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C P Miles

Publications and source records attributed to C P Miles.

At least 19 recordsLinked to original sources
PubMed1981

The use of optical Fourier transforms to diagnose pleomorphism, size and chromatin clumping in nuclear models.

Nuclear features of size, pleomorphism and chromatin clumping are distinctive and quantifiable in the optical Fourier transform of the nucleus. This is shown in photographs of models, tracings and hematoxylin-stained impression smears of various types of nuclei. The size of the transform is inversely proportional to the size of the nucleus. Irregularities in shape (pleomorphism) produce radially symmetric rays of light in the transform. The effect of chromatin clumping is to give a mottled pattern superimposed on the pleomorphism pattern. The transform features can be measured in real time using a ring-wedge or similar detector. These procedures might be used for both automatic screening and objective quantification of diagnoses.

Cell Nucleus↗
PubMed1977

Conditions predisposing to suicide: a review.

By reviewing causes of death among cohorts of various major disease entities or conditions, one may infer that a large majority of suicides are associated with a relatively small number of conditions. From the available follow-up studies, we might estimate that the following percentage of affected individuals will die by suicide: primary (endogenous) depression, 15 per cent; reactive (neurotic) depression, 15 per cent; alcoholism, 15 per cent; schizophrenia, 10 per cent; psychopathic personality, 5 per cent; opiate addiction, 10 per cent or more. Rough estimates of the number of suicides per year in the United States attributable to each condition might be as follows (using low incidence figures): depression, 12,900; alcoholism, 6,900; schizophrenia, 3,800; psychopathy, 2,000 (?); drug addiction, 900.

Age Factors↗
PubMed1974

Non-random chromosome changes in human cancer.

Chromosome changes in human cancer cells appear to evolve by non-random losses and/or gains of particular homologues or groups. It is probable that some of the apparent losses or gains actually represent formation of new chromosome structures, which are then classified as markers or are misclassified as normal homologues. In many cancers these changes appear to continue at a high rate throughout the life of the cancer (so that in some cancers almost every cell will exhibit a different karyotype). In other cancers the rate of change may be slow or arrested so that all cells will have the same abnormal karyotype. One very common step in karyotype evolution is doubling of the entire chromosome complement (2n → 4n or more commonly, S → 2S where S is the stemline number). The 2S cells tend to replace the original stemline. Homologues which have larger amounts of concentrated blocks of heterochromatin (i.e. late replicating DNA) seem more apt to be lost.

Breast Neoplasms↗
PubMed1970

Labeling and other effects of actinomycin D on human chromosomes.

(3)H-actinomycin D, a guanine-binding agent, labels fixed human chromosomes nonrandomly. Actinomycin D added in G2 inhibits secondary constrictions and breaks chromosomes. There is some tendency for label to be concentrated at the ends of chromosomes and near the centromere. Labeling with (3)H-thymidine in the late stage of DNA synthesis shows a different pattern and in general lacks the telomeric concentrations. The sites of actinomycin D-induced breaks do not show good correspondence with the sites of actinomycin D label.

Chromosomes↗