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Biomedical subjects

K C Smith

Publications and source records attributed to K C Smith.

At least 145 records · Page 8Linked to original sources
PubMed1985

Percutaneous trephine biopsy of the vertebral body in the rhesus monkey (Macaca mulatta).

Two methods of percutaneous vertebral body biopsy were performed in the Rhesus monkey, using a 3-mm diameter trephine and a pneumatic driver placed at a 30 degrees angle of approach to the transverse plane of the spine. The freehand method involved placing needle landmarks in the spine, followed by examination of a lateral radiograph of the lumbar region to verify landmark positioning and to estimate placement of the trephine. In the 2nd method, a pneumatic trephine guide was oriented according to a trigonometric calculation based on radiographic data. The pneumatic trephine guide allowed precise placement of the driver and steadied the trephine as it passed through the bone.

Anesthesia, General↗
PubMed1984

umuC-dependent and umuC-independent gamma- and UV-radiation mutagenesis in Escherichia coli.

The effects of the umuC36 and umuC122::Tn 5 mutations on gamma- and UV radiation mutagenesis (nonsense, missense, and frameshift mutation assays) in Escherichia coli K12 were studied. Although both mutations reduced radiation mutagenesis, the umuC36 mutation appeared to be leaky since considerably more UV radiation mutagenesis could be detected in the umuC36 strain than in the umuC122::Tn 5 strain. In general, the umuC strain showed much larger deficiencies in UV radiation mutagenesis than they did for gamma-radiation mutagenesis. The mutability of the umuC122:: Tn 5 strain varied depending on the radiation dose, and the mutation assay used. For gamma-radiation mutagenesis, the deficiency varied from no deficiency to a 50-fold deficiency; for UV radiation mutagenesis, the deficiency varied from 100-fold to at least 5000-fold. We concluded that both umuC-dependent and umuC-independent modes function for gamma-radiation mutagenesis, while UV radiation mutagenesis seems to depend almost exclusively on the umuC-dependent mode.

DNA Repair↗
PubMed1984

A meta-analytic comparison of the Beck Depression Inventory and the Hamilton Rating Scale for Depression as measures of treatment outcome.

Some clinicians have considered the Beck Depression Inventory, a self-rating scale, too reactive to patient halo effects and, therefore, a liberal measure of treatment outcome. On the other hand, interviewer-rating scales, like the Hamilton Rating Scale for Depression have been viewed as more conservative measures of treatment gain. Studies which compared the Beck Depression Inventory to the Hamilton Rating Scale, as dependent measures, were reviewed for the purpose of determining if the scales provided comparable data for assessing treatment effects. The use of meta-analysis techniques resulted in a comparison of effect sizes which indicated that the Beck Depression Inventory was significantly less liberal than the Hamilton Rating Scale for Depression. The implications of these results for selecting outcome measures and the application of meta-analysis techniques for comparing dependent measures are discussed.

Bipolar Disorder↗
PubMed1984

recF-dependent and recF recB-independent DNA gap-filling repair processes transfer dimer-containing parental strands to daughter strands in Escherichia coli K-12 uvrB.

The processes for repairing DNA daughter-strand gaps were studied in UV-irradiated uvrB, uvrB recB, uvrB recF, and uvrB recB recF cells of Escherichia coli K-12. The dimer-containing parental DNA was found to be joined to daughter strands during postreplication repair in all four strains examined. Therefore, both the major (recF-dependent) and the minor (recF recB-independent) gap-filling processes repair DNA daughter-strand gaps by transferring parental strands into daughter strands.

DNA Repair↗
PubMed1984

Characterization of a new radiation-sensitive mutant, Escherichia coli K-12 radC102.

A new radiation-sensitive mutant, radC , has been isolated. The radC gene is located at 81.0 min on the Escherichia coli K-12 linkage map. The radC mutation sensitized cells to uv radiation, but unlike most DNA repair mutations, sensitization to X rays was observed only for rich medium-grown cells. For cells grown in rich medium, the radC mutant was normal for gamma-radiation mutagenesis, but showed less uv-radiation mutagenesis than the wild-type strain; it showed normal amounts of X- and uv-radiation-induced DNA degradation, and it was approximately 60% deficient in recombination ability. The radC strain was normal for host cell reactivation of gamma-and uv-irradiated bacteriophage lambda; the radC mutation did not sensitize a recA strain, but did sensitize a radA and a polA strain to X and uv radiation and a uvrA strain to uv radiation. Therefore, we suggest that the radC gene product plays a role in the growth medium-dependent, recA gene-dependent repair of DNA single-strand breaks after X irradiation, and in postreplication repair after uv irradiation.

Cell Survival↗
PubMed1983

New mutation (mmrA1) in Escherichia coli K-12 that affects minimal medium recovery and postreplication repair after UV irradiation.

