Hydrops of the gallbladder.
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Biomedical subjects
Publications and source records attributed to J Neu.
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Determinations of C3, C4, and C5 concentrations by radial immunodiffusion, and assays for the activation products of C3, C3c and C3d by counterimmunoelectrophoresis, were performed on 80 infants. Seven nonbacteremic preterm infants with necrotizing enterocolitis (NEC) or probable NEC (PNEC) were found at the time of diagnosis to have a significantly lower mean concentration of C3 (P less than 0.05, 1-tailed) without C3 activation when compared to other noninfected preterm infants. Ten full-term and 63 preterm infants were studied prospectively during the first days of life, and were then followed for the postnatal development of localized or systemic infection. Assays for the detection of C3 activation products were negative in all these infants. Four preterm infants who developed PNEC after 5 or more days without clinical illness had low original concentrations of complement components. The pathogenesis of NEC may not involve primarily complement activation, and susceptibility to this condition may be related to pre-existing deficiencies in complement component concentrations relative to gestational age, or to defective activation of C3 in the presence of certain bacterial species and strains.
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The purpose of this study was to assess the usefulness of the white cell ratio of immature neutrophils (PMNs) to total (immature plus mature) PMNs as an indication of infection in the very small premature infant. We retrospectively reviewed the charts of 59 premature infants less than or equal to 1,250 g admitted to our Newborn Intensive Care Unit over a one-year period who had at least one white count determined. Twenty-three were born after rupture of membranes for greater than or equal to 24 hours (PROM), 47 had a one-minute Apgar score less than or equal to 6 and 31 had a five-minute Apgar scores less than or equal to 6, 38 had respiratory distress syndrome (RDS), and 4 had confirmed infection. Thirty-one of the infants had a ratio greater than or equal to .15 in the first day of life, a value which has been suggested in the literature as being abnormal and an indication to suspect sepsis. This ratio bore no statistical relationship to PROM, low Apgar scores, or RDS. We analyzed these same relationships using a ratio greater than or equal to .25, another ratio derived from data in the literature which has been said to suggest infection. No statistical correlation was found for low Apgars or RDS, but there was a significant relationship between PROM and attainment of a ratio greater than or equal to .25 (p less than .005). It is notable that 2 out of the 4 infants with infection had a ratio less than .15. We wish to cast doubt on the applicability of the currently defined WBC ratios in the literature as they apply to the infant with birth weight less than 1,250 g and emphasize the apparent effect of PROM as a factor upon these ratios.
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The timing of the first meconium stool has been considered a marker for proper gastrointestinal functioning in the term infant. There is limited information on the meconium passage patterns of very-low-birth-weight infants of less than 32 weeks' gestation. It is unknown whether feeding practices influence the timing of the first stool in these infants. We retrospectively studied 47 very-low-birth-weight infants with birth weights of 1250 g or less who were previously enrolled in a study of gastrointestinal (GI) priming. Infants whose mothers desired to breast feed (n = 7) were given GI priming with their own mother's milk. The remaining infants had been randomly assigned to receive total parenteral nutrition alone (n = 21) or GI priming with infant formula (n = 19) during the first 14 days of life. We attempted to advance all infants to full enteral nutrition by 21 days of age. There was no statistically significant difference in timing of the first stool among the three groups. The overall median age at first stool was 43 hours, and the 75th percentile was 10 days. The range was 1/2 hour to 27 days. There was no concordance between time of first stool and birth weight within the range studied. There was no concordance between time of first stool and necrotizing enterocolitis, although there was little statistical power to detect this. There was also very little concordance with feeding tolerance. Other than necrotizing enterocolitis, no significant GI disease developed in any of the infants studied.(ABSTRACT TRUNCATED AT 250 WORDS)
Glutamine is an important energy source for small intestinal epithelial enterocytes and serves as a key precursor for de novo synthesis of purines and pyrimidines in these rapidly dividing cells. Although glutamine synthetase (GS) is known to be the major enzyme of glutamine biosynthesis, the precise localization of this enzyme in the small intestine is not known. Because glutamine is an important precursor for nucleic acids biosynthesis, we hypothesized that GS is preferentially expressed in the crypt region, which contains the rapidly proliferating cells in the small intestine. Accordingly, immunofluorescence with a specific polyclonal antibody and in situ hybridization using a riboprobe were performed to localize GS protein and mRNA, respectively, in adult rats. Both GS protein and GS mRNA were detected primarily in the crypt region. This finding suggests that GS is located in the region with the highest nucleotide synthesis and cell proliferation. This finding is in support of the use of parenteral glutamine in patients with severe mucosal injury affecting the crypts.
