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Biomedical subjects

K C Smith

Publications and source records attributed to K C Smith.

At least 181 records · Page 10Linked to original sources
PubMed1978

Hypoxic cell sensitizers and heavy charged-particle radiations.

Stationary-phase populations of Chinese hamster V-79 cells were irradiated with 250 kV X-rays and the Bragg peaks (spread to a width of 4 cm) of energetic He-, C-, Ne-, and A-ion beams produced at the 184-inch cyclotron and BEVALAC at Lawrence Berkeley Laboratory. Survival curves were generated with each radiation for cells suspended in air-saturated and nitrogen-saturated medium with and without sensitizer present. The oxygen enhancement ratios (OERs) measured for X-rays with 1mM metronidazole and 0.5 mM misonidazole were 2.0 and 1.6 respectively. The OERs without sensitizer for He-, C-, Ne-, and A-ion Bragg peaks were 2.4, 1.7, 1.6 and 1.4 respectively. For each type of radiation tested the presence of hypoxic-cell sensitizers resulted in an additional reduction in the measured OERs, indicating that these drugs should be of benefit in the radiotherapy planned with these and other high LET radiations.

Cell Survival↗
PubMed1978

Multiple pathways of DNA repair and their possible roles in mutagenesis.

In studies on bacteria, the excision repair of UVR-induced DNA base damage has been divided into two major pathways on the basis of physiologic requirements and genetic control. The major pathway requires a functional polA+ gene, does not need complete growth medium, is largely error free, and produces short patches during repair. The second pathway requires complete growth medium and functional recA+, recB+, recC+, lexA+, uvrD+, and polC+ genes, is mutagenic, and produces long patches during repair. A second type of ecision repair exists, in which the modified base is removed by a DNA glycosylase, and the chain is nicked by an apurinic (apyrimidinic) acid endonuclease. Subsequent events are presumed similar to the above excision repair process. The postreplication repair system has been divided into at least four distinct pathways, three of which depend on functional recB+, lexA+, and uvrD+ genes, and are error free. A fourth pathway depends on the above gene products but is blocked by postirradiation treatment with chloramphenicol, and may be the UV-inducible, error-prone, mutagenic pathway of repair ("SOS repair"). A possible fifth pathway is dependent on a functional recF+ gene and is independent of the recB+-dependent pathway. Mutagenesis is the result of error-prone DNA repair, and evidence is growing that carcinogenesis is also the result of error-prone repair. Therefore, a complete understanding of DNA repair is crucial to a complete understanding of the molecular basis of carcinogenesis.

DNA Ligases↗
PubMed1977

The involvement of polynucleotide ligase in the repair of UV-induced DNA damage in Escherichia coli K-12 cells.

The effect of the ligts-7 mutation on cell survival and the extent of DNA repair after UV (254 nm) irradiation was determined for wild-type and uvrB5 cells of E. coli K-12 at 30 degrees and 42 degrees C. At the restrictive temperature (42 degrees C) the ligts-7 mutation resulted in (i) a decrease in the extent of repair of DNA incision breaks arising during the excision repair process, and (ii) a decrease in the extent of post-replicational repair of gaps in newly-synthesized DNA. These deficiencies in DNA repair correlated with increases in cellular sensitivity to killing by UV radiation. Thus, DNA lagase plays an important role in vivo in both the excision and post-replicational repair processes.

DNA Repair↗
PubMed1977

Influence of a uvrD mutation on survival and repair of X-irradiated Escherichia coli K-12 cells.

The presence of a uvrD mutation increased the X-ray sensitivities of E. coli wild-type and polA strains, but had no effect on the sensitivities of recA and recB strains, and little effect on a lexA strain. Incubation of irradiated cells in medium containing 2,4-dinitrophenol or chloramphenicol decreased the survival of wild-type and uvrD cells, but had no effect on the survival of recA, recB and lexA strains. Alkaline sucrose gradient sedimentation studies indicated that the uvrD strain is deficient in the growth-medium-dependent (Type III) repair of DNA single-strand breaks. These results indicate that the uvrD mutation inhibits certain rec+lex+-dependent repair processes, including the growth-medium-dependent (Type III) repair of X-ray-induced DNA single-strand breaks, but does not inhibit other rec+lex+-dependent processes that are sensitive to 2,4-dinitrophenol and chloramphenicol.

Cell Survival↗
PubMed1977

Sensitization of Escherichia coli C to gamma-radiation by 5-bromouracil incorporation.

Escherichia coli C cells, unifilarly substituted with 5-bromouracil (BrUra) were 2-25 times as sensitive as unsubstituted cells to killing by gamma-irradiation under aerobic conditions. The yield of DNA double-strand breaks in BrUra-substituted cells was increased by a factor only 1-55, suggesting that other lesions also contribute to cell-killing. Alkaline sucrose density gradient analysis of the 3H-thymine labelled DNA strand showed there was less repair of gamma-ray-induced single-strand breaks when BrUra was in the complementary strand. Since there are more of these unrepaired breaks than can be accounted for by BrUra-induced DNA double-strand breakage, some fraction of the lethal events in BrUra-substituted E. coli cells may be unrepaired DNA single-strand breaks.

Bromouracil↗
PubMed1976

Measurement of the pre-ejection period during labor with the use of arterial pulse time.

A new fetal parameter, the arterial pulse time, is described. It is the time from the onset of the fetal electrocardiographic recording to the arrival of the arterial pulse wave recorded at the fetal head. Since arterial pulse time differs from the pre-ejection period by only an apparently constant value, it is proposed as a potential method for obtaining the pre-ejection period during labor.

Arteries↗