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Biomedical subjects

B L Nichols

Publications and source records attributed to B L Nichols.

At least 37 records · Page 2Linked to original sources
PubMed1992

Developmental changes in lactase-phlorizin hydrolase precursor isoforms in the rat.

The purpose of this study was to determine whether the developmental decline in lactase specific activity (mumol/min/g protein) in the rat was associated with (a) changes in the relative quantities of immunoisolated precursor and mature forms of the enzyme purified by SDS-PAGE and/or (b) immunohistologic changes in the jejunal mucosa. We studied 10- and 16-day-old suckling rat pups, 22-day-old weaned rat pups, and adult female rats (nongravid, pregnant, and lactating). Lactase activity was three- to fourfold higher in 10-day-old pups than in adult rats. Lactase activity was 27% greater in lactating compared with nongravid or pregnant rats. Three molecular forms of the enzyme that migrated identically in all animals were observed on SDS-polyacrylamide gels stained with Coomassie blue: 140-kDa (mature brush border form), 200-kDa, and 220-kDa (apparent precursor forms). There was a striking difference in the proportions of the three polypeptides at different ages that was unrelated to animal status, i.e., pregnant or lactating. As the animals aged, the relative amount of the 140-kDa band declined from 86 +/- 1.1% of the total immunoprecipitated lactase in 10-day old suckling pups to 68 +/- 0.7% in adults. Simultaneously, the relative concentration of the 200-kDa band rose from 1.7 +/- 0.4% in the 10-day-old to 19 +/- 0.6% in adults. The relative concentration of the 220-kDa polypeptide did not change as a function of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

Energy requirements of breast-fed infants.

Current recommendations for energy intake are reviewed in light of emerging data on energy intakes of breast-fed infants and on total daily energy expenditure of infants. For determination of energy requirements, the historical approach based on observed intakes of healthy infants is compared with a newly proposed approach based on energy expenditure and deposition. A data set of exclusively breast-fed infants is used to illustrate the circuity of either approach. Energy intake, expenditure, and stores must be evaluated in an assessment of dietary adequacy. Ultimately, energy requirements of infants should reflect growth rate, body composition, and level of physical activity conducive to optimal health and neurobehavioral development.

Basal Metabolism↗
PubMed1990

Preliminary study of breastfeeding and bacterial adhesion to uroepithelial cells.

The oligosaccharide content of breast-milk and urine from ten nursing mothers and their babies, collected 30 days after delivery, was analysed by thin-layer and high-performance liquid chromatography. Each woman's milk and urinary oligosaccharide profiles were very similar, and the pattern of oligosaccharides excreted by her infant was also strongly correlated with that of her milk. The babies excreted 300-500 mg/day oligosaccharides and the mothers 500-800 mg/day. The effect of oligosaccharide fractions from a 500 ml pool of colostrum on bacterial adhesion to uroepithelial cells was tested on a strain of Escherichia coli isolated from an infant with urinary tract infection. The high-molecular-weight sialylated oligosaccharides had no effect but neutral oligosaccharides caused inhibition of bacterial adhesion which rose as the size of the oligosaccharides decreased. These findings suggest that breastfeeding may have a preventive effect on urinary tract infection in both mother and infant.

Adolescent↗
PubMed1990

Pathogenesis of small-intestinal mucosal lesions in chronic diarrhea of infancy: I. A light microscopic study.

In an effort to increase our understanding of the pathogenesis of chronic protracted diarrhea in infants, we examined 44 jejunal mucosal specimens. Only 3 of the 44 specimens showed a normal mucosa (grade 1). Partial villous atrophy was seen in 17 mucosal specimens (grade 2) with marked patchiness in all of the specimens. Subtotal or total villous atrophy (grade 3) was found in the remaining 24 mucosal biopsies. Plasma cells and macrophages were variably increased and intraepithelial lymphocytes were moderately increased in grades 2 and 3. Eight of ten mucosal biopsy specimens embedded in plastic material and cut at 1-2-mm thickness, showed bacteria of unidentified nature, situated either above the microvillous layer or on the mucosal surface. Both adherent and nonadherent bacteria could be identified in the same specimen. We concluded that severe pathological mucosal changes are common in young infants with protracted diarrhea and that the presence of bacteria may be more common than has previously been documented.