After UV irradiation, Escherichia coli uvrA mutant cells show higher survival on minimal than on rich growth medium, i.e., they show minimal-medium recovery. This effect of rich growth medium on survival is not observed in a uvrA mutant carrying an mmrA1 mutation, and the uvrA mmrA strain showed the same survival rate on minimal and rich growth media as the uvrA strain did on minimal medium plates. The mmrA1 mutation was isolated as a hidden mutation from a uvrA polA mutant strain and shown to map at 84.3 min on the E. coli K-12 linkage map. In contrast to the uvrA strain, the repair of DNA daughter strand gaps was not inhibited in the uvrA mmrA strain by rich growth medium after irradiation. However, the uvrA and uvrA mmrA strains were similar in their ability to repair DNA when compared in minimal medium. These data are consistent with the idea that the mmr gene product is not involved directly in the repair of UV radiation-induced DNA damage, but rather allows rich growth medium to inhibit a portion of postreplication repair.

Chromosome Mapping↗
PubMed1983

Mechanisms for recF-dependent and recB-dependent pathways of postreplication repair in UV-irradiated Escherichia coli uvrB.

The molecular mechanisms for the recF-dependent and recB-dependent pathways of postreplication repair were studied by sedimentation analysis of DNA from UV-irradiated Escherichia coli cells. When the ability to repair DNA daughter strand gaps was compared, uvrB recF cells showed a gross deficiency, whereas uvrB recB cells showed only a small deficiency. Nevertheless, the uvrB recF cells were able to perform some limited repair of daughter strand gaps compared with a "repairless" uvrB recA strain. The introduction of a recB mutation into the uvrB recF strain greatly increased its UV radiation sensitivity, yet decreased only slightly its ability to repair daughter strand gaps. Kinetic studies of DNA repair with alkaline and neutral sucrose gradients indicated that the accumulation of unrepaired daughter strand gaps led to the formation of low-molecular-weight DNA duplexes (i.e., DNA double-strand breaks were formed). The uvrB recF cells were able to regenerate high-molecular-weight DNA from these low-molecular-weight DNA duplexes, whereas the uvrB recF recB and uvrB recA cells were not. A model for the recB-dependent pathway of postreplication repair is presented.

DNA Repair↗
PubMed1983

The effect of growth conditions on inducible, recA-dependent resistance to X rays in Escherichia coli.

Escherichia coli cells grown to logarithmic phase in, and plated on, rich medium (yeast extract-nutrient broth) were more resistant to X rays, ultraviolet (uv) radiation, and methyl methanesulfonate (MMS) than cells grown in, and plated on, minimal medium. We have called this enhanced survival capability medium-dependent resistance (MDR). The magnitude of MDR observed after oxic X irradiation was greater than that observed after anoxic X irradiation, uv irradiation, or MMS treatment. MDR was not observed in stationary-phase cells with X or uv radiation. MDR was associated with an increased ability to repair X-ray-induced DNA single-strand breaks, and with reduced X-ray-induced DNA degradation and protein synthesis retardation. Postirradiation protein synthesis was concluded to be critical in allowing the high X-ray survival associated with MDR, because of the large radiosensitization caused by a postirradiation growth medium shift down or treatment with rifampicin (RIF), recA protein must be at least one of the proteins whose synthesis is critical to MDR, as judged by the absence of MDR or a RIF effect in X-irradiated recA and lexA mutants. The results with X-irradiated temperature-conditional recA cells suggest that it is only after cells have been damaged that the recA gene plays a role in MDR.

Bacterial Proteins↗
PubMed1983

Characterization of an Escherichia coli mutant (radB101) sensitive to gamma and uv radiation, and methyl methanesulfonate.

After N-methyl-N'-nitro-N-nitrosoguanidine mutagenesis of Escherichia coli K-12 (xthA14), and X-ray-sensitive mutant was isolated. This sensitivity is due to a mutation, radB101, which is located at 56.5 min on the E. coli K-12 linkage map. The radB101 mutation sensitized wildtype cells to gamma and uv radiation, and to methyl methanesulfonate. When known DNA repair-deficient mutants were ranked for their gamma-radiation sensitivity relative to their uv-radiation sensitivity, their order was (starting with the most selectively gamma-radiation-sensitive strain): recB21, radB101, wild type, polA1, recF143, lexA101, recA56, uvrD3, and uvrA6. The radB mutant was normal for gamma- and uv-radiation mutagenesis, it showed only a slight enhancement of gamma- and uv-radiation-induced DNA degradation, and it was approximately 60% deficient in recombination ability. The radB gene is suggested to play a role in the recA gene-dependent (Type III) repair of DNA single-strand breaks after gamma irradiation and in postreplication repair after uv irradiation for the following reasons; the radB strain was normal for the host-cell reactivation of gamma- and uv-irradiated bacteriophage lambda; the radB mutation did not sensitize a recA strain, but did sensitize a polA strain to gamma and uv radiation; the radB mutation sensitized a uvrB strain to uv radiation.

Chromosomes, Bacterial↗