An unusual presentation of opportunistic mucormycosis.
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Biomedical subjects
Publications and source records attributed to J A Elliott.
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Direct treatment of L5178Y mouse lymphoma TK+/- cells with N-acetyl-2-aminofluorene (AAF) from two commercial sources produced small, but reproducible increases in mutant frequency over background in the absence of exogenous microsomal enzymes. Unlike most direct-acting mutagens which typically produce regular, dose-dependent increases in mutant frequency; AAF treatment caused very slight dose-related increases or a saturation phenomenon which could be overcome by increased exposure time. Direct mutagenicity following prolonged (24h) exposure was confirmed when a third highly purified (99.9%) AAF sample was tested. Microsomal enzyme analyses of disrupted L5178Y cell preparations revealed negligible benzo[a]pyrene hydroxylase but measurable AAF-N-hydroxylase activity. These data demonstrate that L5178Y mouse lymphoma cells are capable of limited metabolism of AAF to an active mutagen.
Immunoperoxidase labeling showed that the F-1 antigen of Legionella pneumophila is located on the bacterial cell surface. Protection against lethal intraperitoneal challenge with serogroup 1 L. pneumophila was induced in guinea pigs by heat-killed cells and F-1 antigen from serogroup 1, but not by heat-killed cells or F-1 antigens from serogroup 2, 3, or 4.
Flagella were isolated from virulent Legionella pneumophila serogroups 1, 2, and 3. Antiserum made against purified serogroups 1 flagellin agglutinated live, flagellated serogroups 1, 2, and 3 but not heat-killed or nonflagellated bacteria. A single line of identity was seen in immunodiffusion slides between the flagella isolated from the three serogroups and antibody to flagellin isolated from serogroups 1, 2, and 3. Indirect immunoperoxidase staining showed that antibody to flagellin isolated from serogroup 1 organisms reacted with flagella on serogroup 1, 2, and 3 bacteria. Indirect immunoperoxidase staining was also showed that antibody to flagellin isolated from serogroup 1 L. pneumophila did not react with the serogroup-specific cell surface antigen, thus demonstrating that the flagella- and the serogroup-specific antigen are separate antigens. The amino acid content of the flagella from the three serogroups was essentially the same, with aspartate, glutamate, alanine, and threonine comprising 41% of the total. Thirty-five percent of the amino acids were hydrophobic, and there were not detectable amounts of cysteine, tryptophan, or tyrosine.
Serum from 109 coal workers with simple pneumoconiosis, 114 with progressive massive fibrosis, and 130 with normal chest radiographics as control subjects was examined for rheumatoid and antinuclear factors, and antibodies against both native human IgG and Mycobacterium tuberculosis. A significantly greater prevalence of autoantibodies was observed in subjects with pneumoconiosis than in control subjects; however, a rheumatoid factor prevalence of 16% with observed inthe control subjects. No serologic differences were observed between subjects with simple pneumoconiosis and those with progressive massive fibrosis.
One hundred and seventy-four unrelated white patients with biopsied and clinically diagnosed sarcoidosis and a reference population of 97 were tested for HLA antigens. Selected comparisons showed a statistically significant association of HLA-B8 with the sarcoidosis group (28.9%) when compared to the reference group (15.5%).
Sera from 84 white patients with inactive sarcoidosis were analyzed for immunoglobulins, complement, autoantibodies, alpha 1-antitrypsin and lysozyme. The levels of serum factors were compared with levels in serum from a reference population which was matched for age, sex, ethnic background and geographic location. IgG, IgA, IgD, and C3 levels were similar for both groups, as were frequencies of rheumatoid factor, antinuclear antibody and anti-DNA antibody. Lysozyme levels were significantly lower in the inactive sarcoidosis group but the acute phase reactants alpha 1-antitrypsin, IgM as well as complement consumption were increased. The data suggest that the underlying etiological events of sarcoidosis continue, albeit at a subclinical level.
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We isolated a high molecular weight antigen of the Legionnaires' disease (LD) bacterium by column chromatography. The antigen was composed of 35% carbohydrate, 2.6% protein, 1.8% phospholipid, and 1% 2-keto-3-deoxyoctonate and was important in the host's antibody response because it inhibited the indirect immunofluorescent and microagglutination titers of convalescent sera from patients with Legionnaires' disease. The antigen also formed precipitin bands with seven of 10 convalescent sera from patients with Legionnaires' disease. We found chemical and biological evidence of endotoxinlike activity associated with the antigen. Cell sonicates and acid extracts of the LD bacterium gave multiple bands in immunodiffusion with human convalescent serum and rabbit antisera prepared against heat-killed LD bacteria. The antigenic structure of the LD bacterium therefore appears complex.
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Ground whole rye and airborne rye dust of comparable size distribution were tested for their ability to activate the complement cascade via the alternative pathway. Precipitin-negative pooled normal human serum was incubated with increasing amounts of the two rye dusts. Electrophoresis of the resultant supernatant fluids demonstrated the conversion of the proactivator of the third component of complement to the gamma-migrating activator of the third component. This activation was completely prevented by pre-treating the serum with the chelator EDTA, while pre-treatment with EGTA allowed suboptimal arc conversion, strongly implying that complement was activated via the alternative pathway. Quantification of the supernanant fluids showed dose-dependent complement consumption as defined by both CH100 immunodiffusion and CH50 tube haemolytic techniques. Airborne rye dust showed a greater quantitative potential than ground whole rye for activating the alternative pathway. These results indicate the possibility of the direct action of airborne organic dusts on the induction of inflammatory sequelae in the lungs of both sensitized and unsensitized individuals.
The rate and extent of disappearance of two DNA lesions (pyrimidine dimers and covalently bound acetylaminofluorene), both thought to be removed by the so-called wide-patch (approximately 100 nucleotides) repair process, were studied in a variety of cultured mammalian cells. With the exception of mouse cells, dimers were removed more rapidly and extensively than covalently bound acetylaminofluorene. In human cells, for example, about 50% of the dimers were excised from DNA in 1 hr while only 25-50% of the chemically induced lesions were excised from DNA after 48 hr. Surprisingly mouse cells, which remove few dimers, were about as competent as control human fibroblasts at removing acetylaminofluorene lesions; however, xeroderma pigmentosum cells (group D) removed fewer N-acetoxy-2-acetylaminofluorene-induced lesions than control human cells. Our data raise the possibility of separate repair processes for these two types of lesions and suggest that their expression may be under similar genetic control in human cells.
Charcoal haemoperfusion used to treat a 56-year-old woman who had taken a very large overdose of meprobamate was followed by fully recovery. The plasma clearance of meprobamate was 153 ml/min and this compares favourably with values obtained for haemodialysis. The indications for haemoperfusion are reviewed.
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