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Biomedical subjects

J B Boyd

Publications and source records attributed to J B Boyd.

At least 109 records · Page 6Linked to original sources
PubMed1981

Mutants partially defective in excision repair at five autosomal loci in Drosophila melanogaster.

Primary cell cultures derived from mutants in seventeen different genes were analyzed for their ability to excise pyrimidine dimers from DNA. Five of these mutagen-sensitive mutants [mus(2)205A1, mus(3)302D1, mus(3)304D3, mus(3)306D1, mus(3)308D2] display a significantly reduced excision capacity relative to control cultured. In addition, two of the five [mus(3)306D2, mus(3)308D2] are defective in the accumulation of single-strand breaks normally seen after ultraviolet irradiation. This study, therefore, brings the total number of Drosophila mutants known to be defective in excision repair to seven. The results are discussed relative to other genetic and biochemical properties of these mutants.

Animals↗
PubMed1981

Effects of radiation on the survival of excision-defective cells from Drosophila melanogaster.

The effect of various doses of ultraviolet light and ionizing radiation on the survival of excision-defective Drosophila cells has been determined by cloning treated and untreated cells in agarose. Although excision-defective cells survive moderate amounts of DNA damage, they display a severe hypersensitivity to both types of radiation relative to excision-proficient cells. Exposure of ultraviolet-irradiated cells to fluorescent light results in a reduction of the density of pyrimidine dimers in cellular DNA and a 10-to 20-fold increase in survival. Parallel analysis of dimer density and survival, however, suggests that much of the lethal effect of ultraviolet light is due to nondimer damage. Cell proliferation was monitored in both excision-proficient and excision-defective cells exposed to doses of ultraviolet light that reduced survival by 90%. Under these conditions excision-proficient cells displayed exponential growth whereas excision-defective cells exhibited no cell proliferation for 12 days.

Animals↗
PubMed1981

Genetic analysis of X-linked mutagen-sensitive mutants of Drosophila melanogaster.

Mutants at 2 new loci which control mutagen-sensitivity are described. Mutants of both foci are female-sterile and are hypersensitive to killing by MMS; neither increases the frequency of sex-linked recessive lethals. A screen of previously described female-sterile and meiotic mutants has revealed that a number of these are also sensitive to mutagens. In addition, several new mutants have been identified on the basis of sensitivity to either HN2 or MMS. An analysis of complementation data suggests that all of the X-linked genes controlling sensitivity to MMS may now have been identified. Among the new mei-41 alleles are mutants which show very little meiotic nondisjunction or loss. Cytogenetic mapping of previously known mutants is also described. The mutants mus(1)104D1 and mei-41D5 are located in the region 14B13+/- -14D1,2 on the polytene chromosome map, and they map very close to each other genetically. Cytogenetically mus(1)101D1 is between salivary chromosome bands 12A6,7 and 12D3, mus(1)103D1 is between bands 12A1,2 and 12A6,7 and mus(1)109A1 is in section 8F3--9A2.

Animals↗
PubMed1981

Ameloblastoma: a tumour to recognize.

The clinical presentation of ameloblastoma is illustrated by two contrasting cases; in one case the tumour was identified preoperatively while in the other it masqueraded as a dentigerous cyst. The authors stress the importance of making a positive diagnosis and the need for a thorough histologic examination of excised tissue because this tumour is potentially disfiguring and sometimes lethal if it is not adequately excised.

Adolescent↗
PubMed1980

Excision repair in Drosophila. Analysis of strand breaks appearing in DNA of mei-9 mutants following mutagen treatment.

Excision repair of DNA damage has been analyzed in primary and established cell cultures of Drosophila melanogaster. Chemical and enzymatic assays for pyrimidine dimers reveal a strong deficiency in dimer excision from cells which are mutant at the mei-9 locus. Single-strand interruptions, which appear in high molecular weight DNA after ultraviolet irradiation of control cells have been monitored by alkaline elution. The appearance of such breaks is greatly enhanced by inhibitors of DNA synthesis. In mutant mei-9D2 cells, on the other hand, the level of ultraviolet-induced breaks is much reduced and inhibitors fail to potentiate the response. These results imply that the inhibitors cause an accumulation of the transient strand interruptions that normally occur in excision repair by reducing the rate of the resynthesis step. Failure of the mei-9D2 cells to accumulate such intermediates strongly suggests that the initial nicking never occurs in these cells. Confirmatory experiments have also been performed with the alternate mutagen N-acetoxy-N-acetyl-2-aminofluorene.

