Rating of the radiopharmaceuticals for brain imaging.
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Biomedical subjects
Publications and source records attributed to R Chandra.
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Light and electron microscopy were used to observe acute radiation nephritis. By light microscopy the changes were of fibrinoid necrosis of the arteries and atrerioles with segmental necrosis of the glomerular tufts. By electron microscopy the endocapillary cells reacted by hypertrophy and hyperplasia with increase in cytoplasmic organelles. In addition, disruption of endothelial and epithelial cells from the basement membranes were seen. It is concluded that the electron microscopic changes were unique and may be helpful in differentiating the necrotizing glomerulitis seen in other conditions, especially malignant hypertension.
Three groups of 24 C57BL/6J black mice were studied. One group was implanted with B16 malignant melanoma, another was implanted with mammary adenocarcinoma, and the third was not given tumor implants. After 14 to 17 days, the mice were given injections i.v. of technetium-99m sulfur colloid and killed 30 min later. Organs were weighed, and radioactivity was counted. The ratios of specific radioactivities of the spleens to those of the liver were higher only in the group of mice bearing malignant melanomas. This finding suggests that the "hot spleen" phenomenon observed in humans with malignant melanomas may be due to increased specific activity rather than increased splenic volume.
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Studies in vitro of human macrophage function in health and disease have been impeded by the difficulty of obtaining such cells in sufficient number. Unlike animal species, the only readily available source of human macrophages are circulating monocytes. Herein, a method is described whereby the phagocytic rate of small numbers of glass-adherent mononuclear cells can be accurately measured. The method utilizes the ingestion by macrophages of technetium labelled polystyrene particles; both the radiolabel and ingestible substrate are readily available and the labelling process simple and efficient. The phagocytic rate can be expressed as radioactive counts per microgram of cell protein; data is also presented showing that the number of particles ingested per cell can be accurately derived.
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Reperfusion following myocardial ischemia has been postulated to cause myocardial edema resulting in increasing interstitial pressure and retardation of the microcirculation. If ischemia then is repeated, the additional insult results in increasing edema and possible infarction. In order to test this hypothesis, 15 pigs were placed on cardiopulmonary bypass with coronary perfusion maintained at 100 mm. Hg by a separate pump through the clamped aortic root. Coronary flow and vascular resistance were recorded. Distribution of coronary blood flow was monitored by injection of radioactively labeled microspheres (15 mu). Myocardial extravascular water was measured by simultaneously determining myocardial intravascular water with radioactive iodinated serum albumin (RISA) and total myocardial water with tritiated water (THO). Three 30 minute periods of myocardial ischemia and 5 minutes of coronary perfusion produced (1) a loss of the reactive hyperemic response to ischemia (coronary vascular resistance increased--from 0.295 +/- 0.024, control, to 0.366 +/- 0.042, after anoxia--rather than decreasing with reactive hyperemia induced vasodilatation); (2) a significant maldistribution of coronary flow away from the endocardium (endocardial: epicardial perfusion ratio 1.10 +/- 0.05, control, to 0.69 +/- 0.08, following ischemia, p less than 0.05); and (3) significant myocardial edema. Myocardial extravascular water rose from 46.4 +/- 1.7 ml. per 100 Gm., control, to 52.6 +/- 2.0 ml. per 100 Gm., after ischemia (p less than 0.05), whereas intravascular myocardial volume did not change significantly. Both light and electron microscopic examination of the postischemic myocardium shows interstitial and intracellular edema with typical ischemic changes at a cellular and subcellular level. The significant increase in myocardial extravascular water content associated with this injury supports the concept that myocardial reperfusion plays a role in its development.
Thirty-one patients were treated by portoenterostomy procedures for extrahepatic biliary atresia. In 20, there was unequivocal evidence of bile drainage. Eleven of these 20 were restudied from 3 to 23 mo postoperatively by liver biopsy. The clinical condition of most of these infants was satisfactory. Despite absence of clinical jaundice, normal rose bengal scan, and normal liver function studies, eight showed progressive degrees of hepatic fibrosis when compared to the results of the biopsy taken at the time of portoenterostomy. Two patients showed stable histology and one, after progressing on a second biopsy, had normal liver histology on a third study. The implications of progressive hepatic histopathology despite bile drainage are discussed.
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Normothermic anoxic arrest of 15 and 30 minutes, repeated for up to a total of 90 minutes of anoxia was employed in 24 pigs. The purpose was to determine the effect of varying the duration of anoxia on coronary blood flow, coronary vascular resistance, and the distribution of coronary flow to the free wall of the ventricle. Five minutes of reperfusion at pressures of 50 and 100 mm. Hg with the ventricle fibrillating, was employed between each anoxic interval. Results were compared to control studies performed during ventricular fibrillation without anoxic arrest in 12 pigs. Prolonging the anoxic interval to 30 minutes served to create a maldistribution of coronary flow away from the left ventricular endocardium and to reduce the reactive hypermic response to anoxia. Increasing the perfusion pressure to 100mm. Hg accentuated these changes. Both light and electron microscopy of sections demonstrated edema and early myocardial necrosis in the subendocardial layer of the left ventricle subjected to repeated 30 minute intervals of anoxia at a high perfusion pressure. We postulate that repeated anoxic insults with inadequate repayment of oxygen debt results in subendocardial edema, a decrease in perfusion, increasing necrosis, and further edema. A myocardial infarction must result if this vicious cycle cannot be interrupted.
Myocardial infarction may develop during an uneventful open-heart operation. In order to better understand this complication, we undertook an experimental study. The left circumflex coronary artery of 20 dogs was narrowed to 50 per cent of its area by a metal screw clamp to produce a localized coronary stenosis. Regional myocardial perfusion in the distribution of both the stenotic circumflex and normal left anterior descending (LAD) coronary arteries was measured by injection of a radioactive-labeled microsphere (15 +/- 5 mu). Circumflex coronary artery flow was measured with an electromagnetic flow probe. An epicardial electrogram was recorded in the distribution of the left circumflex. Measurements of regional myocardial perfusion, circumflex flow, and the epicardial electrogram were performed in each animal during the control (prebypass) state and during cardiopulmonary bypass with a beating and fibrillating ventricle. Half the animals had cardiopulmonary bypass performed at 50 mm. Hg perfusion pressure and half at 100 mm. Hg. The animals were put to death at the end of the study, and the hearts were sectioned, weighed, and counted. A cast was made of the stenotic circumflex coronary artery, the degree of stenosis is measured, and the per cent area stenosis calculated. The study showed that the effect of a 50 per cent coronary stenosis in reducing distal flow is apparent only during cardiopulmonary bypass at reduced pressure. The mechanism whereby a myocardial infarction develops during cardiopulmonary bypass could evolve from the development of a "critical" stenosis out of a mild-moderate one at a reduced perfusion pressure during cardiopulmonary bypass.
Results of a study on the relative frequencies of tumors in American black and Nigerian children were compared with data from the Childhood Cancer Registries in Manchester, United Kingdom, and Kampala, Uganda. The American black child living in Washington, D.C. and the Caucasian child living in Manchester had similar high frequencies for leukemia and glioma, whereas the incidence of lymphoma and retinoblastoma was low. African children living in Nigeria or Uganda had the opposite frequency patterns. These differences in frequencies of tumors between two ethnologically related population groups, American black and Nigerian, suggested the influence of environmental factors in the etiology of these tumors, even though exposure to environmental carcinogens was short. The rarity of Ewing's sarcoma and testicular tumors in American black and Nigerian children suggested a genetic influence.
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