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Biomedical subjects

B F White

Publications and source records attributed to B F White.

8 recordsLinked to original sources
PubMed1992

Assignment of a human DNA double-strand break repair gene (XRCC5) to chromosome 2.

The Chinese hamster ovary (CHO-K1) cell mutant XRS-6 is defective in rejoining of DNA double-strand breaks and is hypersensitive to X-rays, gamma-rays, and bleomycin. Radiation resistance or sensitivity of somatic cell hybrids constructed from the fusion of XRS-6 cells with primary human fibroblasts strongly correlated with the retention of human chromosome 2 isozyme and molecular markers. Discordancies between some chromosome 2 markers and the radiation resistance phenotype in some of the hybrid cells suggested the location of the X-ray repair cross complementing 5 (XRCC5) gene on the p arm of chromosome 2. Introduction of human chromosome 2 by microcell-mediated chromosome transfer into the radiation-sensitive XRS-6 cells resulted in hybrid cells in which the radiation sensitivity was complemented. The chromosome 2p origin of the complementing human DNA in the microcell hybrids was supported by fluorescent in situ hybridization analysis of human metaphases using human DNA amplified from the hybrids by inter-Alu-PCR as chromosome-painting probes. XRCC5 is therefore provisionally assigned to human chromosome 2p.

Animals↗
PubMed1987

Identification of nucleotide-excision-repair genes on human chromosomes 2 and 13 by functional complementation in hamster-human hybrids.

The CHO UV-sensitive mutants UV24 and UV135 (complementation groups 3 and 5, respectively) are defective in nucleotide excision repair. After fusing each mutant with human lymphocytes, resistant hybrid clones showing genetic complementation were isolated by repeated exposure to UV radiation. Using a combination of isozyme markers, DNA probes, and cytogenetic methods to analyze the primary hybrids and their subclones, correction of the repair defect was shown to be correlated with the presence of a specific human chromosome in each case. Chromosome 2 corrected UV24, and the gene responsible was designated ERCC3. Line UV135 was corrected by human chromosome 13 and the gene designated ERCC5. The UV-sensitive mouse cell line, Q31, was shown not to complement UV135 and thus appears to be mutated in the same genetic locus (homologous to ERCC5) as UV135. Breakage of complementing chromosomes with retention of the genes correcting repair defects allowed the following provisional assignments: regional localization of ERCC5 to 13q14-q34, exclusion of ERCC3 from the region of chromosome 2 distal to p23, and relief of the ambiguity of ACP1 assignment (2p23 or 2p25) to 2p23 proximal to MDH1.

Animals↗
PubMed1983

Electrophoretically detectable mutations induced in CHO cells by varying doses of ultraviolet radiation.

Chinese hamster ovary (CHO) cells were subjected to ultraviolet radiation (UV) at doses resulting in 100% (no irradiation), 50-30%, 20-10% and approximately 1% survival. 2 divisions after UV exposure surviving cells were cloned and clones expanded for electrophoretic analysis of the products of approximately 40 enzyme loci. 4 different classes of variants (electrophoretic shifts, nulls, enzyme re-expression and enzyme modification) were detected in 29 of 1329 clones analyzed and proven mutants by subclone analysis. The frequency of mutants in the irradiated groups (28/38391 loci screened or 7.3 X 10(-4) was significantly higher than controls. The frequency of shift mutants at 10-20% survival was higher than shifts at 30-50% survival and was significantly higher than shifts at approximately 1% survival. The frequency of nulls increased with dose. 12 of the 28 mutants obtained in the irradiated groups were at only 3 of the mean 41 loci screened/clone. These results indicated that shift mutants could be detected more efficiently than nulls at lower dose and that loci varied widely with respect to their susceptibility to UV mutagenesis. Multiple null mutants at 2 loci, isocitrate dehydrogenase 2 and hexokinase 2, indicated they may be hemizygous in CHO cells.

Animals↗
PubMedDate not supplied

Knee injury in skiing. A multifaceted approach.

During the past four ski seasons, all 1,141 ski injuries which occurred in a large northern Vermont ski area were evaluated prospectively. Of these injuries, 21.6% involved knee ligaments and 18.6% involved sprains of the medial collateral ligament. Females sustained a disproportionately high incidence of Grade I medial collateral sprains, but suffered the more severe sprains at a rate similar to that of males. Individuals who were smaller, younger, less experienced, and less skilled sustained a higher incidence of Grade I injuries. Skiers suffering complete tears of the medial collateral ligament were no smaller, younger, or less skilled or experienced than our control population. Medial collateral sprains are produced primarily by external rotation and valgus forces. Two-mode release bindings are insensitive to several loading configurations which could produce knee sprains. Bindings which allow release in roll, shear, and twist at the heel, as well as twist at the toe and forward lean, appear to be necessary to protect the knee.

Athletic Injuries↗
PubMedDate not supplied

Knee impedance testing machine.

A device is described that measures the mechanical impedance of the human knee in vivo. The device and method were tested in a reliability study, on a normal control population, and in a follow-up test of previously injured subjects. Finally, impedance measurement was compared with the clinical examination, the currently employed test for ligament injuries. This impedance method to measure ligament stiffness was found useful in diagnosing acute injuries.

Biomechanical Phenomena↗