Atrophy↗
PubMed1990

Pathogenesis of small-intestinal mucosal lesions in chronic diarrhea of infancy: II. An electron microscopic study.

Our electron microscopic study of biopsies taken from 10 infants with protracted diarrhea was conducted in an effort to determine the pathogenesis of the disorder. In this article, the ultrastructure of the jejunal mucosa of the infants is described in relation to overlying or adherent bacteria of unidentified type. In addition to the known changes on the enterocyte surface caused by adherent bacteria (cupping and effacement), other cytopathic changes, not previously reported, are documented. Included are widespread loss of enterocytes, including intraepithelial lymphocytes, into the bowel lumen; cytopathological changes within the enterocytes; and marked thickening of the basal laminae of the enterocytes and the endothelium of lamina propria blood vessels. In addition, we noted deposition of collagen fibrils in the lamina propria below the basal laminae, active phagolysis within macrophages, and lack of cisternal material (immunoglobulin) in the plasma-cell cytoplasm. Although these changes are nonspecific, they may be related in part to the presence of the nonadhering and adhering bacteria, and their identification may further our understanding of the "sick mucosa" that occurs in chronic diarrhea of infancy.

Bacteria↗
PubMed1990

Iron is not required in the lactoferrin stimulation of thymidine incorporation into the DNA of rat crypt enterocytes.

Lactoferrin has been identified as a factor in human colostrum that accounts for increased incorporation of thymidine into the DNA in an in vitro rat crypt enterocyte bioassay. We have examined lactoferrin-stimulated thymidine incorporation by comparing the effects of iron-free lactoferrin (apolactoferrin) with those of iron-saturated lactoferrin (diferric lactoferrin) under conditions that inhibit the transfer of iron between these iron-binding proteins in the bioassay system. In addition, we have compared the dose-response relationships of diferric lactoferrin and apolactoferrin. The results demonstrated that lactoferrin, independent of iron-binding states, promoted the incorporation of thymidine into the DNA of rat crypt enterocytes. These observations suggest a previously unreported nutritional role for lactoferrin that is independent of its iron-binding capacity.

Animals↗
PubMed1989

Nutrient intake and growth performance of older infants fed human milk.

STUDY OBJECTIVE: To determine whether the ad libitum addition of solid foods to the diet of exclusively human milk-fed infants will increase energy intake and reverse the decline in weight-for-age percentiles observed during the exclusive breast-feeding period. DESIGN: Weekly or biweekly measures of growth were made longitudinally on a cohort of infants from birth to 36 weeks of age, and monthly measures of nutrient intake were made from 16 weeks of age until 10 weeks after solid foods were introduced into the diet. SUBJECTS: Volunteer mother-infant pairs from middle and upper income groups who met entry criteria, including the intention to breast-feed exclusively for at least for 16 weeks; 58 pairs entered and 45 pairs completed the study. INTERVENTION: Solid foods were introduced at a time determined by the mother and the pediatrician; solid foods from controlled lot numbers were provided for each infant. MEASUREMENTS AND MAIN RESULTS: After solid foods were added, daily human milk intake declined at a rate of 77 gm/mo (p less than 0.001). Milk composition did not change during the observation period. Daily total energy intake increased 29 kcal/mo, but no changes were noted in energy intake when consumption was normalized for body weight. Weight (National Center for Health Statistics percentiles) at 28 weeks was 13 percentiles lower than that at birth, and length at 28 weeks was 1 percentile lower than at week 1. Weight and length percentiles at 28 weeks, when compared with peak values at 8 weeks, had dropped 19 and 14 percentiles, respectively. CONCLUSIONS: Energy intake of human milk-fed infants did not increase after solid foods were added to their diet but was maintained at approximately 20% below recommended levels. Energy intake appeared to reflect infant demands. These data suggest that the recommendations for the energy requirements of infancy should be reevaluated. The growth pattern of exclusively breast-fed infants differs from that of the National Center for Health Statistics reference population. These observations raise questions about the adaptive response of human milk-fed infants to different levels of energy intake and about the estimations of energy requirements based on the sum of basal metabolism, activity, growth, and diet-induced thermogenesis.

