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Biomedical subjects

G M Jones

Publications and source records attributed to G M Jones.

At least 91 records · Page 5Linked to original sources
PubMed1986

Cytomorphologic evaluation of the neoplastic potential of 28 cell culture lines by a panel of diagnostic cytopathologists.

A panel of 7 diagnostic cytopathologists, i.e., physicians trained to diagnose the malignant potential of human cells in Papanicolaou-stained smears, was asked to evaluate two sets of microscope slides of stained coverslip preparations of 28 cell culture lines, 15 of which were neoplastic. Slide Set I consisted of 13 pairs of cell lines, one member of each pair being nontumorigenic and the other tumorigenic; the lines were of mouse (9 pairs), rat (3 pairs), and human (1 pair) origin. Slide Set II contained 4 human lines: one lung cancer, one melanoma, and two fibroblast lines. Of a total of 114 diagnostic decisions by the panel, 88 were correct (66/86, 77%) in choosing which member of a pair was neoplastic and 22 were correct (22/28, 79%) in choosing whether a given individual human line was or was not neoplastic. Two members of the panel were correct more frequently, with 16/17 (94%) correct diagnoses, each. Five nuclear morphologic criteria of malignancy used by cytopathologists were prominent in the tumorigenic lines: altered chromatin pattern characterized by increasing size of chromatin granules and chromatin clumping, sharp angularity of large nucleolar and/or chromocenter borders with spicule formation (pointed projection), irregular parachromatin clearing (increase in the clarity of the clear spaces between chromatin threads, granules and clumps), uneven thickness of chromatin at the nuclear border, and variability in nuclear size and shape from cell to cell. These markers of neoplastic transformation, when added to those previously reported, should increase overall accuracy in the diagnosis of neoplastic transformation of mammalian cells in culture.

Animals↗
PubMed1986

A splint for the unstable zygomatic arch fracture.

A case report is presented in which circumferential wires tied over a short length of anaesthetic tubing on the face were used for the fixation of an unstable fracture of the zygomatic arch.

Equipment Design↗
PubMed1986

Chromosomal radiosensitivity during the G2 cell cycle period and cytopathology of human normal x tumor cell hybrids.

The relationship between tumorigenicity and enhanced chromosomal radiosensitivity during the G2 cell cycle phase was examined through the use of nontumorigenic human cell hybrids and their nontumorigenic and tumorigenic segregants. The hybrid cells were produced by fusion of a normal and tumor cell. The parental lines, including HeLa and three fibroblast lines, one of skin and two of fetal lung origin, were also examined. The tumorigenic lines, which had cytological features associated with clinical cancer, showed a significantly higher incidence of chromatid breaks and gaps following X-irradiation during G2 than the normal skin line or the nontumorigenic hybrids. The hybrids and their nontumorigenic subclones had cytological features which are predominantly found with a benign clinical course and had the G2 chromosomal radiosensitivity more characteristic of the normal parental cells. Like tumorigenic cells, fetal cells exhibited enhanced G2 chromosomal radiosensitivity which could be suppressed in fetal X tumor cell hybrids. This observation suggests that the molecular basis for radiosensitivity in fetal cells differs from that of tumor cells. The enhanced G2 chromosomal radiosensitivity of a tumor cell, which appears to result from deficient DNA repair, is suppressed by fusion with a normal cell. Thus, the radiosensitivity, like tumorigenicity, behaves as a recessive trait. Although a Mendelian analysis is not possible with this material, the segregation of enhanced G2 chromosomal radiosensitivity with the neoplastic phenotype suggests that the two may be genetically linked.

Cell Line↗
PubMed1985

G2 chromosomal radiosensitivity of ataxia-telangiectasia heterozygotes.

Five lines of skin fibroblasts from individuals heterozygous for ataxia-telangiectasia (A-T), compared with six cell lines from age-matched normal controls, show a much higher frequency of chromatid breaks and gaps following x-irradiation during the G2 phase of the cell cycle. The magnitude of this difference suggests that G2 chromatid radiosensitivity could provide the basis for an assay to detect A-T heterozygotes. Though clinically normal, A-T heterozygotes share a high risk of cancer with A-T homozygotes and constitute approximately 1% of the human population. Further, we propose that G2 chromosomal radiosensitivity, which appears to result from a DNA repair deficiency, may be associated with a genetic predisposition to cancer.

Ataxia Telangiectasia↗
PubMed1985

The response of small blood vessels in rat skin and skeletal muscle to repeated application of histamine: a chemical, topographical and electron microscopic study.

Quantitative studies of increased vascular permeability, employing vascular labelling with colloidal carbon and measurement of the rate of escape of intravascular 99Tc labelled antimony sulphide (Sb2S3) colloid, show that local injection of histamine into the skin or cremaster muscle of rats reduces for a period of 6-8 h the leakage induced by a second injection of histamine into the same site. Electron microscope studies employing multiple marker particles show that individual blood vessels are able to respond to two successive applications of histamine, and that the diminished leakage seen after the second injection is due to a reduced response of individual vessels and not to leakage from vessels unaffected by the first injection. Prior administration of bradykinin does not reduce the response to local injection of histamine into rat skin. The result suggest that sustained release of histamine is unlikely to be important in the production of prolonged increase in vascular permeability in acute inflammation. Bradykinin may be involved in such response but the findings provide no evidence for its participation.