BACKGROUND: There is growing evidence that glutamine may be a conditionally essential amino acid for critically ill patients, including preterm infants cared for in neonatal intensive care units (NICUs). In a randomized study of 68 very-low-birth-weight (VLBW) infants, we found evidence of lower morbidity in a group fed glutamine-supplemented preterm infant formula from postnatal day 3 to day 30 than in a group fed a standard formula. We report here the effects of the glutamine supplementation on hospital costs in these infants. METHODS: The costs were analyzed by log-rank tests and Kaplan-Meier plots. RESULTS: The median costs for hospitalization, radiology, pharmacy, laboratory, and the NICU, and the median number of utilization units were reduced with glutamine supplementation. CONCLUSIONS: This study provides the first evidence for decreased hospital costs in VLBW neonates who receive enteral glutamine supplementation.
BACKGROUND: We have previously shown that glutamine synthetase protein and mRNA are concentrated in the crypt region of the rat small intestine and that the activity of this enzyme is highest around the time of weaning. This anatomical location and time of peak activity are sites and periods of active enterocyte differentiation. This led to our current hypothesis that glutamine synthetase is important in the differentiation of enterocytes. METHODS: To test our hypothesis, we treated Caco-2 cells with physiologic (0.6 mM) glutamine concentrations in cell culture medium. The experimental group was treated with methionine sulfoximine, an irreversible glutamine synthetase inhibitor, and the control group with phosphate buffered saline. Three standard and well-defined markers of intestinal differentiation-sucrase-isomaltase activity, microvillus formation, and electrical impedance in transwell plates-were compared between the two groups. RESULTS: The methionine-sulfoximine-inhibited group was found to have lower sucrase-isomaltase activity, a lower density of microvilli, and lower electrical impedance values over time compared with the control group. CONCLUSION: The experimental group was found to be less differentiated by all three markers of differentiation. Therefore, glutamine synthetase is important for Caco-2 cell differentiation.
Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in the neonatal intensive care unit. It is a disease of medical progress in that more very low-birth-weight neonates are surviving than ever before and are thus susceptible to this potentially devastating disease. NEC received very little attention in the literature before the 1970s but now is well known to all neonatologists and pediatric surgeons. The 1500 to 2000 infants that die every year from this disease in the United States and the large number of infants who develop short gut syndrome from this disease only represent the tip of the iceberg of the problems NEC causes. The widespread fear of NEC among neonatologists and pediatric surgeons has contributed in large part to the use of the IV route rather than the gastrointestinal tract for nourishing these infants for relatively long periods. The consequences of this include a high incidence of sepsis, high hospital costs, and potential long-term neurodevelopmental disability because of poor nutrition during a very vulnerable period of growth and development. The purpose of this review is to provide a brief overview of the clinical presentation and current treatment for NEC, then provide a discussion of the pathophysiology on which strategies for prevention can be formulated.
Very low-birth-weight infants have minimal endogenous nutritional reserves and are at high risk for stresses that induce further breakdown of these diminished reserves. They frequently receive very little glutamine because enteral feedings are often delayed and glutamine is not included in parenteral nutrition. Here we describe studies of glutamine supplementation in very low-birth-weight infants and discuss potential mechanisms for the beneficial effects.