Radiologist variability in assessing the position of the cavoatrial junction on chest radiographs.

OBJECTIVE: To assess the variability in identifying the cavoatrial junction (CAJ) on chest X-rays (CXRs) amongst radiologists. METHODS: 23 radiologists (13 consultants and 10 trainees) assessed 25 posteroanterior erect CXRs (including 8 duplicates) and marked the positions of the CAJ. Differences in the CAJ position both within and between observers were evaluated and reported as limits of agreement (LOA), repeatability coefficients (RCs) and intraclass correlation coefficients and were displayed graphically with Bland-Altman plots. RESULTS: The mean difference for within-observer assessments was -0.2 cm (95% LOA, -1.5 to +1.1 cm) and between observers, it was -0.3 cm (95% LOA, -2.5 to +1.8 cm). Intraobserver RCs were marginally lower for consultants than for trainees (1.1 vs 1.5). RCs between observers were comparable (2.1 vs 2.2) for consultants and trainees, respectively. CONCLUSION: This study detected a large interobserver variability of the CAJ position (up to 4.3 cm). This is a significant finding considering that the length of the superior vena cava is reported to be approximately 7 cm. We conclude that there is poor consensus regarding the CAJ position amongst radiologists. ADVANCES IN KNOWLEDGE: No comparisons exist between radiologists in determining CAJ position from CXRs. This report provides evidence of the large observer variability amongst radiologists and adds to the discussion regarding the use of CXRs in validating catheter tip location systems.

Colorectal cancer mimics: a review of the usual suspects with pathology correlation.

Colorectal cancer is the third most commonly diagnosed cancer in men and second most commonly diagnosed cancer in women worldwide. Initial diagnosis of colorectal malignancy is generally made on colonoscopy, sigmoidoscopy or digital rectal examination; however, with increased use of CT as primary investigation in patients with lower gastrointestinal symptoms, the diagnosis of colon cancer is often first apparent to a radiologist prior to more invasive tests. CT can demonstrate a discrete soft-tissue mass that narrows the colonic lumen or focal nodular wall thickening/stricture and a variety of pericolonic changes. Pattern of wall thickening has been described as an aid to differential diagnosis; however, significant overlap remains between primary colonic tumor and non-colonic tumors or benign conditions. Imaging is non-specific, and appropriate clinical history, direct inspection, histological analysis, and sometimes discussion at MDT are essential for accurate diagnosis and treatment planning. In this article, we will review the imaging features of some of these benign and malignant mimics of colorectal cancer, with accompanying histology slides where appropriate.

Differential proteomics analysis of synaptic proteins identifies potential cellular targets and protein mediators of synaptic neuroprotection conferred by the slow Wallerian degeneration (Wlds) gene.

Non-somatic synaptic and axonal compartments of neurons are primary pathological targets in many neurodegenerative conditions, ranging from Alzheimer disease through to motor neuron disease. Axons and synapses are protected from degeneration by the slow Wallerian degeneration (Wld(s)) gene. Significantly the molecular mechanisms through which this spontaneous genetic mutation delays degeneration remain controversial, and the downstream protein targets of Wld(s) resident in non-somatic compartments remain unknown. In this study we used differential proteomics analysis to identify proteins whose expression levels were significantly altered in isolated synaptic preparations from the striatum of Wld(s) mice. Eight of the 16 proteins we identified as having modified expression levels in Wld(s) synapses are known regulators of mitochondrial stability and degeneration (including VDAC1, Aralar1, and mitofilin). Subsequent analyses demonstrated that other key mitochondrial proteins, not identified in our initial screen, are also modified in Wld(s) synapses. Of the non-mitochondrial proteins identified, several have been implicated in neurodegenerative diseases where synapses and axons are primary pathological targets (including DRP-2 and Rab GDP dissociation inhibitor beta). In addition, we show that downstream protein changes can be identified in pathways corresponding to both Ube4b (including UBE1) and Nmnat1 (including VDAC1 and Aralar1) components of the chimeric Wld(s) gene, suggesting that full-length Wld(s) protein is required to elicit maximal changes in synaptic proteins. We conclude that altered mitochondrial responses to degenerative stimuli are likely to play an important role in the neuroprotective Wld(s) phenotype and that targeting proteins identified in the current study may lead to novel therapies for the treatment of neurodegenerative diseases in humans.