Animals↗
PubMed1985

Chromatid damage induced by fluorescent light during G2 phase in normal and Gardner syndrome fibroblasts. Interpretation in terms of deficient DNA repair.

Skin fibroblasts from Gardner syndrome (GS) compared with those from normal donors showed a significantly higher incidence of chromatid gaps and breaks following exposure to low-intensity, cool-white fluorescent light during G2 phase of the cell cycle. Considerable evidence supports the concept that chromatid gaps and breaks seen directly after exposure to DNA-damaging agents represent unrepaired DNA single- and double-strand breaks respectively. The changes in incidence of chromatid aberrations with time after light exposure are consistent with the sequence of events known to follow DNA damage and repair. Initially, the incidence of light-induced chromatid gaps was equivalent in GS and normal fibroblasts. In the normal cells, the chromatid gaps disappeared by 1 h post-exposure, presumably as a result of efficient repair of DNA single-strand breaks. In contrast, the incidence of gaps increased in GS cells by 0.5 h followed by a decrease at 1 h and concomitant increase in chromatid breaks. It appears from these findings that the increased incidence of chromatid damage in GS fibroblasts results from deficient repair of DNA single-strand breaks which arise from incomplete nucleotide excision of DNA damage during G2 phase.

Cells, Cultured↗
PubMed1985

Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture.

The generation of hydrogen peroxide (H2O2) and the derivative free hydroxyl radical (. OH) in cultures of mouse cells grown in the presence of visible light and ambient oxygen was shown previously to be implicated in chromatid damage. Furthermore, chromosome alterations appear to be associated with the spontaneous neoplastic transformation of mouse cells in culture. An attempt was made in this study to reduce the incidence of chromosomal aberrations and delay or prevent the onset of spontaneous neoplastic transformation of freshly isolated mouse cells, both fibroblasts and epidermal keratinocytes, by adding catalase to the culture medium, shielding the cultures from wavelengths less than 500 nm and providing a gas phase of 0-1% O2. These conditions significantly decreased the incidence of chromosomal aberrations in both cell types, and in fibroblasts prevented tumourigenicity in non-irradiated syngeneic mice, and increased latent periods for tumour development in X-irradiated mice. The epidermal keratinocytes were particularly resistant to spontaneous neoplastic transformation under all conditions tested. These observations on the protective effect of extracellular catalase suggest that H2O2, a normal metabolite, and/or the derivative .OH can directly or indirectly produce genetic damage and neoplastic transformation in mouse fibroblasts.

Animals↗
PubMed1985

Chromosomal radiosensitivity during the G2 cell-cycle period of skin fibroblasts from individuals with familial cancer.

We reported previously that human cells after neoplastic transformation in culture had acquired an increased susceptibility to chromatid damage induced by x-irradiation during the G2 phase of the cell cycle. Evidence suggested that this results from deficient DNA repair during G2 phase. Cells derived from human tumors also showed enhanced G2-phase chromosomal radiosensitivity. Furthermore, skin fibroblasts from individuals with genetic diseases predisposing to a high risk of cancer, including ataxia-telangiectasia, Bloom syndrome, Fanconi anemia, and xeroderma pigmentosum exhibited enhanced G2-phase chromosomal radiosensitivity. The present study shows that apparently normal skin fibroblasts from individuals with familial cancer--i.e., from families with a history of neoplastic disease--also exhibit enhanced G2-phase chromosomal radiosensitivity. This radiosensitivity appears, therefore, to be associated with both a genetic predisposition to cancer and a malignant neoplastic state. Furthermore, enhanced G2-phase chromosomal radiosensitivity may provide the basis for an assay to detect genetic susceptibility to cancer.

Adolescent↗
PubMed1985

Paramoeba sp. (Amoebida, Paramoebidae) as the possible causative agent of sea urchin mass mortality in Nova Scotia.

An amoeba resembling Paramoeba has been cultured from tissues of diseased sea urchins. Cultures containing the amoeba produced signs of the disease when injected into the coelom of healthy urchins. Control treatments lacking the amoeba did not cause the disease. The amoeba was cultured from radial nerve fragments and seen in tissue sections from experimentally infected urchins. Cultures of the amoeba from these experimentally infected urchins reproduced the disease in healthy urchins by both injection and water-borne routes. These observations suggest involvement of Paramoeba in recent mass mortalities of sea urchins in Nova Scotia.

Amoeba↗
PubMed1984

Are patients with abnormal cervical smears adequately managed?

The outcome was assessed for all 1062 women in Nottingham who had a first report of abnormal cervical cytology in 1981. Satisfactory follow up could be found for only 628 (59%) of them. For 275 (26%) one subsequent normal smear had been reported but no further follow up requested. For 43 (4%), no subsequent test, after the abnormal smear, had been requested by the patient's general practitioner. Thirty patients (3%), 22 of whom had been tested at a special clinic, had not responded to a request for follow up. Even after extensive efforts we could not find the outcome in the remaining 86 (8%) of the patients. Adequate follow up of patients with abnormal cervical cytology is not being achieved. Improvements in the records systems and some changes in procedure should be made to reduce this problem.

Adult↗