Unscientific manufacture of blood donor sets.
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Biomedical subjects
Publications and source records attributed to S Rao.
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The relation of coronary artery disease to plasma lipoproteins was examined in 104 men aged 35-65 years undergoing coronary angiography for suspected myocardial ischaemia. A score reflecting the number, degree, and length of stenoses in seven major coronary arteries was assigned to each angiogram. Lipid concentrations in lipoprotein subfractions were measured after preparative ultracentrifugation; plasma apolipoprotein concentrations were measured by electroimmunoassay. Men with high coronary scores tended to have lower plasma high-density lipoprotein (HDL) cholesterol concentrations and higher low-density lipoprotein (density 1.019-1.063 g/ml) cholesterol concentrations than subjects of similar age with low coronary scores (p approximately equal to 0.1). The strongest relation, however, was with the cholesterol concentration in the HDL2 subfraction (density 1.063-1.125 g/ml) of HDL, which averaged 44% lower in the severely affected patients (p less than 0.005). No associations were found between the coronary score and HDL3 cholesterol, the cholesterol content of lipoproteins of density less than 1.019 g/ml, plasma triglyceride, or the concentrations of apolipoproteins AI, AII, and E. The high coronary scores associated with low HDL2 concentrations reflected an increase in the number of both partial and complete stenoses distributed throughout the coronary tree. In contrast the sizes of the lesions and the proportion producing complete occlusion were unrelated to HDL2.
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Since Apoprotein A-I (apo A-I) is partially synthesized in the intestine and is secreted into plasma via chylomicrons, we have tested the effects of the daily distribution of fat intake on the concentration and composition of plasma high density lipoprotein (HDL). Ten normal subjects ingested 136 g fat either as a single load (SL) at 0 h or in 6 divided doses from 0 to 10 h (DL). Serial blood samples were obtained over a 24-h period. Studies were performed 7 days apart using a double crossover design and paired comparisons. HDL apo A-I increased during DL (+11% at 9 h, P < 0.01) but was not significantly altered after SL. The HDL Apo A-II concentration did not change. HDL cholesterol decreased significantly (-4 to -7%) during postprandial lipaemia in both phases of the study. Apo A-I and A-II were detected in lipoproteins of d < 1.006 during alimentary lipaemia but not in fasting plasma. These results indicate that HDL apo A-I increases when fat intake is distributed throughout the day (DL), perhaps due to intestinal production of particles with a higher protein/lipid ratio during DL than after a large bolus of oral lipid (SL). Alimentary lipaemia is associated with acute alterations in HDL components including a transient reduction in HDL cholesterol and an increase in the apo A-I/A-II ratio during DL.
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Indirect immunofluorescence staining in two thymomas, one case of thymic hyperplasia, 10 malignant lymphomas and three seminomas was done with an antibody prepared against keratins from human epidermis. Staining was observed only in the epithelial cells of the thymomas and thymic hyperplasia and correlated well with electron microscopic studies. Immunofluorescence staining of thymic tumors with antikeratin antibody provides a simple, specific, and sensitive method for distinguishing thymoma from lymphoma and seminoma. The method may also prove to be useful in other instances in the distinction between epithelial and nonepithelial tumors.
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An 11-month-old boy had an episode of generalized convulsions followed by a right peripheral facial palsy, which resolved gradually within 3 weeks. Three months later he had another similar episode of convulsions followed by a left peripheral facial palsy. On both occasions it was found that he had polycythaemia. A careful physical examination discovered that the child had severe hypertension. Extensive laboratory investigations did not reveal a cause for his hypertension. Haematologic investigations showed that the polycythaemia was due to a contracted plasma volume as a result of the hypertension. The peripheral facial palsy most probably was due to a blood clot in the facial canal, below the origin of the nerve to m. stapedius, as audiograms were normal and lacrimation preserved. Control of the hypertension resulted in resolution of the facial palsy within 4 weeks and normal haematocrit readings within 6 weeks. It should be stressed that every patient with peripheral facial palsy should be examined for hypertension.
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