Body Weight↗
PubMed1989

Human milk and the rate of small intestinal mucosal recovery in protracted diarrhea.

STUDY OBJECTIVE: To determine whether human milk accelerates the recovery rate of injured small intestinal mucosa. DESIGN: Randomized, controlled trial. SETTING: County and nonprofit, private urban hospitals. PATIENTS: Moderately to severely malnourished infants less than 6 months of age who required parenteral nutrition for treatment of protracted diarrhea. INTERVENTIONS: Either a human milk preparation (n = 7) or sterile water (n = 9) was administered by continuous nasogastric feeding (14 mL/kg/d) over a 2-week study period while the infants received parenteral nutrition. MEASUREMENTS AND MAIN RESULTS: Small intestine perfusion studies and biopsies were performed at the beginning and end of the study. Age, duration of prior illness, severity of malnutrition, glucose and water absorption, disaccharidase activities, atrophy of villi, and nutritional intake were comparable in both groups of infants. At the end of the 2-week study, improvement toward normal sucrase activity and intraepithelial lymphocytes was found in significantly fewer infants in the milk group than in the water group. No differences were noted in glucose and water absorption or in lactase and maltase activities as a function of the milk versus water treatment. CONCLUSIONS: Human milk did not accelerate functional recovery of the small intestinal mucosa.

Clinical Trials as Topic↗
PubMed1989

Acquired monosaccharide intolerance in infants.

To determine the frequency with which acquired monosaccharide intolerance (AMI) occurs in infants less than 3 months of age, we performed a prospective descriptive study of infants admitted to the hospital for diarrhea. We searched for differences between the characteristics and causes of AMI in these infants and those of a cohort of similar-aged infants admitted with acute diarrhea (AD). Five hundred fifty-five infants less than 3 months of age admitted with diarrhea were enrolled. Nine percent of those infants had AMI, 40% had other forms of chronic diarrhea, and 51% had AD. The mean age at hospital admission was 32 days for the infants with AMI and 44 days for the infants with AD. The mean weight loss of AMI infants was 0.3 g/day since birth, and the mean weight gain was 14.3 g/day for AD infants. The mean dehydration by difference in weights at admission and 48 h postadmission was 5% for AMI and 3% for AD infants. Bacterial and viral causes of the diarrhea were similar. At admission to the hospital, infants in whom AMI subsequently developed were younger, more malnourished, had more prolonged diarrhea, and were more dehydrated than the AD infants. Malnutrition stands out as a significant antecedent factor that contributes to the development of AMI.

Acute Disease↗
PubMed1989

Human lactoferrin supplementation of infant formulas increases thymidine incorporation into the DNA of rat crypt cells.

Lactoferrin has been identified as the factor in human colostrum that accounts for the increased incorporation of thymidine into DNA in a rat crypt enterocyte bioassay. Commercially available infant formulas used in the refeeding of infants who have severe dietary intolerance associated with mucosal atrophy were tested in this bioassay. In contrast to human milk, no stimulation was observed with these formulas in the assay. All formulas inhibited basal thymidine incorporation. The degree of inhibition of the basal assay progressed from 14% with cow's-milk formula to 30% with soy-based formulas to 45% with hydrolyzed casein formulas. When the formulas were supplemented with lactoferrin to match the level of that in human milk, the result was a 35% relative increase in thymidine incorporation into DNA. The quantitative level of response was primarily influenced by the baseline inhibitions associated with the specific formulas. The most profound effect was observed with the hydrolyzed casein formula, when lactoferrin supplementation reversed the baseline inhibition but did not result in a response greater than that seen in control basal bioassays. The supplementation of infant formulas with lactoferrin improved the thymidine incorporation in rat crypt enterocytes; a response equivalent to that of human milk, however, would require a redesign of other formula components to reduce basal inhibition.

