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Biomedical subjects

B L Nichols

Publications and source records attributed to B L Nichols.

At least 91 records · Page 5Linked to original sources
PubMed1981

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↗
PubMed1981

Total body sodium, calcium, and chloride measured chemically and by neutron activation in guinea pigs.

Body sodium (Na), calcium (Ca), and chloride (Cl) of guinea pigs weighing between 227 and 600 g were measured by total body neutron activation analysis (TBNAA) followed by chemical analysis (CA) on 12-17 animals. Paired t test was used to compare any differences in the results obtained by the two methods. There was no significant difference in the results for the three elements. The means and standard deviation for Ca (g/100 g body wt) 1.070 +/- 0.132 (TBNAA) and 1.107 +/- 0.125 (CA); for Na 0.149 +/- 0.019 (TBNAA) and 0.143 +/- 0.021 (CA); and for Cl 0.126 +/- 0.009 (TBNAA) and 0.132 +/- 0.024 (CA). Neutron activation analysis alone, in a series of 27 animals, gave means (g/100 g body wt) and standard deviation of 1.110 +/- 0.084 for Ca, 0.120 +/- 0.009 for Cl, and 0.153 +/- 0.011 for Na. TBNAA has potential usefulness, particularly in longitudinal studies in the same animal, because of its accuracy and the rapidity and ease with which the measurements can be made.

Animals↗
PubMed1980

Intracellular concentration of elements in normal and dystrophic skeletal muscles of the chicken.

In this study, the intracellular concentrations of six elements (mmole/kg dry weight) were directly measured in the muscle fibers of pectoralis major muscles of eight week old, genetically dystrophic and normal chickens by the X-ray microanalysis technique. The extent of muscle degeneration was evaluated by morphometric measurements of muscle fiber diameter and other histological changes. A significant increase in the concentration of intracellular sodium and chlorine was evident in dystrophic muscles. The concentration of intracellular sodium was 127.0 +/- 35.0 in the muscle fibers of dystrophic chicks compared to 65.7 +/- 16.5 in normal controls. The concentration of chlorine was 90.5 +/- 27.5 and 54.1 +/- 5.5 in the muscle fibers of dystrophic and normal chicks respectively. The intracellular concentrations of potassium, magnesium, phosphorous, and sulfur remained unchanged in the dystrophic condition. Morphometric studies revealed that the dystrophic pectoralis muscles contain fewer but thicker fibers per unit area compared to normal pectoralis muscles. The importance of these findings are discussed in relation to the results of earlier investigations.

Animals↗
PubMed1980

The effect of intestinal solute load on water secretion in infants with acquired monosaccharide intolerance.

The osmotic effect of unabsorbed glucose on intestinal secretion of water and electrolytes was investigated by jejunal perfusion in eight infants ranging from 2 to 17 months of age. All infants had or were recovering from acquired monosaccharide intolerance. Isocaloric solutions of glucose and glucose polymer containing 1% polyethylene glycol as a nonabsorbable marker were tested. The osmolalities of the glucose polymer solutions were 1/3 to 1/6 that of the glucose. No major differences were noted in carbohydrate absorption whereas mean water flux changed from secretion of 0.37 ml/min to absorption of 0.023 ml/min when glucose was replaced by glucose polymer. Sodium and potassium flux followed the same pattern. The results of this study indicate that the increased intestinal secretion in acquired monosaccharide intolerance may be a function of osmolar load in the presence of a reduced absorptive capacity.

Body Water↗
PubMed1980

Neonatal salt loss in the hypertensive form of congenital adrenal hyperplasia.

The 11 beta-hydroxylase deficiency (11OHD) form of congenital adrenal hyperplasia is diagnosed infrequently during the newborn period. A child presumed to have the 21-hydroxylase deficiency form of congenital adrenal hyperplasia was studied extensively as an infant. The diagnosis was based on ambiguous genitalia, elevated 17-ketosteroids, evidence of urinary 11-ketopregnanetriol, and salt loss. Severe hypertension was detected at 11 years, and 11 beta-hydroxylase deficiency was confirmed with elevated plasma 11-deoxycorticosterone and 11-deoxycortisol, low cortisol, and normalization of blood pressure following glucocorticoid replacement. Impaired aldosterone biosynthesis and salt loss were demonstrated during dexamethasone therapy. Salt loss during infancy does not distinguish between the 11 beta- and 21-hydroxylase deficiency forms of congenital adrenal hyperplasia.

