William R. Beisel
United States Army Medical Research Institute of Infectious Diseases
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International Review of Neurobiology#R##N#Supplement 1 | 1972
William R. Beisel; Robert S. Pekarek
Publisher Summary This chapter discusses acute stress and trace element metabolism. While considering the effect of acute stress upon the metabolism of a trace element, one must consider the fundamental physiological role of the element, methods available for its analysis, and the status of general and specific trace-metal nutrition in the host. Within cells, magnesium is related functionally to the activity of enzyme systems, especially those that generate high-energy phosphate bonds and control mitochondrial oxidative phosphorylation. Magnesium is a necessary cofactor of DNA, RNA, and ribosomes. It is needed for the binding of mRNA to polysomal subunits and for the activation of aminoacyl-sRNA complexes during protein synthesis. The extracellular concentration of magnesium ions influences both the nerve-cell conduction and myoneural junction activity. Excessive magnesium ions can produce local or general anesthesia, asystole, and curare-like paralysis. Deficiency of magnesium produces a syndrome of central nervous system irritability. The primary functional role of iron is oxygen transport via hemoglobin. Iron further serves as an essential cofactor for a number of heme and non-heme metalloenzymes that are important for oxygen and hydrogen exchange or electron transport. Iron also plays a role in maintaining the structure and integrity of polyribosomes and is important in protein synthesis. Zinc is an integral constituent and cofactor of more than twenty metalloenzymes. Because of relatively high concentrations of zinc found in various endocrine glands, this element may influence the secretion of several hormones. The important role of zinc in promoting the healing of thermal and surgical wounds adds further support to this hypothesis.
Scandinavian Journal of Infectious Diseases | 1984
Göran Friman; Nils-Gunnar Ilbäck; William R. Beisel
Since opinions differ as to whether the oxidative and glycolytic capabilities of skeletal muscle are altered in acute infection, enzyme activities in oxidative, glycolytic and degradative (acid hydrolases) pathways and total protein and DNA were determined in skeletal muscle of rats infected with Streptococcus pneumoniae, Salmonella typhimurium or Francisella tularensis. Studies were performed separately in red (slow twitch) and white (fast twitch) muscle tissue because these fibers function during different types of exercise. In the salmonella- and tularemia-infected rats, the intramitochondrially located oxidative enzymes of muscle were decreased to 56–83 % of controls whereas the glycolytic enzyme situated in the cytosol showed an earlier and more pronounced loss of activity, 30–75 % of controls. In the pneumococcal infection, only reduced glycolytic activity was significant. DNA concentrations were unchanged in any infection. Reductions during tularemia were statistically correlated with whole-cell pr...
Experimental Biology and Medicine | 1972
R. W. Wannemacher; Robert S. Pekarek; William R. Beisel
Summary Live D. pneumoniae, but not endotoxin or double-stranded polynucleotides, stimulated a flux of cycloleucine into liver. Sterile, 2-hr serum from D. pneumoniae-infected rats and secretions obtained from rat peritoneal leukocytes can also mediate a flux of cycloleucine into liver of normal recipient rats. The data were interpreted as evidence that one or more proteins synthesized and excreted by leukocytes can act as humoral intermediates in the stimulation of amino acid flux into liver tissue.
Experimental Biology and Medicine | 1971
R. H. Fiser; J. C. Denniston; R. B. Rindsig; William R. Beisel
Summary Rhesus monkeys acutely infected with D. pneumoniae or S. typhimurium exhibited an increased rate of 3H-mevalonic acid incorporation into free cholesterol in comparison with values observed in control monkeys. When studied early in either infection, there was no evidence for an inhibition of squalene synthesis or its conversion to cholesterol. The estimated volume of plasma cholesterol did not change. Total hepatic cholesterol was decreased and entry of radioactivity into plasma cholesterol esters was reduced in the Samonella-infected monkeys.
Experimental Biology and Medicine | 1972
Robert S. Pekarek; R. W. Wannemacher; F. E. Chapple; Michael C. Powanda; William R. Beisel
Summary A degree of cross species susceptibility was observed on the effects of leukocytic endogenous mediator (LEM) on serum zinc depression and amino acid flux. LEM was shown to be protein in nature, and relatively stable under a wider range of pH and conditions of storage. Although LEM shares several chemical and physical characteristics with endogenous pyrogen (EP), some differences between the chemical properties and species specificity of these two mediators were noted.
Experimental Biology and Medicine | 1972
R. H. Fiser; J. C. Denniston; M. D. Kastello; R. B. Rindsig; William R. Beisel
Summary The presence of chronic, experimentally induced hypercholesterolemia in rhesus monkeys led to atypical patterns of lipid response during acute pneumococcal infection. When compared to infection in previously normal monkeys, hypercholesterolemic monkeys showed an impaired synthesis of cholesterol with accumulation of squalene in the plasma, an increased conversion of newly formed cholesterol to an esterified form, and an impaired utilization of triglycerides.
The American Journal of Clinical Nutrition | 1976
Robert W. Wannemacher; A S Klainer; R E Dinterman; William R. Beisel
The Journal of Infectious Diseases | 1972
Robert H. Fiser; Joseph C. Denniston; William R. Beisel
The American Journal of Clinical Nutrition | 1975
Robert W. Wannemacher; R E Dinterman; R S Pekarek; Peter J. Bartelloni; William R. Beisel
Journal of Laboratory and Clinical Medicine | 1970
Pekarek Rs; Burghen Ga; Bartelloni Pj; Calia Fm; Karen A. Bostian; William R. Beisel
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United States Army Medical Research Institute of Infectious Diseases
View shared research outputsUnited States Army Medical Research Institute of Infectious Diseases
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View shared research outputsUnited States Army Medical Research Institute of Infectious Diseases
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