Acetoxyacetylaminofluorene↗
PubMed1980

Advances in the management of gastroschisis.

Twenty-eight cases of gastroschisis have been treated over a five-year period. Twenty-two silos were placed and 19 infants had uncomplicated silo closure. Enlargement of the abdominal wall defect to allow optimum reduction of the edematous bowel was essential to closure in less than a week. Rapid removal of the prosthesis and strict adherence to aseptic technique prevented septic complications. Inability to return the bowel to the abdominal cavity within five to six days mandated re-exploration to determine the cause for failure to reduce the silo. Accordingly, three infants were re-explored. Two patients had unrecognized intestinal lesions and a third infant, whose defect had not been enlarged, had infarction of the midgut. Six infants underwent primary closure; two with preinatal evisceration and four who had concomminant cutaneous enterostomies performed for intestinal atresia. Intestinal atresia or stenosis occurred in 25% of these infants. Postoperative management was facilitated by insertion of a gastrostomy tube, early peripheral venous nutrition and later insertion of a central venous catheter for nutrition. The one postoperative death (3.5% mortality rate) resulted from failure to follow the principles of silo management as outlined in this report.

Abdominal Muscles↗
PubMed1980

Operative risk factors of colon resection in the elderly.

Between January 1, 1974, and December 31, 1978, patients over 50 years of age underwent colon resections in three West Virginia Hospitals. The patients were studied by decades of age to compare the operative risks in younger and elderly patients. Preoperative assessments of cardiovascular, pulmonary, renal, hepatic, metabolic and nutritional states were compared with the postoperative morbidity and mortality rates. Complications occurred in 33% of all the patients who had resections, with 17 (4.8%) deaths. Mortality rates compared by decades of age correlated with the number of pre-existing conditions, and not with age as an isolated factor. There were no deaths in patients with no pre-existing conditions. The rate of infectious complications increased because the number of emergency procedures increased. This was also true for the mortality rate. Preoperative pulmonary and nutritional problems were significant contributing factors in the patients who died from sepsis. Careful preoperative assessment, correction of pre-existing pulmonary and nutritional deficiencies, and avoidance of emergency procedures may improve the morbidity and mortality rates associated with colon resections in elderly patients.

Age Factors↗
PubMed1979

Production and secretion of proteolytic enzymes by normal and neoplastic cells.

A possible mechanism for tumor cell invasion of normal tissue might be secretion of proteolytic enzymes. This study compares and contrasts production and secretion of proteinases by cell cultures of normal and chemically transformed mouse epithelial cells. Lysates of normal and neoplastic cells contain similar amounts of neutral proteinase, cathepsin D and plasminogen activator. Neither collagenase nor elastase could be identified in lysates of, or serum-free culture medium bathing, normal or neoplastic cells. Neoplastic cells secrete ten times more plasminogen activator than normal cells. Our data support the hypothesis that plasminogen activator produced by neoplastic cells could fuction to activate latent proteolytic enzymes secreted by connective tissue cells which might result in spread of neoplastic cells into normal tissue.

Animals↗
PubMed1979

Sensitivity of drosophila mutants to chemical carcinogens.

