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Biomedical subjects

J M Mason

Publications and source records attributed to J M Mason.

At least 109 records · Page 6Linked to original sources
PubMed1986

Immunoglobulin G subclasses and isoimmunized pregnancy outcome.

Immunoglobulin G antibodies are the most frequent type of red blood cell isoantibodies. They possess the ability to traverse the placenta and may cause hemolytic disease in newborn infants. Of the four subclasses, IgG1 and IgG3 are effective at binding erythrocytes to monocyte-macrophages and therefore are potentially destructive to erythrocytes. IgG2 and IgG4 are unable to react effectively with receptor sites on phagocytic cells and so are totally inactive relative to hemolysis. IgG subclasses were identified in 22 consecutive isoimmunized antepartum patients. Fifteen patients were subsequently delivered of babies who were either affected by or susceptible to hemolytic disease of the newborn. When maternal antibodies consisted of IgG1 only, hemolytic disease of the newborn developed in four of five cases. When only IgG3 was present, each of two patients developed hemolytic disease of the newborn. In eight cases both IgG1 and IgG3 were present and all the babies were born with hemolytic disease of the newborn. Determination of IgG subclasses might prove to be a useful adjunct in evaluating isoimmunized pregnancies. However, the limited information available does not permit the use of IgG subclasses exclusive of traditional means of diagnosis and management of isoimmunized pregnancies.

Amniocentesis↗
PubMed1986

Cloning and nucleotide sequencing of genes for three small, acid-soluble proteins from Bacillus subtilis spores.

Three Bacillus subtilis genes (termed sspA, sspB, and sspD) which code for small, acid-soluble spore proteins (SASPs) have been cloned, and their complete nucleotide sequence has been determined. The amino acid sequences of the SASPs coded for by these genes are similar to each other and to those of the SASP-1 of B. subtilis (coded for by the sspC gene) and the SASP-A/C family of B. megaterium. The sspA and sspB genes are expressed only in sporulation, in parallel with each other and with the sspC gene. Two regions upstream of the postulated transcription start sites for the sspA and B genes have significant homology with the analogous regions of the sspC gene and the SASP-A/C gene family. Purification of two of the three major B, subtilis SASPs (alpha and beta) and determination of their amino-terminal sequences indicated that the sspA gene codes for SASP-alpha and that the sspB gene codes for SASP-beta. This was confirmed by the introduction of deletion mutations into the cloned sspA and sspB genes and transfer of these deletions into the B. subtilis chromosome with concomitant loss of the wild-type gene.

Amino Acid Sequence↗
PubMed1986

Essential role of small, acid-soluble spore proteins in resistance of Bacillus subtilis spores to UV light.

Bacillus subtilis strains containing deletions in the genes coding for one or two of the major small, acid-soluble spore proteins (SASP; termed SASP-alpha and SASP-beta) were constructed. These mutants sporulated normally, but the spores lacked either SASP-alpha, SASP-beta, or both proteins. The level of minor SASP did not increase in these mutants, but the level of SASP-alpha increased about twofold in the SASP-beta- mutant, and the level of SASP-beta increased about twofold in the SASP-alpha- mutant. The growth rates of the deletion strains were identical to that of the wild-type strain in rich or poor growth media, as was the initiation of spore germination. However, outgrowth of spores of the SASP-alpha(-)-beta- strain was significantly slower than that of wild-type spores in all media tested. The heat resistance of SASP-beta- spores was identical to that of wild-type spores but slightly greater than that of SASP-alpha- and SASP-alpha(-)-beta- spores. However, the SASP-alpha- and SASP-alpha(-)-beta- spores were much more heat resistant than vegetative cells. The UV light resistances of SASP-beta- and wild-type spores were also identical. However, SASP-alpha(-)-beta- spores were slightly more sensitive to UV light than were log-phase cells of the wild-type or SASP-alpha(-)-beta- strain (the latter have identical UV light resistances); SASP-alpha- spores were slightly more UV light resistant than SASP-alpha(-)-beta- spores. These data strongly implicate SASP, in particular SASP-alpha, in the UV light resistance of B. subtilis spores.

Bacillus subtilis↗
PubMed1985

Chemical mutagenesis testing in Drosophila. II. Results of 20 coded compounds tested for the National Toxicology Program.

Results are presented from mutagenesis testing in Drosophila of 20 coded compounds. Two compounds were positive in the sex-linked recessive lethal test, and two were inconclusive. The positive compounds were calcium chromate in adult feeding experiments and ferrocene after adult injection. The two inconclusive compounds were 2,4-diaminophenol dihydrochloride and hexachlorocyclopentadiene. Compounds that produced a positive response were assayed for chromosome breakage using the conventional translocation test. Calcium chromate was negative in the translocation test, and ferrocene was positive. Many of the test compounds were poorly soluble in water, raising questions regarding the effective concentration to which the flies were exposed.

