Wild-type Escherichia coli cells are sensitive to nitrofurazone (NF) and many other nitrofuran derivatives. A variety of evidence indicated that these compounds are converted to toxic "active" metabolites by reductases present in the bacteria. Sensitive E. coli K-12 acquired threefold-greater resistance to NF in one mutational step. These partially resistant mutants could undergo a second mutation that made them 10 times as resistant as the wild type. Mutation of wild-type strain K-12 to the higher level of resistance in a single step was not observed. The first mutational step was associated with partial loss of reduced nicotinamide adenine dinucleotide phosphate-linked, 02-insensitive NF reductase activity, and the second step was associated with loss of the remaining activity. The two-step mutants did, however, contain other NF reductases that were inhibited by 02 and reduced NF only under anaerobic conditions. We designated the genes that control reductase activity "nitrofuran sensitivity genes" (nfsA and nfsB). Thus, wild-type strains are nfsA+ nfsB+, and the resistant double mutants are nfsA nfsB. A variety of crosses established that these genes are both located close to gal, that the most probable sequence is lac nfsB gal nfsA, and that the singlestep mutants with an intermediate level of resistance are nfsA nfsB+. The nfsA+ nfsB strains contained about 70 to 80% of the wild-type reductase I activity-apparently enough to confer wild-type sensitivity. This reductase activity was resistant to 2 M urea. The nfsA nfsB+ strains had only 20 to 30% of the wild-type activity, and this residual activity was sensitive to 2 M urea. Bacbmann, Yale University, New Haven, Conn. The isolation and properties of resistant mutants are described in Table 1 and in Results. Media and culture condition. Bacteria were routinely cultured on nutrient agar (Oxoid, London, England) plates or in nutrient broth no. 2 (Oxoid) or Penassay broth (Difco Laboratories, Detroit, Mich.). Defined medium consisted of Davis-Mingioli medium

When Escherichia coli strain B/r is exposed to 10 to 20 ug of nitrofurazone per ml, mutants with roughly threefold resistance are obtained. Treatment of these mutants with higher concentrations of nitrofurazone yields strains with six-to sevenfold resistance over strain B/r. Each of these steps toward nitrofurazone resistance is accompanied by loss of soluble nitrofurazone reductase activity. When sensitive bacteria are exposed to labeled nitrofurazone or labeled 2-nitrofuran, a considerable amount of radioactivity becomes bound to the cold trichloroacetic acid-insoluble fraction. Very little activity becomes bound in the mutants with sixto seven-fold resistance; mutants with intermediate resistance show intermediate levels of binding. Partially purified nitrofurazone reductase preparations catalyze the conversion of nitrofurazone to compounds which bind to protein and are not removed by prolonged dialysis against 8 M urea or by cold acid. Nitrofurazone reduced by xanthine oxidase or electrolytically reduced also yields compounds which react with protein to form stable derivatives.

Monensin, at concentrations which depended on the multiplicity of infection, was found to prevent DNA replication of human cytomegalovirus (HCMV) as well as production of viral progeny in human foreskin fibroblasts. The drug did not affect DNA replication of herpes simplex virus. Inhibition of consecutive HCMV DNA synthesis was also observed following delayed addition of the drug within 12-24 hours postinfection, but was fully reversible upon its removal. Viral replication proceeded, however, without impairment in cultures treated with monensin prior to infection. Induction of viral DNA polymerase activity was not impeded by the inhibitor. Analysis of protein- and glycoprotein synthesis revealed that monensin interfered with the production of a number of HCMV-specific polypeptides. Furthermore, evidence was obtained that the drug may hinder intracellular transport of a 135 kd glycopolypeptide.

No abstract

Back pain and diseases of the spine are today a health disorder of outstanding epidemiological, medical, and health economic importance. The cost of care for patients with lumbosciatic complaints are steadily increasing. Accordingly, the guidelines and treatments are constantly renewed. One concept is the orthotic care. In the following we want to give an overview of the literature and the effectiveness of lumbar orthoses in low back pain supplemented by our own data. A prospective randomized study with 230 patients, divided into three groups, each with two subgroups. Three Orthoses by the TIGGES-Zours GmbH were prescribed; a demountable two-step lumbar orthosis, three-step bridging orthosis and a four-step flexion orthosis modular system. Each were compared to the nonmodular equivalent. All six groups showed improvement in pain intensity and functional capacity at 6 and 12 weeks. The modular groups were found to have improvement in the frequency of use. The subjective effectiveness and sensitivity for the modular and non-modular groups was assessed as being good. In the literature, there are no clear guidelines for an orthotic supply. The studies do not seem to be meaningful and universal due to the difficult ascertainability of pain. There is a need for further research here. Nevertheless, the authors of this review are of the opinion that the implementation of trunk orthoses is void of side effects and beneficial to patients. The modular systems seem to have an advantage as well as higher patient satisfaction.