A consistent, quantitative, observer-independent method of characterising mammographic parenchymal pattern is described. The method is based on the calculation of the 'fractal dimension' of digitised mammograms. The degree of correlation between the parenchymal pattern classifications by a fractal-based system and those of radiologists is assessed. For a set of 70 mammograms, average weighted proportion agreement among three radiologists in calling Wolfe grades was 85%, while agreement between the radiologists and our fractal classifier was 84%. The method developed may prove to be useful in establishing an index of risk for breast cancer and, ultimately, in determining intervals between examinations for individuals in a mammographic screening programme.
The addition of latex particles to native (no anticoagulant) or citratcd human platclctrich plasma (PRP), or to a once-washed platelct suspension causes platelet aggregation. This aggregation is associated with phagocytosis of t'ae latex particles by the platelets and appcars to be due to release of adenosine diphosphate (ADP) from the platclets. Adenosinc and adenosine monophosphate, which are known to inhibit platelet aggregation induced by ADP, also block that induced by latex. These compounds do not prevent the phagocytosis of latex particles by the platelet. The addition of iodoacctate and 2,4-dinitrophcnol in appropriate concentrations to the PRP, prior to the addition of the latex, blocks platelet aggregation and phagocytosis. This is also true for the chelating agent ethylenediaminetetraacetate (EDTA). Platclets left in contact with latex for a sufficient period of time show loss of their granules. Leucocytcs phagocytose both latex and platelets that had themselves phagocytosed latex. It is concluded that phagocytosis of latex particlcs by platelcts rcscmblcs that by white cells, and that in both processes metabolic changes appear to bc involved.
We present clinical and laboratory results (including nuclear imaging) obtained over a period of two years in two nonsmoking miners who were exposed to high concentrations of sulfur dioxide (SO2) after a mine explosion. Within 3 wk of the accident, both miners had evidence of severe airways obstruction, hypoxemia, markedly reduced exercise tolerance, ventilation-perfusion mismatch, and evidence of active inflammation as documented by positive gallium lung scan. Serial ventilation-perfusion scans over the first 12 months showed progressive improvement without returning to normal. After the initial recovery, there has been no significant change over the subsequent two years postinjury. Pulmonary function and exercise tests also displayed a similar pattern of initial improvement. We conclude that (1) acute exposure to high concentrations of SO2 results in severe airways obstruction, (2) pulmonary function abnormalities are partially reversible, and (3) most of the improvement occurs within 12 months after the initial injury.
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