A note on the characterization of an estuarine microbial community enriched with the herbicide Fenuron

M inney , S.F., P arkes , R.J. & B ull , A.T. 1985. A note on the characterization of an estuarine microbial community enriched with the herbicide Fenuron. Journal of Applied Bacteriology 59 , 17—22.
A stable, five-membered estuarine microbial community was enriched in the presence of 1,1 dimethyl-3-phenylurea (Fenuron), phenylurea and aniline. At a dilution rate of 0μD01/h in the chemostat, partial aniline utilization occurred and the rate increased with dilution rate. At the higher dilution rates the phenylurea component was also utilized. At a dilution rate of mD015/h in a fluidized bed system, complete removal of both aniline and phenylurea occurred. There was no evidence of Fenuron degradation under any of the conditions examined. The importance of the use of heterogeneous culture conditions in the laboratory is discussed.     

Repair inhibition of potential mutations of ultraviolet-irradiatedEscherichia coli by chloroquine and quinacrine

The frequency of ultraviolet(UV)-induced mutations drops rapidly whenEscherichia coli Hcr⁺ cells (strains WP-2 Hcr⁺; B/r) are incubated on phosphate-buffered agar (PBA), but is reduced only slightly if chloroquine or quinacrine are incorporated into the medium. The excision-deficient WP-2 Hcr^– strain shows little reduction in the number of mutants when incubated on PBA. During postirradiation incubation on PBA, cell viability was relatively unaffected by the presence of the chemicals in the PBA (25 g/ml quinacrine; 50 g/ml chloroquine). When cells were given optimal doses of photoreactivating light, no further decline in mutations was obtained during subsequent incubation on PBA. Approximately 64% of the mutants seen when cells are treated with UV-PBA-chloroquine and 90% seen with UV-PBA-quinacrine can be repaired if cells are incubated on PBA. When these chemicals were added to the PBA, both excision-proficient strains (WP-2 Hcr⁺; B/r) demonstrated a marked reduction in the repair of UV-induced mutations to streptomycin resistance. Our results indicate that these chemicals interfere with the excision of UV-induced pyrimidine dimers, a process that normally occurs during postirradiation incubation on PBA.     

Differentiation properties of pure populations of human dystrophic muscle cells

The interpretation of the majority of studies of Duchenne muscular dystrophy (DMD) has been complicated by the heterogeneous composition of the cultures used. In addition to muscle cells, muscle tissue contains adipocytes and fibroblasts and the proportion of these cell types varies, especially in disease states. To overcome this problem we developed culture conditions which permitted isolation and characterization of pure populations of clonally derived human muscle cells [1, 2]. Here we report the successful application of these methods to muscle cells from biopsies of individuals with diagnosed DMD. The normal and mutant human muscle cells were used in experiments of muscle differentiation in the same manner as cell lines. Frozen-stored cells were thawed, plated in a series of replicate plates, and allowed to differentiate under similar culture conditions. Yet, in contrast with cell lines, the cells were karyotypically normal, not altered by adaptation to long-term culture, and had a finite lifespan. We have systematically analysed specific properties of the normal and DMD muscle cells which differentiated in culture. The kinetics and extent of myoblast fusion, myotube morphology, and the accumulation and distribution of membrane acetylcholine receptors were monitored. In addition, the isozyme composition of creatine kinase and its intracellular and extracellular distribution were determined. Our results indicate that DMD muscle cells are fully capable of initiating myogenesis in culture and do not differ from normal muscle in several important parameters of differentiation.     

Studies on the lipid composition of the rat liver endoplasmic reticulum after induction with phenobarbitone and 20-methylcholanthrene

1. The cholesterol content, proportions of different phospholipids and fatty acid components of phosphatidylcholine and phosphatidylethanolamine were studied in rat liver endoplasmic-reticulum membrane, after a single injection of 20-methylcholanthrene or injections of phenobarbitone for 5 days. 2. A marked decrease in the proportion of cholesterol occurred 5 days after injection of 20-methylcholanthrene or phenobarbitone. 3. The proportion of phosphatidylcholine was increased by injection of phenobarbitone and minor changes occurred in other phospholipids. 4. Phenobarbitone caused the proportion of linoleic acid in phosphatidylcholine and phosphatidylethanolamine to increase to 120-125% of the control and the proportion of oleic acid, arachidonic acid and docosahexaenoic acid to decrease. 5. 20-Methylcholanthrene caused an increase in the proportion of oleic acid in phosphatidylcholine and ethanolamine to 125-140% of the control, 1 day after injection. 6. The increased proportion of linoleic acid in phosphatidylcholine after phenobarbitone injection occurs simultaneously with the increase of cytochrome P-450 concentration, the rate of oxidative demethylation of aminopyrine and the rate of hydroxylation of biphenyl. It is therefore considered that distinct species of phosphatidylcholine or phosphatidylethanolamine containing linoleic acid in the beta position are essential in the endoplasmic-reticulum membrane for optimal activity of oxidative demethylation.     

The efficacy of biobehavioral and compliance interventions in the adjunctive treatment of mild pregnancy-induced hypertension

This investigation assessed the efficacy of a biobehavioral intervention in the adjunctive treatment of mild pregnancy-induced hypertension (PIH), a potentially serious complication of pregnancy in which normotensive women develop hypertension, proteinuria, and edema of unknown etiology late in gestation. Forty-five women with symptoms of PIH were randomly assigned to one of three treatment conditions: bed rest alone (the most common obstetrical treatment), bed rest with individualized compliance enhancement training, or a four-session biobehavioral treatment consisting of bed rest, compliance enhancement training, and individualized thermal biofeedback-assisted relaxation training. Results indicated that while blood pressure for the bed rest and compliance enhancement groups continued to rise and pose an increasing health risk to maternal and fetal well-being, subjects in the biobehavioral group maintained their blood pressure at a significantly lower, and presumably safer, level. The biobehavioral treatment is hypothesized to affect blood pressure levels in subjects with mild PIH through the mediation of the sympathetic nervous system, decreasing peripheral vascular resistance and cardiac output. The results of this investigation suggest that the biobehavioral intervention may be an effective adjunct to bed rest in the treatment of mild PIH remote from term.     

A new major histocompatibility complex class I b gene expressed in the mouse blastocyst and placenta

 Because of the role major histocompatibility complex (MHC) class I b molecules may play during mouse embryonic development, we thought it would be interesting to search for additional MHC class I b molecules that might be expressed in preimplantation embryos, and in particular in the trophoblastic lineage. We therefore screened a mouse preimplantation blastocyst cDNA library for MHC class I sequences. This search led to the identification and characterization of a new MHC class I b gene, blastocyst MHC. Sequences identical to the exons and 3′ untranslated region of this gene have been found in many laboratory mouse strains, as well as in the related mouse species Mus spreciligus. The presence of this gene in mouse strains of different MHC class I haplotypes argues that blastocyst MHC is a unique, newly-described gene rather than a new allele of a previously described mouse MHC class I gene. Blastocyst MHC has the structure of an MHC class I b gene, with the six exons characteristic of T-region genes. It is linked to H2-D. The amino acid sequence encoded by this gene maintains all the features of a functional antigen-presentation domain. The blastocyst MHC gene, like the human class I b gene HLA-G, is expressed at the blastocyst stage and in the placenta, and may be the mouse analog for HLA-G. Received: 31 May 1996 / Revised: 19 August 1996