Stand-off nuclear reactor monitoring with neutron detectors for safeguards and non-proliferation applications.

Safeguards measures are employed at nuclear reactor facilities worldwide, to ensure that nuclear material is not diverted from peaceful uses. Typical safeguards measures involve periodic inspections, off-line verification and video surveillance of fuel cycle activities. Real-time verification of the fissile contents via stand-off monitoring can enhance continuity of knowledge for non-traditional reactor types, including research reactors and small modular reactors. Here we demonstrate the feasibility of using large-area neutron detectors for monitoring nuclear reactors at stand-off distances up to 100 m outside reactor shielding, as a potential reactor safeguards tool. Since the neutron yield per unit reactor power depends upon the isotopic composition of the reactor core, declared changes in fissile composition can be verified without accessing the core. The supporting results of experiments conducted at the National Research Universal reactor in Canada, are presented.

The course of the radial nerve in the distal humerus: A novel, anatomy based, radiographic assessment.

METHODS AND FINDINGS: Measurements were done on both arms of ten specially embalmed specimens. Arms were dissected and radiopaque wires attached to the radial nerve in the distal part of the upper arm. Digital radiographs were obtained to determine the course of the radial nerve in the distal 20 cm of the humerus in relation to bony landmarks; medial epicondyle and capitellum-trochlea projection (CCT). Analysis was done with ImageJ and Microsoft Excel software. We also compared humeral nail specifications from different companies with the course of the radial nerve to predict possible radial nerve damage. RESULTS: The distance from the medial epicondyle to point where the radial nerve bends from posterior to lateral was 142 mm on AP radiographs and 152 mm measured on the lateral radiographs. The average distance from the medial epicondyle to point where the radial nerve bends from lateral to anterior on AP radiographs was 66 mm. On the lateral radiographs where the nerve moves away from the anterior cortex 83 mm to the center of capitellum and trochlea (CCT). The distance from the bifurcation of the radial nerve into the posterior interosseous nerve (PIN) and superficial radial nerve was 21 mm on AP radiographs and 42 mm on the lateral radiographs (CCT). CONCLUSIONS: The course of the radial nerve in the distal part of the upper arm has great variety. Lateral fixation is relatively safe in a zone between the center of capitellum-trochlea and 48 mm proximal to this point. The danger zone in lateral fixation is in-between 48-122 mm proximal from CCT. In anteroposterior direction; distal fixation is dangerous between 21-101 mm measured from the medial epicondyle. The more distal, the more medial the nerve courses making it more valuable to iatrogenic damage. The IMN we compared with our data all show potential risk in case of (blind) distal locking, especially from lateral to medial direction.

CTP:phosphocholine cytidylyltransferase activation by oxidized phosphatidylcholines correlates with a decrease in lipid order: a 2H NMR analysis.

The enzyme CTP:phosphocholine cytidylyltransferase (CT) binds reversibly to membranes and is active only in its membrane-bound form. Membrane lipid composition influences the equilibrium between its soluble and membrane-bound forms. Whereas the enzyme is not activated by phosphatidylcholine (PC) vesicles, it is activated by PC vesicles that have been oxidized with HClO(4) [Drobnies, A. E., et al. (1998) Biochim. Biophys. Acta 1393, 90-98]. Here we explore the mechanism of activation of CT by a PC oxidized with lipoxidase. Multilamellar vesicles (MLVs) containing > or =5 mol % oxidized 1-palmitoyl-2-arachidonoylPC (PAPC) progressively activated the enzyme, which was fully activated by 25 mol % oxidized PC. The effect of oxidized PAPC on lipid order was investigated by (2)H NMR, using MLVs containing PAPC perdeuterated on the palmitoyl chain. Spectral depaking generated order parameter profiles along the sn-1 chain. The average order parameter (S(CD)) in the plateau region at 37 degrees C decreased from 0.18 to 0.15 with increasing percent of oxidized PAPC (0-25%). The change in S(CD) was even greater near the end of the palmitoyl chain. CT activation was inversely related to lipid order. The major component of the lipoxidase-oxidized PAPC was purified and characterized by mass spectrometry and NMR. This component, 1-palmitoyl-2-(11,15-dihydroxy)eicosatrienoylPC (dihydroxyPAPC), incorporated into PAPC MLVs, also stimulated CT activity and reduced the lipid order parameter. Both effects were reversed by egg sphingomyelin. We propose that CT activation by oxidized PAPC is mediated by effects on lipid packing perturbations. This is the first study to report the effects of a purified oxidized PC on the orientational order along the acyl chain and to correlate the lipid disordering of the oxidized PC with the activation of a membrane-associated regulatory enzyme.

Familial defective apolipoprotein B-100 is clinically indistinguishable from familial hypercholesterolemia.

BACKGROUND: Familial defective apolipoprotein B-100 is caused by a substitution of adenine for guanine in exon 26 of the gene coding for apolipoprotein B, which results in the substitution of glutamine for arginine in the putative low-density lipoprotein-receptor binding domain of the mature protein. This amino acid substitution diminishes the binding capacity of the low-density lipoprotein particle for the low-density lipoprotein receptor, which in turn leads to an increase in levels of plasma total and low-density lipoprotein cholesterol. METHODS: To identify carriers of this mutation by means of molecular biology techniques in a large cohort of Dutch patients living in the Netherlands and in Canada with primary hypercholesterolemia, to establish the frequency of the disorder, and to investigate its clinical signs and symptoms and the response to cholesterol-lowering therapy. RESULTS: A total of 1248 patients were screened, and the mutation was found in 18 patients who were initially all diagnosed as having familial hypercholesterolemia. Ten of 18 patients had tendon xanthomas or an arcus cornealis or both, and eight of 18 patients had angina or other evidence of coronary artery disease. CONCLUSIONS: The disorder was clinically indistinguishable from familial hypercholesterolemia in terms of physical characteristics and lipoprotein measures. Response to lipid-lowering therapy with beta-hydroxy-beta-methylglutaryl coenzyme A reductase inhibitors was similar to that reported in patients with familial hypercholesterolemia. The mutation was associated with a similar haplotype, which was also reported in other patients of Western European descent with familial defective apolipoprotein B100. This strongly suggests that the mutation has a common chromosomal background that originated in Western Europe.