Radioactive vitamin A acetate was stored in specific cells in the mouse adrenal gland. Radioactivity was detected in lipid droplets of fibroblast-like cells, whose distribution was from the capsule to the medulla. Their population was highest in the cortex. The morphology of these labeled cells was similar to that of vitamin A-storing cells in other organs of mouse (Yamada and Hirosawa, '76). Though functions of these cells are obscure, the fact that they are found in organs where metabolic activity of vitamin A is high suggests that they bear some role in the metabolism and storage of the vitamin.

Adrenal Cortex↗

PubMed1978

Rapid, sensitive detection of myoglobulinemia by improved counterimmunoelectrophoresis in cases of acute myocardial infarction.

A counterimmunoelectrophoresis technique for detection of serum myoglobin (Mb) was improved using non-ionic polymer dextran. Precipitin lines were graded according to their strength, which was ascertained by radioimmunoassay data. By this method, serum Mb in concentrations of 500 ng./ml. before stain and of 200 ng./ml. after stain were detected. Electrophoretic time was 60 minutes. Among 32 cases of acute myocardial infarction (AMI) whose blood samples were collected within 24 hours after disease onset, precipitin lines were detected in 25 cases (78%) before stain and 31 cases (97%) after stain. Considering the early peak concentration time (approximately 10 hours) of serum Mb after AMI onset, diagnosis becomes more rapid and exact with this method, especially in severe cases.

Acute Disease↗

PubMed1978

Relationship between myocardial infarction and preinfarction angina: a histopathological study of coronary arteries in two sudden death cases employing serial section.

Two patients who had previously experienced old myocardial infarction and who died suddenly after an attack of chest pain were examined and discussed. In both cases two of the three main coronary arteries showed severe stenosis with canalization. Ruptured atheromatous plaque was found in the unblocked coronary artery. Fibrin was already formed and surrounded the fractured intimal collagen fiber, foam cells, and cholesterin clefts, but a luminal thrombi had not yet been formed. Fresh occluding thrombi were formed at the site of the ruptured atheromatous plaque. Coronary thrombi containing abscess components such as foam cells, cholesterin clefts, and the fractured intimal collagen fiber were found in our preliminary study. These views support the supposition that this fracture between the lumen and the plaque might precede and be responsible for the formation of the thrombus and the onset of acute myocardial infarction. It was confirmed that the attack of preinfarction angina occurred at the time of the rupture of the atheromatous plaque. The rupture of the atheromatous plaque plays an important part as an initiating factor of peinfarction angina and myocardial infarction. Thus, it is necessary to examine coronary arteries by serial histopathological section method.

Aged↗

PubMed1978

Impact of computerized tomography on epilepsy study.

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Epilepsy↗

PubMed1978

Coronary thrombosis in pathogenesis of acute myocardial infarction. Histopathological study of coronary arteries in 108 necropsied cases using serial section.

An extensive histopathological study was carried out on the hearts of 108 patients with electrocardiographically proven acute myocardial infarction dying after admission to a coronary care unit. The occluded or the narrowest segments of the coronary arteries were examined at intervals of 100 mu using serial sections. Serial sectioning is important in such a study because the pathology of the lumen can vary considerably within a 2 to 3 mm segment. A high incidence (80.3%) of thrombus formation corresponding to the site of infarction was observed. These thrombi occluded the vessel lumen, were usually found proximally in the coronary arteries, and were associated with a ruptured atheromatous plaque in 90.8 per cent of cases. It is postulated that an increase of intraplaque pressure resulting from a honeycomb-like accumulation of foam cells, cholesterol clefts, and blood infiltration through the injured endothelial cells is the cause of rupture of the atheromatous plaque. This rupture into the vessel lumen may precede, and be responsible for, formation of thrombus and the onset of acute myocardial infarction.

Adult↗

PubMed1978