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Biomedical subjects

P I Good

Publications and source records attributed to P I Good.

8 recordsLinked to original sources
PubMed1979

Detection of a treatment effect when not all experimental subjects will respond to treatment.

Non-responders attenuate average response an inflate sample variance, reducing the power of standard parametric tests. A new Fisher's type randomization test, which has no parametric analogue, is recommended when not all subjects may be capable of responding to treatment. The new test was evaluated by Monte Carlo means and applied to drug abuse data and to virus titre data. In most trial applications the new test proved to be more sensitive to treatment effects than Student's t.

Animals↗
PubMed1978

A comparison of two methods for evaluating drug-induced chromosome alterations.

Evaluating the technique and procedure for mutagenicity testing in mammals is a prerequisite to the development of a broad spectrum mutagenic assessment program. Two techniques, chromosome examination and micronucleus scoring, show promise but their applicability for mass screening is uncertain. We determined the slide observation time for these two techniques in mice treated orally, subcutaneously, intravenously, and intraperitoneally with cyclophosphamide (CY). In each instance, we detected a dose-response in less observation time by counting micronuclei in polychromatophilic erythrocytes. The simplicity of the scoring method, the ease of micronucleus identification and the rapidity of scoring all suggest the micronucleus test may be favorably integrated into a mutagenicity screening program.

Animals↗
PubMed1976

Reduced humoral immune activity in long-lived old mice: an approach to elucidating its mechanisms.

Spleen cells from young (3-5 months) and old (22-27 months) mice were assessed in cultures, both in vivo and in vitro, for their anti-sheep RBC response separately and in mixtures. Pooled young spleens, pooled old spleens, and individual old spleens were analysed. The response of pure young spleen cells was always higher than that of pure old spleen cells (approximately 30 times). The responses of mixtures were either less than (i.e. reduced; frequency approximately 65%), comparable to (i.e. additive; frequency approximately 10%), or greater than (i.e. elevated; frequency approximately 30%) the sum of the responses given by equivalent numbers of pure young and pure old spleen cells. The reduced response was observed in mixtures containing cells from histologically normal old spleens, old spleens with tumours and old spleens with atrophic follicles. Additive and elevated responses were observed only in mixutres containing cells from histologically normal old spleens. The reduced response is explicable in terms of excessive numbers of suppressor cells in old spleens that can prevent young immunocompetent cells from responding maximally to the test antigen. The additive response can be accounted for by a reduction in number of immunocompetent cells in old spleens and/or a decrease in their functional efficiency. The elevated response can be explained by a reduction in number of at least one type of immunocompetent cell in old spleens that exists in excess in young spleens. These results indicate that there are several types of cellular changes responsible for the decrease in humoral immune activity in old mice. Pooling of old spleens, as was commonly done in the past, should therefore be discouraged. Not only might it selectively favour the expression of old spleens with an excess of supressor cells but it conceivably could result in an elevated response.

Aging↗
PubMedDate not supplied

Aging in mammalian cell population: a review.

Research on in vitro aging and development is reviewed within a framework provided by three aspects of population growth--birth, canalization and death. Although there are periodic changes in the birth rate coupled to periodic changes in the in vitro environment, there do not appear to be any age-related changes in the birth rate of dividing cells. There appear to be distinct subpopulations of dividing and nondividing cells, each with its own characteristic morphological and functional properties; thus, Weiss-Kavanaugh theory may be applicable to the growth, maturation and senescence of mammalian cell populations. Substantial cell losses occur during subcultivation and transfer; correction for these losses requires substantial reinterpretation of existing experimental findings. The various measures of age are poorly correlated with one another; there is wide variation from population to population. A uniform measure of age has been found in the cell generation, the number of ancestors of a given cell. Studies of intrinsic variation in development can provide additional insight into the developmental process. The framework of birth, canalization and death permits reduction in the number of competing hypotheses of aging in mammalian cell populations. Additional experimental evidence is needed to discriminate among the remaining hypotheses.

Aging↗
PubMedDate not supplied

Colony size distribution as a measure of age in cultured human cells. A brief note.

Individual human diploid cells from the same culture differ greatly in the number of doublings they can achieve and consequently the size of colony they can initiate. Computer simulations suggested that the life-span of a culture could be determined from the distribution of colony sizes. Colony size distributions of cultures of a human diploid fibroblast, WI-38, were determined experimentally and found to be a sensitive measure of in vitro age. In particular, there is a highly significant linear correlation between the percentage of colonies of sixteen or more cells and the number of population doublings remaining in the in vitro life-span. Thus, the colony size distribution can be used to predict the number of population doublings remaining in the vitro life-span of a human diploid fibroblast cell culture without knowledge of its prior history.

Aging↗