Influence of point defects and impurities on the dynamical stability of δ-plutonium.

We use first-principles calculations to provide direct evidence of the effect of aluminum, gallium, iron and uranium on the dynamical stability of δ-plutonium. We first show that the δ phase is dynamically unstable at low temperature, as seen in experiments, and that this stability directly depends on the plutonium 5f orbital occupancies. Then, we demonstrate that both aluminum and gallium stabilize the δ phase, contrary to iron. As for uranium, which is created during self-irradiation and whose effect on plutonium has yet to be understood, we show that it leaves a few unstable vibrational modes and that higher concentrations lead to an almost complete stabilization. Finally, we provide an attempt at a consistent analysis of the experimental Pu-Ga phonon density of states. We show that the presence of gallium can reproduce only partially the experimental measurements, and we investigate how point defects, such as interstitials and vacancies, affect the calculated phonon density of states.

NFkappaB and AP-1 DNA binding activity in patients with multiple sclerosis.

Current evidence suggests that multiple sclerosis (MS) results from an autoimmune response mediated by T lymphocytes, which would be activated in the peripheral blood and migrate into the central nervous system. NFkappaB and AP-1 are two main transcription factors involved in T-cell activation. To investigate possible alterations in the activity of these factors in MS individuals, we have assayed NFkappaB and AP-1 DNA binding activity in peripheral blood mononuclear cells (PBMC). Binding activity was analyzed by gel mobility shift assay in MS patients compared with controls. No significant differences were found between the two groups, indicating no evidence of abnormalities associated with MS in NFkappaB or AP-1 binding activities in PBMC, both basally and after PMA+anti-CD3 antibody induction.

Advances in first-principles modelling of point defects in UO2: f electron correlations and the issue of local energy minima.

Over the last decade, a significant amount of work has been devoted to point defect behaviour in UO2 using approximations beyond density functional theory (DFT), in particular DFT + U and hybrid functionals for correlated electrons. We review the results of these studies from calculations of bulk UO2 properties to the more recent determination of activation energies for self-diffusion in UO2, as well as a comparison with their experimental counterparts. We also discuss the efficiency of the three known methods developed to circumvent the presence of metastable states, namely occupation matrix control, U-ramping and quasi-annealing.

NF-kappaB in Th2 cells: delayed and long-lasting induction through the TCR complex.

Nucelar NFkappaB was analyzed in murine Th2 cells after stimulation via the TCR pathway. Signals delivered through the TCR/CD3 complex induced active NFkappaB translocation to the nucleus of Th2 cells after a late phase (24 h) of the activation process, which is in contrast to the rapid appearance of nuclear NFkappaB (3 h) in Th1 cells after the same stimulation. The slow kinetic of NFkappaB nuclear uptake in Th2 cells was not accelerated by CD28 triggering or under stimulation with antigen plus antigen-presenting cells. Th1 and Th2 cells were also different in the composition of NFkappaB complexes induced. Whereas in Th1 cells TCR triggering induced the presence of nuclear p50.p65 heterodimers, in Th2 cells the complexes induced were shown to be composed of p65 plus another NFkappaB protein distinct from p50. The delayed NFkappaB induction in Th2 cells was dependent on protein synthesis and the significance of this is discussed.

Physiology and biochemistry of endothelial function in children with chronic renal failure.

Premature atherosclerosis is a major cause of morbidity and mortality in chronic renal failure (CRF). Endothelial dysfunction is a key early event in atherogenesis. The aim of this study was to assess the effect of CRF on endothelial function using physiological and biochemical measures. To focus on the effect of CRF itself, 23 children (matched with 23 controls for age and vessel diameter) were selected because they were normotensive, had normal total cholesterol (TC) levels, and were not on vasoactive drugs. Their mean (range) age was 12.0 (7.8 to 17.0) years; GFR 17.5 (8.8 to 34.5) ml/min/1.73 m2. The physiology of endothelial function in the brachial artery was assessed using high resolution ultrasound by measuring its diameter at rest, during reactive hyperemia (endothelium dependent dilation) and after sublingual glyceryl trinitrate (GTN; endothelium independent dilation). Nitric oxide (NO) metabolites and endogenous NO synthetase (eNOS) inhibitors were measured as an assessment of endothelial metabolism. Brachial artery dilation to flow [FMD, mean (SEM)%] was reduced in CRF to 4.9 (0.6) and controls 8.6 (0.6), P < 0.0001. In contrast, the response to GTN was similar in both groups: CRF 25.1 (1.6), controls 23.3 (1.2), P = 0.31. There was no difference in TC, low density lipoprotein (LDL) or high density lipoprotein (HDL) between the patients and the controls. Triglycerides (TG) were higher in the patients but within the normal range. Antibodies against oxidized LDL (ox-LDL) were high in CRF. Endogenous NOS inhibitors were high in CRF, and intermediate NO metabolites were low. There was no correlation between FMD of the brachial artery and lipid subfractions, or with NO metabolites or eNOS inhibitors. Endothelium dependent dilation of the brachial artery is impaired in children with CRF who do not have co-existing risk factors for atherosclerosis. This may represent early evidence of atherogenic vascular disease.