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The presence of materials with different magnetic properties, such as metal implants, causes distortion of the magnetic field locally, resulting in signal voids and pile ups, i.e. susceptibility artifacts in MRI. Quantitative and unbiased measurement of the artifact is prerequisite for optimization of acquisition parameters. In this study an image gradient based segmentation method is proposed for susceptibility artifact quantification. The method captures abrupt signal alterations by calculation of the image gradient. Then the artifact is quantified in terms of its extent by an automated cross entropy thresholding method as image area percentage. The proposed method for artifact quantification was tested in phantoms containing two orthopedic implants with significantly different magnetic permeabilities. The method was compared against a method proposed in the literature, considered as a reference, demonstrating moderate to good correlation (Spearman's rho = 0.62 and 0.802 in case of titanium and stainless steel implants). The automated character of the proposed quantification method seems promising towards MRI acquisition parameter optimization.

The aim of this study is to investigate the effect of edge-enhancing diffusion (EED) denoising on the quality of dual energy CT images, derived by varying the weighting of the two spectra (0.1 to 0.9, 0.1 step). The quality of EED denoised weighted images was quantitatively assessed by means of SNR, contrast and CNR measured on ROIs of phantom images corresponding to 14 mg/ml iodine concentration and bone equivalent. The performance of the EED denoising technique was further compared to the performance of median filtering. EED improves significantly the quality of weighted images.

Background: We reviewed our experience to determine the effect of epidural versus intravenous analgesia on postoperative pulmonary function and pain control in patients with chronic obstructive pulmonary disease (COPD) undergoing open surgery for abdominal aortic aneurysm. Methods: A retrospective study with prospective collection of data of 30 COPD patients undergoing open abdominal aortic aneurysm repair, during a 5-year period. Group I (n = 16) was operated under combined general and epidural anesthesia and epidural analgesia; group II (n = 14), under general anesthesia and intravenous analgesia. All patients performed pulmonary function tests (PFTs) preoperatively and during postoperative days 1 and 4. Pain assessment was performed on all patients during rest and activity on postoperative days 1, 2, and 4 by using the visual analog scale. Data were recorded for PFTs, postoperative pain, length of hospital stay, length of ICU stay, and postoperative pulmonary morbidity, including atelectasis and pulmonary infections. Results: There was no in-hospital mortality. Hospital stay was similar between the two groups (group I: 7.1 ± 1.0, group II: 7.5 ± 1.1). Group I patients showed significantly increased postoperative PFT values compared with group II patients at all time points (postoperative day 1: FEV1(%): 32.3 ± 4.4 vs. 27.1 ± 1.6, p = 0.007, FVC(%): 35.4 ± 8,5 vs. 28.3 ± 2.3, p = 0.035; postoperative day 4: FEV1(%): 50.4 ± 6.8 vs. 41.9 ± 6.8, p = 0.017, FVC(%): 51.3 ± 8.3 vs. 43.0 ± 7.9, p = 0.046). However, postoperative clinical pulmonary morbidity was not different between groups. Group I patients showed significantly reduced postoperative pain at all time points compared with group II patients. These differences were more pronounced during postoperative days 1 and 2, both at rest (visual analog score: 1.1 ± 0.9 vs. 2.6 ± 1.6, p = 0.02 and 0.7 ± 0.8 vs. 1.9 ± 1.1, p = 0.021, respectively) and during activity (2.3 ± 0.8 vs. 4.0 ± 1.7, p = 0.013 and 1.6 ± 0.7 vs. 2.8 ± 1.2, p = 0.019, respectively). Conclusions: Epidural anesthesia and postoperative epidural analgesia improve the postoperative respiratory function, compared with general anesthesia and systemic analgesia, and reduce postoperative pain as well, in COPD patients undergoing elective infrarenal abdominal aortic aneurysm repair. © 2011 Annals of Vascular Surgery Inc.

A part of current research has intensively been focused on the proliferation and metabolic processes governing biological systems. Since the advent of high throughput methodologies such as microarrays, the load of genomic data has increased geometrically and along with that the need for computational methods to interpret these data. In the present study, we investigated in vitro the common proliferation and metabolic processes, associated with common oncogenic pathways, as far as gene expression is concerned, between the T-cell acute lymphoblastic leukemia (CCRF-CEM) and the rhabdomyosarcoma (TE-671) cell lines. We present a computational approach, using cDNA microarrays, in order to identify commonalities between diverse biological systems. Our analysis predicted that JAK1, STAT1, PIAS2 and CDK4 are the driving forces in the two cell lines. This type of analysis may lead to the understanding of the common mechanisms that transform physiological cells to malignant, and may reveal a new holistic approach to understanding the dynamics of tumor onset as well as the mechanistics behind oncogenic drivers.

Blood pressure within prehypertensive levels confers higher cardiovascular risk. As prehypertension is also an intermediate stage for full hypertension, a precocious intervention with lifestyle changes or drugs is therefore appealing. Endothelial injury and dysfunction are thought to contribute to cardiovascular risk in prehypertension. Endothelial progenitor cell impairment has been linked to endothelial dysfunction, atherosclerotic disease progression and cardiovascular events. A potential mechanism contributing to the heightened cardiovascular risk in prehypertension may be linked to abnormalities in endothelial progenitor cell number and/or function. Aim of this review is to be up to date about the recent work on the correlation between endothelial progenitor cells and prehypertension and the possible prevention, treatment, and control of this pathology. The effect of an approach based on dietary intervention on both blood pressure and endothelial progenitor cells will be also shown. © 2011 Bentham Science Publishers.

P>A significant proportion of men with erectile dysfunction (ED) exhibit early signs of coronary artery disease (CAD), and this group may develop more severe CAD than men without ED (Level 1, Grade A). The time interval among the onset of ED symptoms and the occurrence of CAD symptoms and cardiovascular events is estimated at 2-3 years and 3-5 years respectively; this interval allows for risk factor reduction (Level 2, Grade B). ED is associated with increased all-cause mortality primarily due to increased cardiovascular mortality (Level 1, Grade A). All men with ED should undergo a thorough medical assessment, including testosterone, fasting lipids, fasting glucose and blood pressure measurement. Following assessment, patients should be stratified according to the risk of future cardiovascular events. Those at high risk of cardiovascular disease should be evaluated by stress testing with selective use of computed tomography (CT) or coronary angiography (Level 1, Grade A). Improvement in cardiovascular risk factors such as weight loss and increased physical activity has been reported to improve erectile function (Level 1, Grade A). In men with ED, hypertension, diabetes and hyperlipidaemia should be treated aggressively, bearing in mind the potential side effects (Level 1, Grade A). Management of ED is secondary to stabilising cardiovascular function, and controlling cardiovascular symptoms and exercise tolerance should be established prior to initiation of ED therapy (Level 1, Grade A). Clinical evidence supports the use of phosphodiesterase 5 (PDE5) inhibitors as first-line therapy in men with CAD and comorbid ED and those with diabetes and ED (Level 1, Grade A). Total testosterone and selectively free testosterone levels should be measured in all men with ED in accordance with contemporary guidelines and particularly in those who fail to respond to PDE5 inhibitors or have a chronic illness associated with low testosterone (Level 1, Grade A). Testosterone replacement therapy may lead to symptomatic improvement (improved wellbeing) and enhance the effectiveness of PDE5 inhibitors (Level 1, Grade A). Review of cardiovascular status and response to ED therapy should be performed at regular intervals (Level 1, Grade A).