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Biomedical subjects

J Greenberg

Publications and source records attributed to J Greenberg.

At least 235 records · Page 13Linked to original sources

Use of phage F-phi WJ-1 of Mycobacterium fortuitum to discern more phage types of Mycobacterium tuberculosis.

A total of 125 strains of Mycobacterium tuberculosis from the Southeastern area of the United States was subjected to phage typing. In addition to the five major mycobacteriophages, a new phage, F-phi WJ-1, was used in the study. The results obtained with the five major phages were: type A0, 35.2%; TYPE B, 29.6%, and type C, 4.0%. The remaining 21.2% of the strains phaged typed as subgroups A1 through A6. These percentages were similar to the typing results of earlier studies. The new phage, F-phi WJ-1, subdivided each of the phage types, with the exception of type C, into two subgroups. The possible role of host modification-restriction of the phages used in phage typing of strains of M. tuberculosis is discussed.

Bacteriophage Typing↗

Transgingival probing as a potential estimator of alveolar bone level.

The validity of using a periodontal probe for the transgingival sounding of the alveolar crest level has been demonstrated for buccal surfaces of the jaw. The measurements from the occlusal surfaces of the teeth to the estimated level of the alveolar crest using this technique accurately reflected the actual distances measured after surgical exposure of the alveolar crest at these sites.

Alveolar Process↗

Effect of inorganic phosphate on acridine inhibition and plasmid curing in Escherichia coli.

Some mutants and stock strains of Escherichia coli K12 were sensitive to acriflavine in the presence of inorganic phosphate but were resistant to acriflavine in its absence. They mutated spontaneously to resistance to acriflavine plus phosphate. The synergistic effect of phosphate on acriflavine sensitivity was increased at high pH values. Genetic analysis suggested that the mutations occurred in the gene acrA. Electron microscopic observation suggested that the presence of acriflavine plus phosphate affected the structure of the plasma membrane and the cytoplasm under it. This structural alteration was not caused by acriflavine alone. Acridine orange plus phosphate can more effectively eliminate the plasmid F8-gal+ than acridine orange alone.

Acridines↗

Mapping of sul, the suppressor of lon in Escherichia coli.

The suppressor sul, which is allele specific for the ultraviolet sensitivity gene lon, has been mapped by conjugation and transductional crosses in Escherichia coli K-12 and B/r. Previously, sul was reported to lie in the azi region of the Escherichia coli chromosome. Evidence is presented which positions sul close to and clockwise of fabA on the Escherichia coli map. Cotransductional frequencies of 31.3% were obtained between sul and pyrD, and frequencies of 82% were obtained between sul and fabA. Also, the mucoid phenotype of K-12 lon strains grown on minimal glucose agar plates at 37 C was not significantly effected in sul derivatives. No differences between the sul of Escherichia coli B/r and that of K-12 derivatives with regard to map location or effect on mucoid production were observed.

Chromosome Mapping↗

Interaction of the expression of two membrane genes, acrA and plsA, in Escherichia coli K-12.

The mutation acrA1, leading to acriflavine sensitivity through disorganization of the plasma membrane, is located between proC and purE on the Escherichia coli K-12 chromosome. Gene plsA has been reported to determine biosynthesis of membrane phospholipid and to be located very near acrA (1). Genes acrA and plsA fall into different cistrons and are arranged in the order proC-acrA-plasA-purE. The genes were shown to interact with each other. Introduction of acrA mutation into a plsA temperature-sensitive mutant mitigated the heat sensitivity. Plasmid (F-gal+) stability in acrA mutants was restored by introduction of the plasA mutation into the acrA cells. When an Hfr plsA donor was conjugated with an acrA recipient, or when reciprocally conjugated, the exogenotes were eliminated at high frequency during subsequent subcultivation in broth. However, the exogenotes were not eliminated in all other allelic combinations of genes acrA and plsA. When an F-gal+ plasmid was introduced into the unstable heterozygotes (acrA+plsA/acrApls1+), the plasmids were stably hosted, whereas the acrA+ plasA exogenotes were spontaneously lost at a high frequency. On the other hand, when the unstable heterozygotes carrying F-gal+ were cultured in acriflavine-containing medium, the F-gal+ plasmids were preferentially eliminated but the acrA+plasA exogenotes were not affected. The results suggest that the organization of the plasma membrane controls the recombination of the exogenotes introduced into zygotes.

