Biomedical subjects
S A Cook
Publications and source records attributed to S A Cook.
Multifocal osteosarcoma. A case report.
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The incidence of scintigraphically viable and nonviable tissue by rubidium-82 and fluorine-18-fluorodeoxyglucose positron emission tomographic imaging in patients with prior infarction and left ventricular dysfunction.
BACKGROUND: Although reversible perfusion defects, perfusion-metabolism mismatch and match patterns are important for differentiating viable from nonviable myocardium, the frequency of these scintigraphic patterns has not been reported. The study objective was to establish the incidence of these scintigraphic patterns to estimate the clinical need for metabolic positron emission tomography for evaluating tissue viability in patients with prior myocardial infarction (MI). METHODS AND RESULTS: 82Rb perfusion images were interpreted to identify reversible or irreversible defects, followed by determination of their 18F-fluorodeoxyglucose (18F-FDG) uptake pattern. In 155 patients with prior MI, analysis of 613 abnormal segments showed reversible perfusion defects in 13%. The 87% irreversible defects, 18% showed perfusion-metabolism mismatch, whereas 69% showed the match pattern. Reversible perfusion defects and perfusion-metabolism mismatches were noted in 20% (31/155) and 29% (45/155) of patients, respectively, whereas the match pattern was noted in 51% (79/155) of patients. CONCLUSION: Irreversible perfusion defects were common in our patients with prior MI, and distinction between viable and nonviable tissue was not possible by perfusion imaging alone. The identification of hibernating myocardium was possible only with the additional 18F-FDG imaging in about one third of patients. This indicates a significant clinical demand for 18F-FDG imaging that identifies patients who will benefit from revascularization.
Juvenile bare: a new hair loss mutation on chromosome 7 of the mouse.
We describe a new juvenile hair loss mutant in the mouse in which the hair follicle follows irregular pathways to the surface and generally becomes dystrophic when the mouse is about 23 days of age. Skin from mutant mice older than 1 month of age is histologically normal, although adult mutant mice show a slightly more sparse coat than normal. Grafts of mutant littermates skin to SCID hosts indicate that the condition is probably a systemic response rather than one of the follicle per se. The hair loss is caused by a recessive mutation, which we have named juvenile bare (jb), located on proximal chromosome 7.
A new allelic series for the underwhite gene on mouse chromosome 15.
A new allelic series at the underwhite gene is described. Three of the alleles in the series--uw, uwd, and Uwdbr--arose as spontaneous mutations on different genetic backgrounds at The Jackson Laboratory. We report here the visible phenotypes and dominance hierarchy of these alleles, all of which are defined by a reduction of pigmentation in both eye and coat color. Electron microscopic analysis of retinal epithelium suggests that the primary defect is in the melanosome. The degree of severity of melanosome anomalies in the retina correlates with the degree of hypopigmentation in the coat. The perturbed gene and its gene product are unknown. We show that the uw locus is genetically distinct from Myo10, a suggested candidate gene for this mutation.
Balding: a new mutation on mouse chromosome 18 causing hair loss and immunological defects.
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Microcirculatory obstruction in focal cerebral ischemia: albumin and erythrocyte transit.
The objectives were to study plasma and erythrocyte flow in an area of acute focal cerebral ischemia and define their relationship to developing microcirculatory obstruction as determined by morphological techniques. Eighteen adult cats, anesthetized with ketamine hydrochloride, had right middle cerebral artery (MCA) occlusion. Plasma flow was determined by measuring the transit of Iodine-131 (131I) albumin and erythrocyte flow was determined by measuring the transit of Technetium-99 (99Tc) labeled erythrocytes in the right Sylvian region. Transit studies were performed before and immediately after right MCA occlusion and at the end of the ischemic period, 1 hour, 3 hours, or 6 hours after occlusion. Intra-arterial perfusion with a buffered formaldehyde - colloidal carbon solution was carried out after completion of the isotope studies. Swelling of cerebral tissue and impaired carbon filling in the right MCA territory were seen initially after 3 hours occlusion and were more severe after 6 hours occlusion. Ischemic neuronal alterations, edema formation, and capillary luminal narrowing increased with longer periods of occlusion. 131I albumin transit time in the right Sylvian region was 8 +/- 2 seconds before occlusion and 10 +/- 2 seconds immediately after occlusion. 99Tc erythrocyte transit time was 10 +/- 2 seconds before occlusion and 12 +/- 3 seconds immediately after occlusion. 99Tc erythrocyte transit time was 10 +/- 2 seconds before occlusion and 12 +/- 3 seconds immediately after occlusion. Transit times increased progressively with longer periods of occlusion in cats developing cortical ischemic changes. No evidence of complete microcirculatory obstruction to albumin and erythrocyte transit was seen in cats with 6 hours of occlusion despite the impaired filling of the cortical microcirculation with carbon. There were no findings to substantiate the hypothesis that plasmapheresis develops during the early phases of cerebral infarction.