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Biomedical subjects

W R Beisel

Publications and source records attributed to W R Beisel.

At least 37 records · Page 2Linked to original sources

Hypothesis: leukocyte endogenous mediator/endogenous pyrogen/lymphocyte-activating factor modulates the development of nonspecific and specific immunity and affects nutritional status.

We postulate that leukocyte endogenous mediator/endogenous pyrogen/lymphocyte-activating factor (LEM/EP/LAF) integrates the host's nonspecific and specific immune responses to infection by virtue of the panoply of physiological and metabolic activities it is capable of eliciting. The alterations in systemic metabolism modulated by LEM/EP/LAF, although apparently of value to the host in the defense against infection and the repair of tissue damage, result in negative nutrient balances. Severe infections, alone or in conjunction with injury, may result in malnutrition unless the patient is adequately nourished. Preexisting nutritional deficits can compromise host resistance to infection, in part by preventing production of LEM/EP/LAF. Additional studies of the sequelae of LEM/EP/LAF action and effects of nutrition on host resistance to infection appear warranted.

Humans↗

The effects of strenuous exercise on infection with Francisella tularensis in rats.

To investigate the effects of strenuous forced exercise on the course and complications of a bacterial infection and on myocardial responses and performance capacity, rats with tularemia (characterized by pyogranulomatous hepatic and splenic lesions) were exercised by swimming on days 0-6 of infection. Levels of glutamic oxaloacetic and pyruvic transaminases in plasma, densities of pyogranulomatous lesions, and bacterial counts in blood, liver, and spleen were similar in exercising and resting rats. Although a few exercising rats showed an unusual dissemination of infection, the antibody responses were similar in rest and exercise. Plasma concentrations of beta-glucuronidase, lysozyme and alpha 2-macrofetoprotein were higher with exercise, a result that indicated that more vigorous stress responses were elicited with exercise than with infection alone. Physical performance capacity was reduced by the infection, but forced daily exercise limited this reduction substantially and counteracted the myocardial protein-degrading effects of infection. Thus, exercise evoked normal training responses even during this generalized infection.

Animals↗

Single-nutrient effects on immunologic functions. Report of a workshop sponsored by the Department of Food and Nutrition and its nutrition advisory group of the American Medical Association.

Immune system dysfunction can result from singlie-nutrient deficiencies or excesses, alone or in combination with generalized protein-energy malnutriton. Acquired immune dysfunctions in man occur with deficiencies of iron, zinc, vitamins A and B12, pyridoxine, and folic acid and with excesses of essential fatty acids and vitamin E. Additional micronutrients are important for maintaining immunologic competence in animals. Deficits or excesses of many trace elements and single nutrients thus have potential for causing immune dysfunctions in man. Since nutritionally induced immune dysfunction is generally reversible, it is important to recognize and identify clinical illnesses in which immunologic dysfunctions are of nutritional origin. Correction of malnutrition should lead to prompt reversal of acquired immune dysfunctions.

American Medical Association↗

Electrolyte metabolism in rhesus monkeys with experimental salmonella sepsis.

Prior investigations in the human indicate that alterations occur in electrolyte balance and serum concentration during infectious diseases. In order to explore these alterations in greater detail, electrolyte metabolism has been investigated in rhesus monkeys with a sublethal illness induced by intravenous inoculation with Salmonella typhimurium. The response to this illness was evaluated by a variety of measurements including serum and muscle electrolyte composition and renal function studies. In the animals with ad libitum dietary intake, a loss in muscle and serum potassium concentrations was evident within 24 h after inoculation. This was reflected in increased urinary potassium losses during the febrile phase of illness. Serum and muscle K concentrations returned to normal after 5 days of illness. Sodium and water content of muscle responded to infection in a more complex pattern. During the febrile phase, muscle sodium and water increased and sodium concentrations in serum and urine were elevated. During convalescence, renal retention of sodium was marked and overlapped the period of weight loss and the increased urine volume. This asynchrony in recovery of normal renal function appeared to be the cause of relatively large swings in plasma sodium concentrations during the early convalescent period. These investigations indicate that the altered serum concentrations in infectious diseases are the sum of renal and extrarenal factors controlling electrolyte metabolism, and that some of the most remarkable alterations occur during early convalescence as renal function returns to normal.