Animals↗
PubMed1989

Dietary origin of retained H+ in infants with acquired monosaccharide intolerance.

Net external acid balance was studied in 12 malnourished infants with chronic diarrhea (some of whom had acquired monosaccharide intolerance). When the infants achieved an adequate energy intake from a formula that contained either glucose or glucose polymers, seven developed metabolic acidosis and five remained free of acidosis. During the study, the acidotic infants produced a significant excess of acid (3.7 +/- 2 vs. 0.5 +/- 2 mEq/kg/day, p less than 0.005). The amount they excreted in urine (2.9 +/- 2 mEq/kg/day), however, was similar to that excreted by nonacidotic infants (2.7 +/- 2 mEq/kg/day) and indicated renal inability to reduce the excess acid load. The net effect was hydrogen ion (H+) retention (+0.8 +/- 0.8 vs. -2.2 +/- 0.8 mEq/kg/day, p less than 0.001). Good correlation existed between the net acid balance and the acid-base measurement in the blood. We speculate that (a) the increased acid load was a consequence of colonic bacterial production of volatile fatty acids from carbohydrate malabsorbed from the small bowel and (b) the renal incapacity to excrete H+ probably was secondary to potassium and phosphate depletion.

Acidosis↗
PubMed1988

The miniature pig as an animal model for the study of intestinal enzyme development.

Studies of intestinal enzyme development and regulation relevant to the human infant require an animal model with a rate of maturation similar to that of the human infant. Hanford miniature pigs were weaned at 3 days of age to a standard swine weaning formula. At 1, 2, 3, 4, 5, and 6 wk of age, duodenal jejunal, and ileal segments were analyzed for protein content and lactase, sucrase, maltase, glucoamylase, and acid beta-galactosidase activities. Protein content of the small intestine changed significantly with age only in the ileum (p less than 0.05). Lactase activity fell significantly with age in all segments of the small intestine (p less than 0.001); activity was highest in the jejunum. Sucrase and maltase activities were present in all segments of the small intestine at 1 wk of age. Sucrase increased significantly (2-fold, p less than 0.02) with age only in the ileum and maltase increased significantly with age in the jejunum (by 50%, p less than 0.05) and the ileum (3-fold, p less than 0.001). Activities were highest in the jejunum. Glucoamylase activity was present at 1 wk of age and showed a small but significant increase with age only in the duodenum (p less than 0.005). Acid beta-galactosidase activity demonstrated small but significant decreases with age in all small intestinal segments. Glucoamylase and acid beta-galactosidase activities were similar in all segments. In the 6-wk-old pigs, activities of all the enzymes tested were similar to those found in young human infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Macro- and trace-mineral intakes of exclusively breast-fed infants.

Intakes of calcium, phosphorus, magnesium, zinc, sodium, potassium, iron, and copper of 45 exclusively breast-fed infants were determined during the first 4 mo of life. Direct 24-h measurements of milk intake and mineral contents of human milk were used to estimate mineral intakes. Daily intakes of Ca, P, Zn, K, Na, Fe, and Cu decreased significantly over the study period while the intake of Mg increased. With the exception of Mg, mineral intakes on a weight basis displayed significant quadratic trends over the 4 mo. In spite of seemingly low-mineral intakes, growth progressed satisfactorily.

Body Height↗
PubMed1987

Specific effects of weight loss, protein deficiency and energy deprivation on the water and electrolyte composition of young rats.

