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Imperial Chemical Industries

About: Imperial Chemical Industries is a based out in . It is known for research contribution in the topics: Alkyl & Catalysis. The organization has 8189 authors who have published 7809 publications receiving 190252 citations. The organization is also known as: Imperial Chemical Industries Ltd.
Topics: Alkyl, Catalysis, Alkoxy group, Polymer, Coating


Papers
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Journal ArticleDOI
TL;DR: In this article, it has been shown that in dry ammonium nitrate, transformations between forms V, IV, II and I only take place in the presence of moisture and the mechanism appears to be one of dissolution and recrystallization.
Abstract: The thermal transformations which take place in solid ammonium nitrate have been studied with the following techniques: differential thermal analysis, measurement of d.c. electrical conductance, optical microscopy, X-ray diffraction and nuclear magnetic resonance. It has been found that in dry ammonium nitrate, transformations between forms V, IV, II and I only take place and that the transformations appear to be of the order-disorder type. The transformations IV ⇌ III only take place in the presence of moisture and the mechanism appears to be one of dissolution and recrystallization.

71 citations

Journal ArticleDOI
TL;DR: The concept that the formation of mixed disulphides of protein and glutathione is a mechanism for maintaining NADPH levels despite the 'redox' stress caused by the cyclical and NADPH dependent reduction and reoxidation of paraquat is supported.

71 citations

Journal ArticleDOI
TL;DR: The data suggest that any increase in radical production in the livers of rats exposed to peroxisome proliferators is not large enough to give rise to a biologically significant degree of DNA damage and that the mechanism whereby such chemicals produce liver tumours in certain rodent species may be one other than simply DNA damage due to increased production of radical species.
Abstract: This study was undertaken to investigate the hypothesis linking peroxisome proliferation with the production of reactive oxygen species and subsequent DNA damage. Hepatic peroxisomal proliferation was induced in male Wistar-derived rats by the administration of clofibrate, methyl clofenapate, di(2-ethylhexyl)phthalate, or its metabolite mono (2-ethylhexyl)phthalate (MEHP) for periods of up to 28 days. Genotoxicity was monitored using an alkaline elution technique to assay for DNA strandbreaks and cytotoxicity was monitored by measuring lipid peroxidation. Both parameters might be expected to be elevated if peroxisome proliferation is accompanied by an elevated level of oxygen free radicals within the cell. Enzyme measurements made on the livers of the treated rats showed that peroxisomal palmitoyl CoA oxidase activity was markedly increased over control whereas peroxisomal catalase activity was not. In addition, both the cytosolic glutathione peroxidase and superoxide dismutase activities were found to be lowered in the treated animals by up to 50 and 20% respectively. Despite such changes in enzyme activity, no evidence for increases in DNA strandbreaks or lipid peroxidation was obtained with any of the chemicals at any of the time points examined. DNA strandbreaks were also assayed on hepatocytes treated in culture with MEHP (0.5 mM) for 3 days and then exposed to inhibitors of DNA repair for 2 h immediately before assay. Again, no significant increase over controls was observed. Our data suggest that any increase in radical production in the livers of rats exposed to peroxisome proliferators is not large enough to give rise to a biologically significant degree of DNA damage and that the mechanism whereby such chemicals produce liver tumours in certain rodent species may be one other than simply DNA damage due to increased production of radical species.

70 citations

Journal ArticleDOI
TL;DR: Mutants, showing either constitutive (depressed) or non-inducible expression of chromosomally-mediated Type I beta-lactamase were obtained from clinical isolates of Enterobacter cloacae, Ent.
Abstract: Mutants, showing either constitutive (depressed) or non-inducible expression of chromosomally-mediated Type I beta-lactamase were obtained from clinical isolates of Enterobacter cloacae, Ent. aerogenes, Citrobacter freundii, Providencia stuartii, Morganella morganii, Serratia marcescens and Pseudomonas aeruginosa. The wild-type and mutant strains were compared for susceptibility to a range of beta-lactam antibiotics. Derepression of beta-lactamase synthesis generally, but not always, resulted in a marked reduction in susceptibility to the agents tested, including the '3rd generation' cephalosporins. In many cases, the observed resistance would preclude, or severely compromise, the therapeutic efficacy of the drugs. In this context, depressed mutants of Enterobacter spp., Citro. freundii and Ps. aeruginosa could be of primary concern although those of Ser. marcescens, Prov. stuartii and Morg. morganii often exhibited equally high resistance levels to older beta-lactams. Comparison of the susceptibilities of the non-inducible mutants with that of their inducible parents suggested variation in the beta-lactamase inductive potency of different compounds in different organisms. For example, cefoxitin was a powerful inducer in Ent. cloacae, Citro. freundii and one strain of Ps. aeruginosa; similarly cefazolin and cefuroxime were good beta-lactamase inducers in Ser. marcescens and Morg. morganii. Aminothiazolyl-oxime cephalosporins and ureido-penicillins were generally poor inducers. From such comparisons, the contribution of inducible Type I beta-lactamase to resistance phenotype could be ascertained.

70 citations

Patent
02 Feb 1995
TL;DR: In this paper, an internal mold release system consisting of a polysiloxane compound and an amine salt of a carboxylic acid was provided. But this system was not suitable for the use of polysilicon compounds.
Abstract: An internal mold release system is provided which comprises: a) a polysiloxane compound; and b) an amine salt of a carboxylic acid.

70 citations


Authors

Showing all 8189 results

NameH-indexPapersCitations
Richard A. Dixon12660371424
Donald Mackay10346835105
Graham J. Hutchings9799544270
George E. P. Box94276131808
Ian Kimber9162028629
Ian D. Wilson8059433379
Paul D. Beer7654427398
Philip J. White7531426523
Vernon C. Gibson7134022163
A. Keller6230414920
Michael Bowker6230412119
Brian Vincent5922813366
Brian P. Griffin5637314337
Manfred Bochmann5633112573
Diana Anderson5432316177
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20151
20131
20122
201149
201011
200913