Animals↗

Serum antibodies reactant with Korean haemorrhagic fever agent in Scandinavian epidemic (endemic) nephropathy (nephropathia epidemica) demonstrated by immunofluorescence utilizing an in vitro antigen source.

A newly developed spot slide immunofluorescence method utilizing an in vitro antigen source was used for the first time for the assay of antibodies reactant with the Korean haemorrhagic fever (KHF) agent in sera from patients diagnosed with Scandinavian epidemic (endemic) nephropathy (nephropathia epidemica, NE) and from age-matched control patients living in the same area as the NE patients but suffering from other diseases. KHF antibodies were demonstrated in all of 14 NE patients who were followed prospectively, 7 of whom exhibited seroconversion and in 6 of 8 NE patients studied retrospectively, but in only one of 42 controls. Antibodies in NE appeared within the first week of onset of symptoms and persisted for long periods of time as seen in KHF. The time from the onset of the illness until maximum antibody titre was recorded varied from 9 days to 1 month. On an average, the level of the antibody titres measured in NE was lower than that usually encountered in the Korean disease. The results indicate a close antigenic relationship between the KHF and NE agents and demonstrate that the reliability of our new spot slide method is similar to that of another previously reported and more laborious immunofluorescence method using lung from infected rodents as antigen source.

Adolescent↗

Impact of infectious disease upon fat metabolism and immune functions.

Abnormalities in lipid metabolism influence immunological competence. Infectious diseases are accompanied by altered lipid metabolism as well as by suppression or stimulation of generalized defensive mechanisms and immune functions. An infectious disease may therefore introduce variables that must be recognized and evaluated during studies aimed at elucidating possible relationships between dietary lipids and the development of cancer.

Cholesterol↗

Elevated glycosyltransferase activities in infected or traumatized hosts: nonspecific response to inflammation.

Streptococcus pneumoniae infection leads to multifold increases in sialyltransferase, galactosyltransferase, alpha 2-fucosyltransferase, and alpha 3-fucosyltransferase activity of rat liver. Such changes may reflect an increased demand for glycosylation of acute-phase proteins synthesized and secreted by the liver during inflammatory processes. Serum sialyltransferase became elevated in bacteria-infected or burned rats and sandfly fever-infected humans, but did not correlate with acute-phase serum protein changes. These data suggest that nonparenchymal liver cells, such as macrophages, may contribute substantially to elevated sialyltransferase activity in the circulation during infection and, as such, represent a general host response to infection and tissue trauma.

Acetylglucosamine↗

A probable endocrine basis for the depression of ketone bodies during infectious or inflammatory state in rats.

The effects of infection with Streptococcus pneumoniae, Francisella tularensis, and Venezuelan equine encephalitis virus as well as inflammatory stress induced by the administration of turpentine and endotoxin on plasma ketone bodies and insulin were studied in white rats. All of the infectious/inflammatory stresses caused a significant decrease in the ketonemia of fasting and an elevation of plasma insulin. When a pneumococcal infection was initiated in a diabetic rat, inhibition of fasting ketonemia did not occur. Similarly, pneumococcal infection in the hypophysectomized rat did not result in a noticeable depression of either fasting ketonemia or plasma FFA. The increase in circulating insulin appears to be closely correlated with the inhibition of fasting ketonemia noted in the infectious/inflammatory stress.

Animals↗

Effects of infection on nutritional status and immunity.

Generalized infectious illnesses cause a highly predictable series of biochemical, metabolic, and hormonal responses. In combinations with fever and anorexia, these responses lead to hypermetabolic losses of cellular constituents and a depletion of body nutrient stores. Concomitantly, infectious processes stimulate a complex series of defensive measures that include both organism-specific immunological responses and an activation of generalized nonspecific defenses. The possible presence and impact of an infectious process must therefore be considered whenever nutrition-immune system interrelationships are studied in experimental animals. In clinical situations, nutritional depletion and weakened host defenses must be recognized as expected sequelae of acute infectious illnesses and, conversely, the presence of development of an infectious process must be anticipated in patients with malnutrition, both before and during their rehabilitation.

Chronic Disease↗

Alterations of body fluid compartments and distribution of tissue water and electrolytes in rhesus monkeys with rocky mountain spotted fever.

