A neutronradiography facility based on an experimental reactor

A thermal Neutron Radiography (NR) facility based on the use of thermal neutron flux, generated by the PULSTAR experimental reactor, has been designed and simulated using the MCNPX code. The key objective of the proposed facility is to deliver thermal neutron flux in this range for variable values of L/D ratio, instantaneously with acceptable values for all NR parameters. Thus, with suitable aperture and collimators designs, optimization for the parameters for thermal NR was achieved, for a wide range of the collimator ratio. The short time requirements for obtaining the radiography images justify the use of the proposed system for ‘real time radiography’. The system was designed under the limitation that the total Dose Equivalent Rate does not exceed at the external shield surface the limit recommended by ICRP-26.JRC.F.4-Innovative Technologies for Nuclear Reactor Safet

Increases of Corporal Temperature as a Risk Factor of Atherosclerotic Plaque Instability

This work explores for the first time the effects of temperature increments on the development of high shear stresses between plaque and arterial wall due to their different dilatational properties. Data from the literature report febrile reactions prior to myocardial infarction in patients with normal coronary arteries and that coronary syndromes seem to be triggered by bacterial and viral infections, being fever the common symptom. Methods The thermo-mechanical behavior of thoracic aortas of New Zealand White rabbits with different degrees of atherosclerosis was measured by means of pressure–diameter tests at different temperatures. In addition, specific measurements of the thermal dilatation coefficient of atheroma plaques and of healthy arterial walls were performed by means of tensile tests at different temperatures. Results Results show a different thermo-mechanical behavior, the dilatation coefficient of atheroma plaque being at least twice that of the arterial wall. The calculation of temperature-induced mechanical stress at the plaque–vessel interface yielded shear stress levels enough to promote plaque rupture. Conclusions Increases of corporal temperature either local—produced by the inflammatory processes associated with atherosclerosis—or systemic—by febrile reactions—can play a role in increasing the risk of acute coronary syndromes, and they deserve a more comprehensive study

11β-hydroxysteroid dehydrogenase type 2 deficiency accelerates atherogenesis and causes proinflammatory changes in the endothelium in apoe^-/- mice

Mineralocorticoid receptor (MR) activation is pro inflammatory and pro atherogenic. Antagonism of MR improves survival in humans with congestive heart failure caused by atherosclerotic disease. In animal models, activation of MR exacerbates atherosclerosis. The enzyme 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) prevents inappropriate activation of the mineralocorticoid receptor (MR) from inappropriate activation by glucocorticoids by inactivating glucocorticoids in mineralocorticoid-target tissues. To determine whether glucocorticoid-mediated activation of MR increases atheromatous plaque formation we generated Apoe(−/−)/11β-HSD2(−/−) double-knockout (E/b2) mice. On chow diet, E/b2 mice developed atherosclerotic lesions by 3 months of age, while Apoe(−/−) mice remained lesion-free. Brachiocephalic plaques in 3 month-old E/b2 mice showed increased macrophage and lipid content and reduced collagen content compared to similar sized brachiocephalic plaques in 6 month old Apoe(−/−) mice. Crucially, treatment of E/b2 mice with eplerenone, an MR antagonist, reduced plaque development and macrophage infiltration while increasing collagen and smooth muscle cell content without any effect on systolic blood pressure (SBP). In contrast, reduction of SBP in E/b2 mice using the epithelial sodium channel (ENaC) blocker amiloride produced a less profound atheroprotective effect. Vascular cell adhesion molecule 1 (VCAM-1) expression was increased in the endothelium of E/b2 mice compared to Apoe(−/−) mice. Similarly, aldosterone increased VCAM-1 expression in mouse aortic endothelial cells, an effect mimicked by corticosterone only in the presence of an 11β-HSD2 inhibitor. Thus, loss of 11β-HSD2 leads to striking atherogenesis associated with activation of MR stimulating pro-inflammatory processes in the endothelium of E/b2 mice