Animals↗
PubMed1985

Chemical mutagenesis testing in Drosophila. III. Results of 48 coded compounds tested for the National Toxicology Program.

Forty-eight chemicals were tested for mutagenicity in Drosophila melanogaster. Each compound was tested first for the induction of sex-linked recessive lethals (SLRLs) by feeding the chemical in a solution of 5% aqueous sucrose. If it was not mutagenic by this route, the chemical was tested by injection in a solution of 0.7% aqueous NaCl. If found inactive, the compound was not tested further. If it was mutagenic, the compound was tested for the induction of reciprocal translocations (RTs) using the exposure protocol and germ cell stage that yielded positive results in the SLRL assay. Eight chemicals (diglycidylresorcinol ether, AF-2, alloxan monohydrate, 1-aziridine ethanol, p,p'-DDE, dichloroacetonitrile, 1,3-dichloropropene, and 3,3'-dimethylbenzidine dihydrochloride) were found to induce SLRLs. Only diglycidylresorcinol ether also induced RTs.

Animals↗
PubMed1985

Chemical mutagenesis testing in Drosophila. IV. Results of 45 coded compounds tested for the National Toxicology Program.

Results from Drosophila mutagenicity tests of 45 chemical compounds assayed for the National Toxicology Program are presented. Nine compounds were judged positive and four equivocal in the sex-linked recessive lethal test. The nine positive compounds were acetin, allyl glycidyl ether, cyclophosphamide, 1,2-dibromo-3-chloropropane, 2,3-dibromo-1-propanol, dimethylcarbamyl chloride, 1,2-epoxy-butane, lasiocarpine, and N-nitrosopiperidine. The results for chloral hydrate, maleic hydrazide, propantheline bromide, and trifluralin were equivocal. Of the nine compounds positive in recessive lethal induction, only two--allyl glycidyl ether and dimethylcarbamyl chloride--failed to induce translocations. The remaining 32 were judged to be nonmutagenic under the conditions used.

Animals↗
PubMed1985

Genetic drift and seasonal variation in spontaneous mutation frequencies in Drosophila.

Spontaneous sex-linked recessive lethal mutation frequencies may vary with time. Examination of approximately 1.7 X 10(6) Drosophila melanogaster X chromosomes in three laboratories suggests two sources of variation in the spontaneous mutation frequency. First, the underlying mutation rate may change with time, suggesting genetic drift among the genes controlling the spontaneous mutation rate. In one set of experiments, the recessive lethal frequency increased from 0.2% to 0.4% in 6 years. Second, there may be seasonal variation in the mutation frequency even under apparently controlled conditions, suggesting that uncontrolled environmental factors may play an important role in determining the mutation frequency. Therefore, concurrent controls should be used in mutation experiments except in cases in which the frequency in the untreated control is so low as to be unmeasurable in a single experiment or the control frequency can be shown not to vary with time.

Animals↗
PubMed1985

Chemical mutagenesis testing in Drosophila. V. Results of 53 coded compounds tested for the National Toxicology Program.

Fifty-three chemicals were tested for mutagenicity in Drosophila melanogaster by adult feeding and, where results were negative, by adult injection for the induction of sex-linked recessive lethal mutations in meiotic and postmeiotic germ cell stages of Canton-S males. One compound was tested by inhalation. Those compounds that induced lethal mutations were tested further for the induction of reciprocal translocations. Seventeen of the 53 compounds (acetaldehyde, 2-aminoanthracene, bromoform, t-butyl hydroperoxide, chlorambucil, trans-cinnamaldehyde, crotonaldehyde, 1,3-dichloro-5,5-dimethylhydantoin, 3,4-dichloronitrobenzene, dimethoxane, 2,4-dinitrotoluene, 1,2-epoxy-3,3,3-trichloropropane, formaldehyde, furfural, halothane, HC yellow 4, and picric acid) were found to induce lethal mutations and three (2-aminoanthracene, chlorambucil,and crotonaldehyde) also induced reciprocal translocations.

Animals↗
PubMed1984

Chemical mutagenesis testing in Drosophila: I. Comparison of positive and negative control data for sex-linked recessive lethal mutations and reciprocal translocations in three laboratories.

As part of the validation phase of the Drosophila melanogaster segment of the National Toxicology Program, a comparison has been made of positive and negative controls for sex-linked recessive lethal mutations and reciprocal translocations from three laboratories. This comparison involves approximately 700,000 spontaneous recessive lethal mutation tests, 70,000 spontaneous translocation tests, and screens for genetic damage induced by N-nitrosodimethylamine and beta-propiolactone. Spontaneous frequencies for lethal mutations and translocations were homogeneous in the laboratories regardless of solvent or broods sampled. Inhomogeneity was observed in induced frequencies among laboratories, but the variation was no greater than that found within a laboratory.

Animals↗
PubMed1984

mu-2: mutator gene in Drosophila that potentiates the induction of terminal deficiencies.