Acridines↗

Role of pyrimidine dimer excision in loss of potential streptomycin resistance mutations of ultraviolet-irradiated Escherichia coli on phosphate-buffered agar.

The frequency of ultraviolet (UV)-induced mutations to streptomycin resistance dropped rapidly when starved Escherichia coli strains WP-2 B/r and B/r T- were incubated on phosphate-buffered agar (PBA), but was reduced only slightly in a WP-2 hcr- mutant. During postirradiation, incubation viability remained approximately constant. Cells given an optimal recovery treatment with photo-reactivating light showed no further recovery if subsequently incubated on PBA. At least 70% of the mutations induced to streptomycin resistance by UV could be repaired. The loss of potential streptomycin-resistant mutants was markedly reduced in strain B/r T- when 5 mug of acriflavin or 700 mug of caffeine per ml was added to PBA. The excision of UV-induced thymine-containing dimers from E. coli tb/r T- was investigated. Dimer excision progressed more slowly when the cells were incubated on PBA containing acriflavin or caffeine. There was no congruity between the kinetics of dimer excision and the kinetics of mutant loss. Our results indicate that removal of potential streptomycin-resistant mutants is considerably faster than the excision of pyrimidine dimers.

Acriflavine↗

Pallido-pyramidal syndrome treated with levodopa.

Two siblings are reported who developed classical signs and symptoms of Parkinsonism in the first decade of life. In addition, they had evidence of cortical spinal tract disease, thus putting them in the category of Davison's pallido-pyramidal syndrome. Both deteriorated to the point of a non-productive existence until the institution of levodopa treatment, at the ages of 18 and 20 years. The response of the extrapyramidal signs plus the lack of response of the pyramidal tract signs demonstrate the specificity of a pharmacological agent in certain areas of the nervous system. The rapid response of the female patient to very low doses of levodopa is unusual in our experience. Both patients have remained well for eight months after initiation of treatment.

Adolescent↗

Effects on platelet function of removal of platelet sialic acid by neuraminidase.

A number of investigators have implicated sialic acid on the surface of platelets in platelet function. In this study we have quantitated the amount of sialic acid removed by purified neuraminidase from the surface of washed platelets of man, rabbit, or pig and examined the effects of this removal. Purified neuraminidase did not induce the release of platelet granule contents. Platelets were pre-labeled with 14C-serotonin for measurement of the release reaction or with 51Cr for determination of adherence to a collagen-coated surface or damaged aortic surface, and for in vivo platelet survival studies. Washed, neuraminidase-treated platelets were resuspended in Tyrode's solution containing 0.35 per cent albumin or in citrated platelet-free plasma from the same species. Both resuspending fluids contained apyrase. Aggregating agents tested were ADP, acid-soluble collagen, thrombin, ristocetin (with human platelets), polylysine, and serotonin (with rabbit platelets). With all of these agents except polylysine, aggregation of neuraminidase-treated human or rabbit platelets was slightly enhanced compared with control platelets; aggregation of pig platelets was unchanged. When release-inducing agents were used, neuraminidase-treated platelets released more of their 14C-serotonin than control platelets. The extent to which rabbit platelets adhered to a collagen-coated surface or to the damaged surface of everted rabbit aorta was unchanged by pretreatment of platelets with neuraminidase. Therefore it seems unlikely that sialic acid is involved in platelet adherence to collagen. When more than 15 per cent of total sialic acid had been removed from rabbit platelets, they were completely cleared from the circulation within 1 hour of their injection into rabbits. When 8 to 10 per cent of total sialic acid had been removed, the platelets were not cleared immediately from the circulation but were cleared more quickly than control platelets. Thus, although removal of up to 65 per cent of platelet sialic acid has only a slightly enhancing effect on platelet aggregation and release in vitro, removal of as little as 8 to 10 per cent results in the recognition of platelets as "foreign" in vivo.

Adenosine Diphosphate↗