Selective cyclooxygenase-2 (COX-2) inhibitors (coxibs) increase the incidence of cardiovascular and cerebrovascular events. Complete disruption of the murine gene encoding COX-2 (Ptgs2) leads to renal developmental problems, as well as female reproductive anomalies and patent ductus arteriosus of variable penetrance in newborns, thus rendering this genetic approach difficult to compare with coxib administration. Here, we created hypomorphic Ptgs2 (COX-2(Neo/Neo)) mice in which COX-2 expression is suppressed to an extent similar to that achieved with coxibs, but not eliminated, in an attempt to circumvent these difficulties. In LPS-challenged macrophages and cytokine-stimulated endothelial cells obtained from COX-2(Neo/Neo) mice, COX-2 expression was reduced 70-90%, and these mice developed a mild renal phenotype compared with COX-2 mice possessing an active site mutation (COX-2(Y385F/Y385F)), with minimal signs of renal dysfunction as measured by FITC-inulin clearance and blood urea nitrogen. These COX-2 knockdown mice displayed an increased propensity for thrombogenesis compared with their wild-type (COX-2(+/+)) littermates observed by intravital microscopy in cremaster muscle arterioles upon ferric chloride challenge. Measurement of urinary prostanoid metabolites indicated that COX-2(Neo/Neo) mice produced 50% less prostacyclin but similar levels of PGE(2) and thromboxane compared with COX-2(+/+) mice in the absence of any blood pressure and ex vivo platelet aggregation abnormalities. COX-2(Neo/Neo) mice, therefore, provide a genetic surrogate of coxib therapy with disrupted prostacyclin biosynthesis that predisposes to induced arterial thrombosis.

A small number of pRCCs have indeterminate enhancement when renal protocol CT is used. Heterogeneity, irregular margins, and calcification are suggestive diagnostic features; however, quantitative and qualitative CE-MRI can accurately differentiate hemorrhagic/proteinaceous cysts from pRCC.

3 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018;48:882-896.

Cite as: Can Urol Assoc J 2017;11(1-2):E50-7. http://dx.doi.org/10.5489/cuaj.3789 Published online January 12, 2017 AbstractIntroduction: Plasmacytoid urothelial carcinoma (PUC) is a highgrade variant of conventional urothelial cell carcinoma. This study is the first to describe the imaging findings of PUC, which are previously unreported, using clinical and histopathological correlation. Methods: With internal review board approval, we identified 22 consecutive patients with PUC from 2007-2014. Clinical parameters, including age, gender, therapy, surgical margins, and longterm outcome, were recorded. Baseline imaging was reviewed by an abdominal radiologist who evaluated for tumour detectability/location/morphology, local staging, and presence/location of metastases. Pelvic peritoneal spread of tumour (defined as >5mm thick soft tissue spreading along fascial planes) was also evaluated. Followup imaging was reviewed for presence of local recurrence or metastases. Results: Median age at presentation was 74 years (range 51-86), with only three female patients. Imaging features of the primary tumour in this study were not unique for PUC. Muscle-invasive disease was present on pathology in 19/22 (86%) of tumours, with distant metastases in 2/22 (9%) at baseline imaging. Pelvic peritoneal spread of tumour was radiologically present in 4/20 (20%) at baseline. During followup, recurrent/residual tumour was documented in 16/22 (73%) patients and 7/16 (44%) patients eventually developed distant metastases. Median time to disease recurrence in patients who underwent curative surgery was three months (range 0-19). Conclusions: PUC is an aggressive variant of urothelial carcinoma with poor prognosis. Pelvic peritoneal spread of tumour as thick sheets extending along fascial planes may represent a characteristic imaging finding of locally advanced PUC.

Diagnostic performance of CT was highest when an intraluminal contrast agent was used. Meticulous and careful use of an intraluminal contrast agent is therefore important in this patient population.

Purpose: The Royal College of Physicians and Surgeons of Canada (RCPSC) has mandated the transition of postgraduate medical training in Canada to a competency-based medical education (CBME) model divided into 4 stages of training. As part of the Queen’s University Fundamental Innovations in Residency Education proposal, Queen’s University in Canada is the first institution to transition all of its residency programs simultaneously to this model, including Diagnostic Radiology. The objective of this report is to describe the Queen’s Diagnostic Radiology Residency Program’s implementation of a CBME curriculum. Methods: At Queen’s University, the novel curriculum was developed using the RCPSC’s competency continuum and the CanMEDS framework to create radiology-specific entrustable professional activities (EPAs) and milestones. In addition, new committees and assessment strategies were established. As of July 2015, 3 cohorts of residents (n = 9) have been enrolled in this new curriculum. Results: EPAs, milestones, and methods of evaluation for the Transition to Discipline and Foundations of Discipline stages, as well as the opportunities and challenges associated with the implementation of a competency-based curriculum in a Diagnostic Radiology Residency Program, are described. Challenges include the increased frequency of resident assessments, establishing stage-specific learner expectations, and the creation of volumetric guidelines for case reporting and procedures. Conclusions: Development of a novel CBME curriculum requires significant resources and dedicated administrative time within an academic Radiology department. This article highlights challenges and provides guidance for this process.

MTR measurements can be used to monitor early myelination in the developing brain and to help detect changes in tissue that are not shown on T1- and T2-weighted MR images.

An oxidant-initiated, substitution process for dihapto-coordinated ligands is described for the {MoTp­(NO)­(DMAP)} system. Complexes of the form MoTp­(NO)­(DMAP)­(η2-alkene), MoTp­(NO)­(DMAP)­(η2-ketone), and MoTp­(NO)­(DMAP)­(η2-arene) (where Tp = hydridotris­(pyrazolyl)­borate and DMAP = 4-(dimethylamino)­pyridine) undergo an alkene-to-ketone exchange that is catalyzed by the addition of <0.1 equiv of a metallocene oxidant (ferrocenium, permethylferrocenium, or cobaltocenium). A similar acceleration was observed in the presence of the H-bond donor hexafluoroisopropanol (HFIP). From experimental observations, a radical chain propagation mechanism is proposed that is dependent on the equilibrium between dihapto-coordinated (C, O-η2) and monocoordinated (κ-O) isomers and the differing redox characteristics of these two isomeric forms. This concept was then applied to the search of sodium-free reduction conditions for the conversion of MoTp­(NO)­(DMAP)­(I) to various molybdenum(0) complexes of unsaturated ligands, including MoTp­(NO)­(DMAP)­(η2-naphthalene) and MoTp­(NO)­(DMAP)­(α-pinene).