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Biomedical subjects

B F Trump

Publications and source records attributed to B F Trump.

At least 199 records · Page 11Linked to original sources
PubMed1981

Sodium and calcium regulation and the role of the cytoskeleton in the pathogenesis of disease: a review and hypothesis.

Recent years have seen a rapid development in knowledge concerning ion regulation and the cytoskeleton and their roles in many normal and abnormal cell processes. The structure and function of the cytoskeleton plays a key part in a number of cell properties including cell shape, potential mobility of intracellular proteins including receptors, cell to cell adhesion, and many other phenomena such as secretion, phagocytosis and autophagocytosis. Although earlier studies have emphasized the roles of sodium and calcium ion modification following acute and chronic cell injury, it has not been until recently that volume regulation and sodium modification have been found to be intimately linked through mechanisms such as sodium-calcium exchange and that the interaction of these regulations are associated with the cytoskeleton and the cell membrane. Therefore, it is the purpose of this review not only to summarize the vast amount of data which has rapidly accumulated in this field, and to put it into perspective, but also to advance a hypothesis which, we hope, will eventually establish that a wide variety of pathological phenomena ranging from acute cell death to chronic processes such as neoplasia, hypertension and aging are all a common series of cellular reactions.

Animals↗
PubMed1981

Pathophysiology of hemorrhagic shock. II. Anoxic metabolism of the rat liver following acute blood loss in the rat.

Changes in energy metabolism of rat liver in hemorrhagic shock were investigated. The hepatic energy charge level (0.24-0.693) correlated significantly with the mean arterial blood pressure (20-75 mmHg) (r = 0.931, P less than 0.001), as well as the blood volume withdrawn (2.43-2.82 ml/100 g body weight) which, in turn, correlated with the various mortality rates (LD16, LD50, and LD84) (r = -0.728, P less than 0.01). As shown by the changes in adenylate energy charge levels, the liver was very sensitive to acute blood loss. There was no significant difference between the energy charge levels of liver obtained in situ from rats with 84% mortality after hemorrhage and that of the same liver further incubated in vitro in the absence of O2 (0.304 versus 0.235). From these results, it appears that the energy status in the liver of rats dying from severe hemorrhagic shock has changed to anaerobic metabolism, which may not be sufficient to maintain adequate liver function or support individual survival.

Acute Disease↗
PubMed1981

Pathophysiology of hemorrhagic shock. A role of arterial ketone body ratio as an index of anoxic metabolism of the liver in acute blood loss.

The changes in the oxido-reduction state and the adenylate energy charge of the liver were investigated in rats having 16%, 50%, and 84% mortality rates after acute hemorrhage. In the arterial blood, concentrations of ketone bodies, pyruvate, lactate, and the ratios (acetoacetate to beta-hydroxybutyrate and pyruvate to lactate) were measured after hemorrhage and reinfusion of the shed blood. The mitochondrial oxido-reduction state and the blood ketone body ratio decreased 15 minutes after hemorrhage. The values of these parameters of rats having the higher mortality rate were lower than those rats having the lower mortality rate. In addition, the changes in both the adenylate energy charge and the mitochondria oxido-reduction state of the liver were closely correlated with the changes in the ratio of acetoacetate to beta-hydroxybutyrate in the arterial blood (P less than 0.001). Thus, it is suggested that the decreased oxygen supply to the liver mitochondria may play an important role in determining the mortality rate after acute hemorrhage and is reflected in the ratio of acetoacetate to beta-hydroxybutyrate in the arterial blood.

Acute Disease↗
PubMed1980

Changes in mitochondrial lipids of rat kidney during ischemia.

Lipid changes in mitochondria isolated from rat kidney after various periods of ischemia were analysed by thin-layer chromatography and gas-liquid chromatography. Free fatty acids were increased at 30 min and more so thereafter. Total phospholipid fatty acids decreased steadily. The proportion of diphosphatidylglycerol (cardiolipin) in the total phospholipid fraction decreased at 30 min, but the proportion of phosphatidylcholine and phosphatidylethanolamine in the total phospholipid fraction did not change until the irreversible phase of ischemic injury. We have shown that decrease of cardiolipin in mitochondrial membrane occurs early during ischemia, and only during the irreversible phase of ischemia are phosphatidylethanolamine and phosphatidylcholine broken down. It is postulated that these phenomena are due to activation of phospholipase in the mitochondrial membrane.