Adrenal Hyperplasia, Congenital↗
PubMed1979

Lactation.

Explore the source record for details and available documents.

Body Water↗
PubMed1978

Intestinal surface area in infants with acquired monosaccharide intolerance.

Acquired monosaccharide intolerance is characterized by the malabsorption of all carbohydrates, resulting in profuse acidic diarrhea. Five infants with this syndrome, ranging from two to six months of age, were studied by measuring their ability to absorb glucose given by intestinal perfusion. Jejunal biopsies obtained at the time of perfusion were studied by light and electron microscopy, and surface area measurements were obtained. Glucose absorption and surface area were significantly decreased (P less than 0.005) during the acute phase of the disease and improved during convalescence. A linear correlation (r = 0.8757) was observed between the ability to absorb glucose and intestinal surface area. It is concluded that the loss of absorptive surface is a major cause of the reduced carbohydrate absorption and consequent diarrhea.

Atrophy↗
PubMed1978

Magnesium supplementation in protein-calorie malnutrition.

The widespread observation of magnesium depletion in edematous malnutrition has been confirmed in Guatemalan children. The magnesium requirement during initial stages of therapy has been estimated as 2.7 mEq/kg per day. This may be achieved by adding 0.5% MgSO4.7H2O to a solution containing 15% dextromaltase and 1.5% KCl which is used to dilute whole milk; two parts milk and one part dilution mixture. The replacement of magnesium deficits was not essential for recovery from edematous malnutrition, however, the present evidence suggested that the rate of recovery was accelerated by approximately 2 weeks in those children who received the supplement.

Child↗
PubMed1978

Fiber, intestinal sterols, and colon cancer.

It has been postulated that dietary fiber's protective effect against the development of colon cancer, diverticular disease, and atherosclerosis may be due to the adsorption and/or dilution of intestinal sterols such as bile acids and neural sterols and their bacterial metabolites by component(s) of fiber. Dietary fiber is made up of four major components-cellulose, hemicellulose, lignin, and pectin. There is evidence that hemicellulose and pectin may induce an increase in fecal bile acid excretion in man which may be accompanied by a decrease in serum cholesterol. Natural fibers, such as rolled oats, alfalfa, guar gum, and Bengal gram have been shown to have hypocholesterolemic properties of alfalfa, wheat straw, and some other fibers found considerable amounts of bile acids in vitro. On the other hand, wheat bran, oat hulls, and all the synthetic fibers tested bound only negligible amounts of bile acids under the same conditions. Vegetarians in the United States have lower plasma lipids and different plasma lipoprotein patterns than those of comparable control populations on regular mixed diet. They also have smaller daily fractional turnover rates of cholic acid and deoxycholic acid pool size. In addition, populations on a mixed Western diet, where the rate of large bowel cancer is high (North American, English, Scottish, etc.) degraded and excreted cholesterol and bile acid metabolites to a greater degree than populations where the rate of colon cancer is comparatively low (Ugandan, Japanese, etc). It cannot be denied that the fiber theory linking fiber deficiency with the development of colon cancer and other diseases, is simple, attractive and appears to be firmly based in common sense. When subjected to research studies, however, the situation appears much more complex than expected. Although some progress is being made, the data are often contradictory and confusing, probably due to lack of adequate documentation of fiber intake (e.g., use of dietary fiber instead of crude fiber) and/or the absence of detailed information on the chemistry of the fiber itself.

Adult↗
PubMed1977

Cholesterol ester storage disease: clinical, biochemical, and pathological studies.

Of three siblings affected with cholesterol ester storage disease, two died at ages 7 and 9 years, respectively, with hepatic scarring and portal hypertension. Lipid storage was documented in both patients, as were esophageal varices and aortic plaques in the older child. The third affected sibling, followed to 13 years of age, has hepatomegaly, hyperlipidemia, short stature, adrenal calcification, and acid lipase deficiency. Leukocyte extracts demonstrated deficiency of acid lipase in this patient. This autosomal recessive condition may be allelic with Wolman disease with a more malignant course in this family than in most reported cases.

Child↗