients was reviewed retrospectively.

Stomal Stenosis After Continent Urinary Diversion in Bladder Exstrophy: Risk Factors and Management.

Objective: To identify risk factors for stenosis and compare management strategies for stenosis etiology and to examine the efficacy of each approach. Patients with classic bladder exstrophy (CBE), a rare genitourinary malformation, may require construction of a continent urinary stoma (CUS) if incontinence persists. Stomal stenosis is a challenging complication as it is common, progressive, and recurrent.

The nuclear tyrosine kinase BRK/Sik phosphorylates and inhibits the RNA-binding activities of the Sam68-like mammalian proteins SLM-1 and SLM-2.

Expression of the intracellular tyrosine kinase BRK/Sik is epithelial-specific and regulated during differentiation. Only a few substrates have been identified for BRK/Sik, including the KH domain containing RNA-binding protein Sam68 and the novel adaptor protein BKS. Although the physiological role of Sam68 is unknown, it has been shown to regulate mRNA transport, pre-mRNA splicing, and polyadenylation.

Tumor suppressor functions for the Cdk inhibitor p21 in the mouse colon.

The Cdk inhibitor p21 regulates p53-mediated growth arrest following DNA damage. It is expressed during epithelial differentiation in a variety of organs including colon. We investigated susceptibility of p21-deficient mice to the colon carcinogen azoxymethane (AOM).