Search PubMed⌕ Search

Biomedical subjects

C Kidson

Publications and source records attributed to C Kidson.

At least 127 records · Page 7Linked to original sources
PubMed1980

Development of sensitivity to acetylcholine in cultured chick embryo sympathetic ganglion neurones.

Dissociated sympathetic neurones from chick embryos of various ages were maintained in culture for several days and changes in sensitivity to iontophoretically applied acetylcholine (ACh) measured over 5 days in vitro. Neurones from 12-day embryos show a marked increase in ACh sensitivity, neurons from 14-day embryos a smaller change and those from 19-day embryos do not alter. These changes parallel those observed previously for binding of [125I]alpha-bungarotoxin.

Acetylcholine↗
PubMed1980

Diseases of DNA repair.

A number of disparate clinical syndromes have been loosely grouped together under the leading of diseases of DNA repair. More logically they should perhaps be termed diseases of diminished capacity to cope with DNA damage, since in only three has defective DNA repair been established as a basis so far. These are xeroderma pigmentosum, ataxia telangiectasia and Fanconi's anaemia. Increased sensitivity may be to radiation, to particular types of chemical mutagens, or to both. This sensitivity may be reflected in an increased liability to chromosome aberrations, decreased cell survival in culture and, in some cases only, increased mutagenesis. In many cases there is an associated increased liability to develop malignant tumours. These syndromes are genetically autosomal recessive so that it is the relatively rare homozygotes which display the full clinical picture. In some cases, however, the heterozygotes share the increased liability to cancer: since these are of relatively high frequency, they may be quantitatively important in the genetics of some human cancers including leukaemias. Immunological abnormalities are common and frequently are selective. This suggests the possibility that the repair systems whose defects are monitored by decreased capacity to cope with DNA damage may also perform functions essential to differentiation during embryonic development. At a molecular level knowledge of the fundamental defects in each of these groups of human mutants is still rudimentary. There is sufficient evidence, however, to conclude that each group is genetically heterogeneous, involving more than one gene locus, so that the total number of genes involved is probably large.

Adult↗
PubMed1980

Plasmodium falciparum strains from Papua New Guinea: culture characteristics and drug sensitivity.

Seven strains of Plasmodium falciparum from Papua New Guinea have been established in continuous in vitro culture. Samples with a high initial parasitaemia were more likely to form continuous lines, possibly due to the time required for transport of infected blood samples from Papua New Guinea to laboratories in Australia. Most but not all established lines were resistant to chloroquine and all were resistant to pyrimethamine, possibly reflecting the parasite strain characteristics in that region.

Adolescent↗
PubMed1979

Quantitation of DNA repair in brain cell cultures: implications for autoradiographic analysis of mixed cell populations.

Quantitation of DNA repair in the mixed cell population of mouse embryo brain cultures has been assessed by autoradiographic analysis of unscheduled DNA synthesis following UV-irradiation. The proportion of labelled neurons and the grain density over neuronal nuclei are both less than the corresponding values for glial cells. The nuclear geometries of these two classes of cell are very different. Partial correction for the different geometries by relating grain density to nuclear area brings estimates of neuronal and glial DNA repair synthesis more closely in line. These findings have general implications for autoradiographic measurement of DNA repair in mixed cell populations and in differentiated versus dividing cells.

Animals↗
PubMed1978

Cell fusion induced by scrapie and Creutzfeldt-Jakob virus-infected brain preparations.

Cell fusion was induced by brain extracts containing the scrapie virus and the virus of Creutzfeldt-Jakob disease. The assay involved quantitation of colony-forming ability in a double selection system, strandardized against fusion induced by Sendai virus. Correlation between the logarithm of virus dilution and the hybrid colony number gave similar curves for scrapie virus and Sendai virus. Fusion induction may explain some aspects of pathogenesis in these diseases and provide a potential in vitro assay.

Animals↗
PubMed1978

Dependence on cloning method of survival of human melanoma cells after ultraviolet and ionizing radiation.

The resistance of a human melanoma cell line (MM96) to both ultraviolet and ionizing irradiation was compared by two different methods of cloning, on plates and in agar. A high level of resistance to both ultraviolet (D0 = 320 ergs/sq mm) and ionizing irradiation (D0 = 4300 rads) was observed when viability of cells was determined by cloning in agar. In contrast, melanoma cells were found to be as sensitive as were other cells when viability after irradiation was determined by cloning on plastic plates. The difference in sensitivity to radiation between the two methods of cloning can be explained in a model involving damage to membranes as well as to DNA. At least for ionizing radiation, this effect is not restricted to melanoma cells since a HeLa subline, HeLa-QB1, showed a similar response. In contrast, a human lymphoblastoid line (JHP) cloned in agar was sensitive under these conditions (D0 = 120 rads).

Agar↗
PubMed1977

DNA replication and repair in a human melanoma cell-line resistant to ultra-violet-radiation.

The effect of ultra-violet (U.V.)-irradiation on DNA replication was studied in a U.V.-resistant, human melanoma cell-line (MM96). Semi-conservative synthesis of DNA was decreased about five-fold by a U.V.-dose of 100 ergs/mm2. The size of DNA fragments synthesized in irradiated cells at short times after U.V. was smaller than those synthesized in unirradiated cells. Elongation of these fragments occurred with time, and 6 hours after irradiation cells synthesized DNA in fragments of the same size as obtained in unirradiated cells. In this post-replication repair process, elongation appeared to involve de novo synthesis and was not inhibited by theophylline.

