Chalk River Laboratories

About: Chalk River Laboratories is a based out in . It is known for research contribution in the topics: Neutron diffraction & Neutron scattering. The organization has 2297 authors who have published 2700 publications receiving 73287 citations.

Concentration-independent spontaneously forming biomimetric vesicles.

Abstract: In this Letter we present small-angle neutron scattering data from a biomimetic system composed of the phospholipids dimyristoyl and dihexanoyl phosphorylcholine (DMPC and DHPC, respectively) Doping DMPC-DHPC multilamellar vesicles with either the negatively charged lipid dimyristoyl phosphorylglycerol (DMPG, net charge -1) or the divalent cation, calcium (Ca 2 + ), leads to the spontaneous formation of energetically stabilized monodisperse unilamellar vesicles whose radii are concentration independent and in contrast with previous experimental observations

A Mechanistic Study on Lead-Induced Passivity-Degradation of Nickel-Based Alloy

Abstract: The mechanism of lead-induced passivity-degradation in a nickel-based alloy (UNS N06690) was explored in a simulated stream generator alkaline crevice chemistry. The pitting induction test indicated that the detrimental impact of lead contamination on pitting resistance was significantly enhanced by the presence of calcium ions. An X-ray photoelectron spectroscopy analysis revealed the incorporation of lead into the passive film. Calcium ions in the alkaline chemistry entered the passive films with the aid of the lead species but the ingress of calcium did not occur in the solution free of lead contamination. The incorporation of lead reduced chromium and iron content in passive films and hindered the dehydration processes during the passivation. Mott-Schottky and photoelectrochemical measurements showed that passive films on the nickel-based alloy are p-type semiconductors and the incorporation of lead may reduce the acceptors in the passive films. A further analysis suggested that the lead-induced passivity degradation of nickel-based alloys may be related to the increases in M-O and M-OH 2 bonds, the electronic structural changes of spinel oxides in the passive film, and reduced ion-selectivity due to the surface adsorption of the lead species.

Modulation of radiation-induced strand break repair by cisplatin in mammalian cells.

Abstract: PURPOSE: To investigate the repair of ionizing radiation-induced DNA lesions in human skin fibroblasts in the presence of cisplatin-DNA adducts and to determine the persistence of DNA repair inhibition by cisplatin. MATERIALS AND METHODS: Normal human fibroblasts (AG 1522) treated with cisplatin were exposed to 4 Gy 60Co gamma-radiation and assayed for repair of radiation-induced damage under growth-permissive conditions. DNA damage was measured by the fluorescence analysis of DNA unwinding (FADU) and cytokinesis-blocked micronucleus assays. RESULTS: Rejoining of strand breaks caused by 4 Gy radiation in cells without cisplatin pre-treatment appeared to be biphasic with an initial fast component (up to 15 min of repair time) followed by a slower component, and was completed by 90 min. Cisplatin treatment (10 microg/ml, 30 min) immediately before irradiation had no effect on the fast rejoining component, but inhibited the slow component (p<0.01). The same cisplatin treatment 24 h prior to irradiation inhibited both slow and fast components (p<0.01). In contrast, decreasing the cisplatin exposure to 1.0 microg/ml for 30 min, 24h prior to irradiation, resulted in an increased amount of strand break repair at each time point measured compared with irradiated control cells. This mild cisplatin treatment (95% survival) also resulted in a reduction of radiation-generated micronuclei indicating an adaptive response. CONCLUSIONS: Cisplatin used in combination with ionizing radiation can produce differential cellular responses depending upon the severity of the cisplatin treatment and the time interval between cisplatin and radiation exposures.