An x-ray-dependent mutator on chromosome 3 of Drosophila melanogaster is described that specifically increases the recovery of deletions for chromosomal tip regions. Such deficiencies can be induced on any chromosome. More centromere proximal mutations, as assayed by the sex-linked recessive lethal test, are not increased over the wild-type control. As far as can be determined by genetic, cytological, and molecular assays, the deletions extend to the very end of the chromosome involved. In addition, the frequency of these deletions is directly proportional to x-ray dose, suggesting that they are one-break rearrangements. It is proposed that the mutator is blocked in a major pathway for the repair of DNA double-strand breaks, and that a minor repair pathway is responsible for the addition of new telomeres under these conditions.

Animals↗
PubMed1984

Expression of Bacillus megaterium and Bacillus subtilis small acid-soluble spore protein genes during stationary-phase growth of asporogenous B. subtilis mutants.

The small acid-soluble spore proteins alpha and beta were not detected during stationary-phase growth of asporogenous Bacillus subtilis mutants blocked in stages 0, II, or III, but mutants blocked in stages IV or V accumulated nearly wild-type levels of these small acid-soluble spore proteins. Similar results were obtained when production of Bacillus megaterium C protein (also a small acid-soluble spore protein), as well as alpha and beta, were monitored in these mutants containing a recombinant plasmid carrying the B. megaterium C protein gene. The only exception was a spo0H mutant which synthesized a small amount of C protein, but no alpha or beta.

Bacillus megaterium↗
PubMed1983

Statistical analysis and sample-size determinations for mutagenicity experiments with binomial responses.

Two statistical analyses are studied for their applicability to mutagenicity experiments that produce binomial responses from a control group and a single treated group. Attention is focused on experiments with (1) group sample sizes greater than 500 and (2) a probability less than .05 for a binary observation from any experimental unit being "positive." In addition, it is assumed that historical control data will not be included in the statistical analysis. The first analysis is a conditional binomial test, which has been tabulated extensively by Kastenbaum and Bowman [1970], while the second is based on a standard normal approximation to the distribution of the difference between two sample proportions. A formula is presented for each analysis that relates the associated probability of detecting a mutagen to the mutant frequencies and sample sizes of the two groups. Based on extensive numerical results, the conclusion is drawn that the normal test is the preferred analysis for experiments in which the ratio of the two sample sizes is between 0.80 and 1.25. On the further assumption that an experiment is to be conducted with equal experimental group sample sizes, recommendations are offered for values of this common sample size needed to achieve a specified power, ie, a degree of assurance of detecting a postulated level of mutagenic effect.

Animals↗
PubMed1983

Genetic instability associated with the aroC321 allele in Salmonella typhimurium involves genetic duplication.

Strains of Salmonella typhimurium that contain the aroC321 allele require phenylalanine, tyrosine, and tryptophan for growth but revert to tryptophan-prototrophy at high frequencies (about 10(-4) per cell plated). The Trp+ derivatives remain auxotrophic for phenylalanine and tyrosine and are genetically unstable, in that they readily give rise to cells that require all three aromatic amino acids. On the basis of growth characteristics and genetic instability, it has been proposed that reversion to tryptophan-prototrophy in aroC321 strains occurs by genetic duplication. This paper provides genetic evidence in support of that hypothesis. The data indicate, moreover, that the tryptophan prototrophs contain a duplication that extends at least from glpT to xyl, a region of greater than 30% of the Salmonella chromosome. The aroC locus is found within the duplicated region, and aroC321/aroC321 merodiploids apparently grow as tryptophan prototrophs because of a gene-dosage effect.

Chromosome Mapping↗
PubMed1983

Irregular antibodies: an assessment of routine prenatal screening.

In a review of the antenatal-postnatal records of 6062 patients attending the prenatal clinic at a large university perinatal center during 1980, 8.3% of the pregnant patients seen were Rho(D) negative and 91.7% were Rho(D) positive. Through routine antibody screening of all patients, 115 were found to have irregular antibodies which would otherwise not have been detected. Fifteen of these patients were Rho(D) negative, but they would have been included for antibody screening due to their Rho(D) negative status. Of the remaining 100 Rho(D) positive patients, clinically significant antibodies were observed in six patients; however, no maternal morbidity or hemolytic disease of the newborn was reported. Antecedent maternal risk factors for development of irregular antibodies were not sufficiently selective for predicting outcomes of such pregnancies. Furthermore, the only four patients with irregular antibodies requiring blood transfusion were cross-matched without difficulties. Findings suggest that screening all patients for irregular antibodies cannot be justified due to the prohibitive costs involved. However, because of the racially homogeneous population studied, variations in the frequency of red blood cell genotypes between racial groups, and the irregular pattern of occurrence of irregular antibodies, the authors believe that further studies on the clinical impact and cost-effectiveness of screening all antenatal patients for presence of irregular antibodies are necessary.

Blood Group Antigens↗