Search PubMed⌕ Search

Biomedical subjects

B Sedgwick

Publications and source records attributed to B Sedgwick.

42 records · Page 3Linked to original sources
PubMedDate not supplied

Widespread adaptive response against environmental methylating agents in microorganisms.

Many bacterial species have adaptive responses which protect against the toxicity and mutagenicity of methylating agents. Induced 3-methyladenine-DNA glycosylase and O6-methylguanine-DNA methyltransferase activities increase the cellular capacity of E. coli, B. subtilis, and M. luteus to repair toxic and mutagenic methylated base derivatives in DNA. The DNA methyltransferase or Ada protein of E. coli regulates the response and is converted into a strong transcriptional activator by self-methylation on repair of a methylphosphotriester in DNA. The multiple functions of the E. coli Ada protein (39 kDa) are split between two proteins, AdaA (24 kDa) and AdaB (20 kDa), in B. subtilis. Proteins (39 kDa) recognised by anti-Ada antibodies are efficiently induced in several enterobacterial species and correlate with increased DNA methyltransferase activities. In contrast, an "Ada-related" protein is only weakly induced in Salmonella typhimurium and no increase in DNA repair activity is detectable. The existence of adaptive responses in diverged bacterial species suggests the frequent occurrence of methylating agents in the environment. Several direct-acting methylating agents which are known to arise in the environment have been shown to induce the response. These include abundantly occurring methyl chloride, the antibiotic streptozotocin, the precursors of the known labile inducers N-methyl-N'-nitrosourea and N-methyl-N'-nitro-N-nitrosoguanidine and as shown in this paper, methyl radicals which may arise by the irradiation or oxidation of methyl compounds.

Adaptation, Physiological↗
PubMedDate not supplied

Detection of ritalinic acid in urine by thin-layer chromatography and gas chromatography.

A new method for the analysis of ritalinic acid, the major metabolite of methylphenidate in urine, is described. The procedure involves solid-phase extraction of ritalinic acid from urine using C-18 reverse phase columns. The ritalinic acid is methylated to form methylphenidate which, together with an internal standard, is then extracted into chloroform and analyzed by gas chromatography using a flame ionization detector. This procedure gives essentially quantitative recovery of ritalinic acid from 10 mL urine and is linear in the range of 0 to 10 micrograms/mL. A positive analysis for ritalinic acid is confirmed by thin-layer chromatography. Detection sensitivities of greater than or equal to 1 micrograms/mL urine were observed for both procedures.

Chromatography, Gas↗