Cell Line↗
PubMed1977

Repair of ionizing radiation induced DNA damage in human lymphocytes.

Phytohemagglutinin stimulated human lymphocytes exhibit a 20 fold increase in DNA repair synthesis following ionizing radiation damage compared to the level of repair in unstimulated cells. The peak of repair synthesis coincides with that for DNA replication. Stimulated lymphocytes provide a relatively simple assay for ionizing radiation repair defects.

DNA↗
PubMed1977

Differential radiosensitivity of mouse embryonic neurons and glia in cell culture.

The responses of neurons and glial cells to ultraviolet and gamma-radiation were studied in cell cultures of embryonic mouse brains. A decrease in the ratio of glia to neurons occurred after both forms of irradiation. [3H]thymidine labelling followed by autoradiography revealed that all glia were capable of replication wereas 70% of neurons were non-replicating under the conditions of the study. Ultraviolet radiation caused a decrease in the proportion of replicating neurons but did not affect the proportion of replicating glia, whereas gamma-radiation caused a decrease in DNA replication in both cell types. Levels of ultraviolet radiation-induced unscheduled DNA synthesis were lower in neurons than in glia. It is concluded that sensitivity to both ionizing and ultraviolet radiation of neurons and glial cells in embryonic brain cultures is determined primarily by the capacity for and state of DNA replication. Neurons which have already reached the stage of ternimal differentiation are more resistant than replicating neurons of glial cells.

Animals↗
PubMed1976

Aminoacyl-tRNA conformation. Information from steroid and oligonucleotide probes.

The conformations of aminoacyl- and deacylated tRNA Phe (yeast) have been compared by using the steroid progesterone and the tetranucleotides U-C-C-C and C-G-A-A as probes of transfer RNA ordered structure. U-C-C-C is complementary to G18-G19-G20-A21 in the dihydrouridine loop and C-G-A-A is complementary to T54-psi55-C56-G57 in the ribosylthymine loop. None of the probes bound to deacylated tRNA Phe but all three bound to phenylalanyl-tRNA Phe, with molar association constants of the order of 10(4) M-1. The oligonucleotide binding data imply that the tertiary hydrogen bonds between G18 and psi55, G19 and C56, T54 and m1A58, and A21 and the ribose of U8 (Quigley, G. J., Wang, A. H. J., Seeman, N. C., Suddath, F. L., Rich, A., Sussman, J. L., and Kim, S. H., (1975) Proc. Natl. Acad. Sci. U.S.A. 72, 4866-4870) are destabilized or broken on aminoacylation, unmasking the sequence T-psi-C-G thought to be involved in ribosome binding of aminoacyl-tRNA. The presumed progesterone binding site is G18-G19-G20, which is part of the binding site for U-C-C-C. Competition was not, however, observed between these two probes; model building has shown that they could, theoretically, bind simultaneously. Since progesterone bound to N-acetyl-Phe-tRNA Phe, the introduction of the additional positive charge on aminoacylation is not sufficient per se to explain the conformational change. The association of progesterone with peptidyl-tRNA Phe was similar to that with aminoacyl-tRNA Phe, implying that no further conformational change takes place in the region of the steroid binding site on formation of a peptide bond.

Binding Sites↗
PubMed1976

A mammalian nicking endonuclease.

Purification and properties are described for an endonuclease isolated from calf thymus which attacks double-stranded, unmodified DNA, primarily by making single-strand breaks. No detectable acid-soluble products arise from the reaction. Double-strand breaks may occasionally be produced by the introduction of single-strand breaks on opposite strands in close proximity. The enzyme does not attack denatured DNA and is not inhibited by tRNA. Although added divalent cations are not required for activity, the enzyme is inhibited by EDTA, which suggests an essential role for bound cations; reaction is inhibited by Ca2+. The endonuclease has a broad pH optimum and is inactivated by preincubation at temperatures of 45 degrees C and higher. The molecular weight as determined by gel chromatography is about 30 000. Analysis of the products of reaction on a defined substrate, bacteriophage T3 DNA, by sedimentation in alkaline sucrose density gradients indicates limit products with chain lengths of about 0.8 X 10(6) daltons. On electrophoresis in agarose gels these products were shown to be heterogeneous in size. The endonuclease appears to generate 3'-hydroxyl and 5'-phosphate ends. The ability of the endonuclease to utilize bovine DNA as substrate argues against a restriction role for this enzyme.

Animals↗
PubMed1976

Control of DNA repair linked to neuroblastoma differentiation.

Mouse neuroblastoma cells, which can be induced to undergo reversible differentiation in culture, have been used as a model to investigate the effects of ultra-violet (U.V.) radiation on terminally-differentiated nerve cells. Differentiated neuroblastoma cells were found to be extremely sensitive to U.V.-radiation when compared with proliferating cells from the same clone. However, normal resistance was regained if the differentiated cells were allowed to proceed to the next G1 phase of the cell-cycle before irradiation. Neuroblastoma cells in the differentiated mode are capable of carrying out soem excision repair of DNA damage, but they appear to lack a repair mechanism present in proliferating cells.

Cell Division↗