Animals↗
PubMed1980

Metabolism of aflatoxin B1, benzo[a]pyrene, and 1,2-dimethylhydrazine by cultured rat and human colon.

A model system for comparing carcinogen metabolism between human and rat colon has been developed. Tissue explants maintained under chemically defined conditions were treated with radioactively labeled carcinogens. After incubation for 24 hours, the binding of radioactive carcinogen to DNA was quantitated. Further, the carcinogen-DNA adducts and carcinogen metabolites released into the culture media were identified. Both human and rat colon activate benzo[a]pyrene (BP), aflatoxin B1 (AFB), and 1,2-dimethylhydrazine (DMH) into chemical species that reacted with cellular macromolecules. When human and rat colons were compared, the metabolism of AFB and DMH was qualitatively similar - the same major carcinogen-DNA adducts and metabolic profile. However, the mean binding levels of DMH and AFB to colonic DNA were higher in rats than in humans. BP-guanine adducts were the major adducts formed by both rat and human colonic DNA. However, BP-adenine adducts were observed in rat colonic DNA but not in human colonic DNA. A positive correlation for the binding of BP and DMH to human DNA of different individuals was observed, but no correlation was found between BP and AFB. The data suggest that similar enzyme systems may be involved in the metabolism of BP and DMH, whereas different enzymes might be involved in the metabolic activation of AFB.

1,2-Dimethylhydrazine↗
PubMed1980

Putrescine stimulates growth of human bronchial epithelial cells in primary culture.

Explants of adult human bronchus were cultured in CMRL-1066 medium supplemented with heat-inactivated fetal bovine serum, hormones, antibiotics, and either 0.0, 0.1, 1, or 10 mM putrescine. The outgrowth of bronchial epithelial cells was stimulated in medium containing 1 mM putrescine, a concentration that partially inhibited the outgrowth of fibroblasts. In medium containing 10 mM putrescine, the outgrowth of epithelial cells was similar to that observed in the control medium, but the outgrowth of fibroblasts was completely inhibited for periods of at least 4 weeks. When 10 mM putrescine was added to cultures of bronchial fibroblasts, the fibroblasts were not killed. These results suggest that human bronchial epithelial cells have a higher requirement for putrescine for growth than fibroblasts, and the molecular basis for this observation is under investigation.

Bronchi↗
PubMed1980

Glycogen deposition in distal tubular cells during HgCl2 induced acute renal failure.

An unusual cytoplasmic accumulation of glycogen within the distal tubular epithelium of the kidney was produced by subcutaneouse administration of a single dose of HgCl2 (4 mg/kg body weight), used to induce acute renal failure. Since the plasma immune-reactive insulin was increased while plasma and urine glucose levels remained normal, it was concluded that activation of glycogen synthase might have lead to this effect. Furthermore, the accumulated glycogen was considered to contribute to the protection of distal tubular cells against HgCl2-induced injury, since oxidative energy metabolism was severely depressed after HgCl2 administration.

Acute Kidney Injury↗
PubMed1980

Structural changes following hypothermic preservation of human cadaveric kidneys.

Three kidneys preserved as though for transplantation became available for study. The clinical details relating to the donors and methods of preservation by simple hypothermia and pulsatile perfusion are presented. Light microscopic and ultrastructural features observed following perfusion fixation of the kidneys are described. All three kidneys showed some reversible ischemic cell damage, but only one showed evidence of ischemic cell damage that was considered to be irreversible. The latter was seen focally in the pars recta of the proximal convoluted tubules and in the ascending thick limb of the loop of Henle. The irreversible changes were present in the kidney that had undergone the longest period of simple hypothermic storage prior to transfer to pulsatile perfusion preservation. The similarity of the findings to those seen in vivo in the rat after one hour of total renal ischemia, followed by 24 hours' reflow, is discussed; a hypothesis is suggested to explain the site of the irreversible injury seen in the kidneys under study.

Adolescent↗