Quantification of abdominal aortic calcification on CT

[Extract] Calcification of the coronary arteries is associated with cardiovascular end-point, such as myocardial infarction, stroke, and vascular death.1\ud Techniques for quantifying vascular calcification in patients, particularly in arteries outside the chest, are not routinely available.2 In this prospective study, we examined whether CT angiography (CTA) could be used to\ud reproducibly measure severity of infrarenal abdominal aortic calcification. The study involved 50 consecutive patients undergoing aortic CTA for investigation of peripheral vascular disease or aortic aneurysm in 3 stages.\ud For the initial 14 patients, sequential plain and contrast-enhanced CT were obtained and then analyzed on a workstation using 5 different thresholds to define aortic calcification. The calcification volumes were assessed using a number of nonparametric statistical tests to compare\ud clinical measurements to define the most appropriate threshold by which calcification should be measured on CTA by comparison with CT. For the next 24 patients, CTA alone was obtained and analyzed with the threshold defined as optimal from part 1 of the study. The calcification volume measurements were performed by one observer using three different workstation protocols: (1) manual threshold setting without image magnification, (2) manual threshold setting with twice image magnification, and (3) automatic threshold setting with twice image magnification. To assess the most appropriate protocol, the readings were repeated on a second occasion 24 hours apart by the same observer, and the intraobserver reproducibility was assessed by nonparametric statistical tests. Having defined the most appropriate thresholds and workstation settings to analyze the calcification volume on CTA, the interobserver reproducibility of calcification volume measurements was analyzed on the next 12 consecutive patients undergoing CTA and compared with those for CT (using the first cohort of patients)

Assessment of a serum assay for quantification of abdominal aortic calcification

Intimal vascular calcification is an important marker of atherosclerosis, and its severity is an independent risk factor for cardiovascular events. Measurement of coronary or aortic calcification requires CT-based imaging and elaborate data analysis to ensure accuracy. A blood assay which could quantify the severity of vascular calcification would be less expensive, avoid exposure to radiation, and be more accessible than present imaging based methods. Osteoprotegerin (OPG) and osteopontin (OPN) are present in human serum and have been implicated in vascular calcification. In this prospective study we assessed the value of a number of serum assays for OPG and OPN in determining abdominal aortic calcification. Firstly, we investigated the assay characteristics and reproducibility of 5 ELISAs using a subset of patients. Based on the findings of these assessments, we selected 3 assays for full evaluation in the entire cohort

Hyperdiploid tumor cells increase phenotypic heterogeneity within Glioblastoma tumors

Here we report the identification of a proliferative, viable, and hyperdiploid tumor cell subpopulation present within Glioblastoma (GB) patient tumors. Using xenograft tumor models, we demonstrate that hyperdiploid cell populations are maintained in xenograft tumors and that clonally expanded hyperdiploid cells support tumor formation and progression in vivo. In some patient tumorsphere lines, hyperdiploidy is maintained during long-term culture and in vivo within xenograft tumor models, suggesting that hyperdiploidy can be a stable cell state. In other patient lines hyperdiploid cells display genetic drift in vitro and in vivo, suggesting that in these patients hyperdiploidy is a transient cell state that generates novel phenotypes, potentially facilitating rapid tumor evolution. We show that the hyperdiploid cells are resistant to conventional therapy, in part due to infrequent cell division due to a delay in the G0/G1 phase of the cell cycle. Hyperdiploid tumor cells are significantly larger and more metabolically active than euploid cancer cells, and this correlates to an increased sensitivity to the effects of glycolysis inhibition. Together these data identify GB hyperdiploid tumor cells as a potentially important subpopulation of cells that are well positioned to contribute to tumor evolution and disease recurrence in adult brain cancer patients, and suggest tumor metabolism as a promising point of therapeutic intervention against this subpopulation

Relationship between CT anthropometric measurements, adipokines and abdominal aortic calcification

Background: Visceral obesity and aortic calcification are both associated with cardiovascular events. The purpose of this study was to examine if visceral obesity was associated with the severity of abdominal aortic calcification.\ud Methods: One hundred and forty eight patients with peripheral artery disease were assessed by CT angiography. The severity of infrarenal abdominal aortic calcification was measured using a validated technique. The size of the visceral and subcutaneous compartments was estimated from anthropometric measurements made from the same CT. Calcification and anthropometric measurements were compared with Spearman's correlation and multiple logistic regression (adjusting for age, gender, hypertension, diabetes, smoking and cholesterol).\ud Results: The relative size of the visceral compartment estimated from CT diameter ratios was correlated with abdominal aortic calcification severity, r = 0.27, p = 0.001 and independently associated with calcification allowing for other cardiovascular risk factors (OR 6.63, 95% CI 1.90–23.14). The relative size of the visceral compartment was associated with serum osteoprotegerin levels, suggesting a possible mechanism underlying the detrimental influence of visceral adiposity.\ud Conclusion: The association of visceral adiposity and arterial calcification suggests one mechanism, which may contribute to the detrimental effects of central obesity