Chair-restrained rhesus monkeys (Macaca mulatta) were inoculated subcutaneously with 10(2)--10(3) plaque-forming units of virulent Rickettsia rickettsii. The latent period for fever and rickettsemia was three to four days; death occurred six to eight days after infection. Total circulatory electrolyte levels and fluid volumes, including plasma, red blood cell, true circulatory blood, and extracellular fluid, increased. The expansion of the extracellular and plasma volumes resembled findings reported during severe Rocky Mountain spotted fever in humans, guinea pigs, and rabbits. Total water content of the liver also increased. Intracellular concentrations of K+, as well as total Na+ and K+, decreased in the diaphragm. Both the lung and medulla oblongata showed increased levels of intracellular Na+ and water with simultaneously decreased levels of extracellular Na+ and water. Such an intracellular overhydration of the medulla oblongata could contribute to death as a result of depression of the cardiovascular and respiratory centers. On the basis of the findings in monkeys, the intravenous infusion of fluids and electrolytes during clinical therapy of severe rickettsial infections should be considered extremely dangerous.

Animals↗

Effect of glucose infusion on the concentration of individual serum free amino acids during sandfly fever in man.

After an intravenous glucose load in man, total serum amino acid concentrations are rapidly depressed and remain below baseline values for at least 2 to 3 hr after serum glucose and insulin have returned to preload concentrations. Despite the presence of basal hypoaminoacidemia, a decreased glucose disappearance rate, and hyperinsulinemia in volunteers who were ill with sandfly fever, an intravenous glucose load resulted in a further depression of serum amino acids which was equal to or slightly greater than that observed in the same individuals before exposure to the virus. Although the infectious process may have some effect on insulin-stimulated hepatic disposal of a glucose load, it does not appear to influence the ability on insulin to decrease the rate of release of certain amino acids from skeletal muscle.

Adult↗

Magnitude of the host nutritional responses to infection.

This review describes the scope, complexity, and magnitude of host nutritional responses throughout the course of an infectious process. These responses include prominent changes in nitrogen and protein metabolism, altered rates of carbohydrate and lipid production and utilization, and changes in mineral, electrolyte, trace element, and vitamin metabolism. It is postulated that these responses develop in a relatively predictable sequence which is influenced by the adequacy of host antimicrobial defense mechanisms, the severity and duration of illness, and specific localization of an infectious process within the body. In addition to hormonal regulatory effects, the metabolic and nutritional responses of the host are also influenced by biologically active substances released when host cells participate in phagocytic activity and local inflammatory responses.

Carbohydrate Metabolism↗

Sequential changes in body composition during infection: electron probe study IV.

Alterations occur in human muscle electrolyte and water composition in response to infection. There appear to be at least two basic mechanisms; the first is an exchange of sodium for potassium without alteration in water content of muscle. The second is an increase in cellular Na and water without a loss of K on a dry weight basis. In a series of studies in monkeys, Salmonella typhimurium sepsis was induced as an experimental model. Both patterns of muscle response to infection were detected. Electron probe microanalysis revealed that the loss of K concentration was due to an accumulation of intracellular saline which dilute the K content. The mechanism of this is unclear; however, a concomitant increase in undertermined osmoles in the serum suggests that there may be an increase in organic osmoles within the cell which leads to the dilution of intracellular K concentration.

Animals↗

Studies on Macaca mulatta infected with Rocky Mountain spotted fever.

Acid-base alterations and changes in other selected serum constituents (free fatty acids, triglycerides, cholesterol, copper, cortisol, alpha1-acid glycoprotein, haptoglobin, and albumin) were measured during a study of Rocky Mountain spotted fever in 16 male rhesus macaques. Blood samples were taken from nonanesthetized macaques conditioned to repeated handling. Arterial pH increased and PCO2 decreased during the febrile period. Free fatty acids, triglycerides, copper, cortisol, alpha1-acid glycoprotein, and haptoglobin increased, whereas albumin decreased during the disease. Significant changes were not observed in arterial PO2. Cholesterol remained unchanged. The increase in arterial pH and decrease in PaCO2 indicated that respiratory alkalosis was present in macaques acutely affected with Rocky Mountain spotted fever.

Animals↗