The novel 48-h VVR was a robust predictor of outcome following paediatric cardiac surgery and outperformed the VIS and peak postoperative lactate.

Ultrasound and magnetic resonance imaging (MRI) are both capable of diagnosing full-thickness rotator cuff tears. However, it is unknown which imaging modality is more accurate and precise in evaluating the characteristics of full-thickness rotator cuff tears in a surgical population. This study reviewed 114 patients who underwent arthroscopic repair of a full-thickness rotator cuff tear over a 1-year period. Of these patients, 61 had both preoperative MRI and ultrasound for review. Three musculoskeletal radiologists evaluated each ultrasound and MRI in a randomized and blinded fashion on 2 separate occasions. Tear size, retraction status, muscle atrophy, and fatty infiltration were analyzed and compared between the 2 modalities. Ultrasound measurements were statistically smaller in both tear size (P=.001) and retraction status (P=.001) compared with MRI. The 2 image modalities showed comparable intraobserver reliability in assessment of tear size and retraction status. However, MRI showed greater interobserver reliability in assessment of tear size, retraction status, and atrophy. Independent observers are more likely to agree on measurements of the characteristics of rotator cuff tears when using MRI compared with ultrasound. As tear size increases, the 2 image modalities show greater differences in measurement of tear size and retraction status. Additionally, compared with MRI, ultrasound shows consistently low reliability in detecting subtle, but clinically important, degeneration of the soft tissue envelope. Although it is inexpensive and convenient, ultrasound may be best used to identify a tear, and MRI is superior for use in surgical planning for larger tears. [Orthopedics. 2017; 40(1):e124-e130.].

Background Wnt/β-catenin signaling is important for prostate development and cancer in humans. Activation of this pathway in differentiated luminal cells of mice induces high-grade prostate intraepithelial neoplasia (HGPIN). Though the cell of origin of prostate cancer has yet to be conclusively identified, a castration-resistant Nkx3.1-expressing cell (CARN) may act as a cell of origin for prostate cancer. Methods To activate Wnt/β-catenin signaling in CARNs, we crossed mice carrying tamoxifen-inducible Nkx3.1-driven Cre to mice containing loxP sites in order to either conditionally knock out adenomatous polyposis coli (Apc) or constitutively activate β-catenin directly. We then castrated and hormonally regenerated these mice to target the CARN population. Results Loss of Apc in hormonally normal mice induced HGPIN; however, after one or more rounds of castration and hormonal regeneration, Apc-null CARNs disappeared. Alternatively, when β-catenin was constitutively activated under the same conditions, HGPIN was apparent. Conclusion Activation of Wnt/β-catenin signaling via Apc deletion is sufficient to produce HGPIN in hormonally normal mice. Loss of Apc may destabilize the CARN population under regeneration conditions. When β-catenin is constitutively activated, HGPIN occurs in hormonally regenerated mice. A second genetic hit is likely required to cause progression to carcinoma and metastasis.

Introduction: Renal failure occurs in approximately 20% admissions with cirrhosis. Spontaneous bacterial peritonitis (SBP) is one of the most common reasons for admissions in cirrhotics with ascites and contributes 10-30% of the mortality. Acute kidney injury (AKI) is reported to be the most important predictor for mortality in few studies, with mortality approaching 100% in progressive renal failure. However, the role of dialysis in this group has not been studied. We aim to fulfill this knowledge gap. Methods: Using the Nationwide Inpatient Sample 2006-2009, patients older than 18 years, cirrhotic discharged with any diagnosis of SBP and AKI were identified through ICD-9-CM codes as described in literature. Outcome variables included frequency, in-hospital mortality and length of stay (LOS). Chi square test and Wilcoxon rank test was used to compare categorical and continuous variables respectively. Results: There were 56,973 discharges with SBP from 2006 to 2009. Of these, 19,251 (33.8%) developed AKI and of these 3,005(15.6%) received hemodialysis. The in hospital mortality in those with SBP not developing AKI was 9.5% and 34.9% in those developing AKI. The rates of hemodialysis in SBP with AKI increased from 11.8% in 2006 to 17.5% in 2009 (p=0.04). The in hospital mortality however did not change significantly through these years (51.6% in 2006 to 54.3% in 2009, p=0.76). Median LOS in SBP with AKI requiring dialysis was significantly longer than those not requiring hemodialysis (16 days vs. 8 days, p<0.001). LOS in this group has increased from 13.5 days to 16 days in this time period. Conclusions: AKI in SBP is associated with high mortality. The rates of dialysis have been increasing from 2006 to 2009 and patients have been staying longer but this has not been accompanied by improvement in mortality.