7 single-mutant and five double-mutant strains of Drosophila melanogaster were tested for their relative sensitivity to the chemical carcinogens: 1-acetylaminofluorene, benzo(alpha)pyrene, N-methyl-N'-nitro-N-nitrosoguanidine, 4-nitro quinoline-1-oxide and aflatoxin B1. Among the single mutants, mei-9a, mei-41D5 and mus(1)104D1 are hypersensitive to all 5 chemicals, whereas mus(1)107D1 is hypersensitive only to 4-nitroquinoline-1-oxide and is slightly sensitive to benzo(alpha)pyrene. The mei-9a mei-41D5 double-mutant is the most sensitive of 5 tested double-mutants which carry the mei-9a allele. When treated with 0.025 mM benzo(alpha)pyrene this double-mutant produces significantly more sex-linked recessive lethals and dominant lethals than does the control. Analysis of double-mutants reveals that the mei-9+ product functions in a different repair pathway of methyl methanesulfonate-induced damage than do the normal products of the mus(1)103, mus(1)104 and mus(1)107 loci. Our findings suggest that the sensitivity of Drosophila repair-deficient mutants could be exploited in screening for potential mutagens and carcinogens.

4-Nitroquinoline-1-oxide↗
PubMed1978

Correction of prognathism with fixed and removable partial dentures.

Prognathism in those patients for whom surgical orthodontic procedures are contraindicated can be successfully treated by the use of fixed and removable partial denture prosthodontics. Careful neuromuscular evaluation of the patient is necessary for the success of the treatment rendered. The nonsurgical treatment of prognathism by this method was described.

Acrylic Resins↗
PubMed1977

Sensitivity of wild type and recombination-deficient strains of Drosophila melanogaster to ultraviolet radiation.

The sensitivity of Drosophila melanogaster to ultraviolet light has been studied in wild type and recombination-deficient strains. Survival was measured as the proportion of irradiated embryos or larvae which developed to adult flies. In view of the fact that males of this species do not participate in meiotic recombination, emphasis was placed on the relative sensitivity of males and females. The results show that young wild type male larvae are more sensitive to UV radiation than are young female larvae. This difference in sensitivity, however, is not apparent in some recombination-deficient strains. In addition, young embryos of the recombination-deficient strain Df(3)sbd105/T(2;E)Xa are exceptionally sensitive to UV radiation.

Animals↗
PubMed1976

Genetic controls of meiotic recombination and somatic DNA metabolism in Drosophila melanogaster.

Recombination-defective meiotic mutants and mutagen-sensitive mutants of D. melanogaster have been examined for their effects on meiotic chromosome behavior, sensitivity to killing by mutagens, somatic chromosome integrity, and DNA repair processes. Several loci have been identified that specify functions that are necessary for both meiotic recombination and DNA repair processes, whereas mutants at combination and DNA repair processes, whereas mutants at other loci appear to be defective in only one pathway of DNA processing.

Animals↗
PubMed1976

Isolation and characterization of X-linked mutants of Drosophila melanogaster which are sensitive to mutagens.

Thirteen X-linked mutants have been isolated in Drosophila melanogaster which render male and homozygous female larvae sensitive to the mutagen methyl methanesulfonate. Their characterization and preliminary assignment to functional groups is described. Four of these mutants are alleles of mei-41 (Baker and Carpenter 1972). Like previously isolated alleles of this locus, these mutants reduce fertility and increase loss and nondisjunction of the X-chromosome in homozygous females. The remaining mutants have been tentatively assigned to six functional groups (two mutants to the mus(1)101 locus, two to mus(1)102 , two to mus(1)103, and one each to mus(1)104, mus(1)105 , and mus(1)106). Several of the complementation groups can be distinguished on the basis of nondisjunction and cross sensitivity to mutagens. Females homozygous for the mei-41, mus(1)101 and mus(1)102 mutants exhibit elevated levels of nondisjunction. Mutants belonging to complementation groups mei-41, mus(1)101, and mus(1)104 are sensitive to nitrogen mustard (HN2) in addition to their MMS sensitivity. Among these mutants there is currently a direct correlation between sensitivity to HN2, sensitivity to 2-acetylaminofluorene and a deficiency in post-replication repair ( Boyd and Setlow 1976). Only the mei-41 mutants are hypersensitive to UV radiation, although several of the mutants exhibit sensitivity to gamma-rays. Semidominance is observed in female larvae of the mei-41, mus(1)104, and mus(1)103 mutants after exposure to high concentrations of MMS. The properties of the mutants generally conform to a pattern which has been established for related mutants in yeast. Additional properties of these mutants are summarized in Table 9.

Alleles↗