Specific effects of weight loss, protein deficiency and energy deprivation on the water and electrolyte content of the body were studied. Longitudinal changes in total body Na and Cl were measured by neutron activation analysis in young rats fed either a low protein diet (LP) ad libitum or a control diet in restricted amounts (ER). Total body Ca was determined to monitor growth of skeletal mass. Four balance periods were defined to represent various stages of protein or energy deprivation. The chemical composition of the rats was determined at the end of the study and compared with that of rats killed at the start of the study. Changes in body composition of LP rats were attributable chiefly to wasting of body cell mass. There was no retention of Na and Cl until severe hypoalbuminemia and edema developed after chronic protein deprivation; at this time, Na and Cl were retained in the same proportion as their molar ratio in extracellular fluid (ECF). The resulting increase in ECF volume accounted for the high total body water values in LP rats. Energy restriction to approximately 80% of maintenance requirements for 20 d resulted in Na retention in a compartment distinct from either the Cl or Ca space. With prolonged ER, there was preferential wasting of cell mass and adipose tissue but relative preservation of the ECF compartment; there was no net retention of Na and Cl, and hydration of fat-free mass was normal. The differences in the body compositions of ER and LP rats suggested that protein and energy deprivation can have separate effects on Na and Cl homeostasis that are distinct from changes induced by a loss of cell mass.

Animals↗
PubMed1987

Electrolyte composition changes of chronically K-depleted rats after K loading.

The responses of whole body, skeletal muscle, and plasma to oral K loading were studied in K-depleted male rats. Potassium depletion was induced by feeding the rats a K-deficient diet for 4 wk and injecting deoxycorticosterone acetate during the first week. After 4 wk, the rats were growth retarded and hypokalemic (1.9 mmol/l plasma) and had low whole-body and muscle K content, 188 +/- 27 and 276 +/- 19 mmol/kg fat-free dried tissue (FFDT), respectively, compared with 296 +/- 10 and 454 +/- 13 mmol/kg FFDT for the control group. Sodium and water retention also occurred in the K-deficient group. After K depletion, the rats were divided into four groups and received either 0, 1, 2, or 3 intragastric doses of 10 mmol KCl/kg at 8-h intervals. The rats were killed 8 h after the last dose. Control rats were treated similarly. K-depleted and control rats responded differently to K loading. In the normal rats, plasma K remained at 5.0 +/- 0.5 mmol/l, muscle K increased to 502 +/- 24 mmol/kg, and muscle K/N ratio increased from 3.0 to 3.4 mmol/g. In the K-depleted rats, plasma K increased to 7.2 +/- 0.7 mmol/l, muscle K increased to 453 +/- 50 mmol/kg, and muscle K/N ratio increased from 1.8 to 3.1 mmol/g. These data indicate that the capacity of the muscles to accumulate K was impaired after severe K depletion and caused elevated plasma K levels when repletion was complete.

Animals↗
PubMed1987

Human lactoferrin stimulates thymidine incorporation into DNA of rat crypt cells.

In a search for dietary factors that might stimulate enterocyte proliferation, we developed an assay for thymidine incorporation into DNA using harvested crypt cells from mature rat small intestine. Human colostrum stimulated a significant increase in thymidine incorporation into rat crypt cell DNA during a 60-min period of incubation. When the protein with biological activity was purified to a single peak by sequential ion exchange and gel filtration chromatography, it was found to have the characteristics of lactoferrin. The protein was identical to lactoferrin standards by sodium dodecyl sulfate polyacrylamide gel electrophoresis, isoelectric focusing, and double-diffusion immunologic precipitation. All available human lactoferrins stimulated thymidine uptake and all reacted with a lactoferrin polyclonal antibody. Human lactoferrin appears to be a potent activator of thymidine incorporation into DNA in incubated rat crypt cells, a nutritional function not previously reported.

Animals↗