摘要:

Motor activity was recorded in 19 preterm infants three times during the first postnatal month. There was a paucity of small intestinal motor quiescence during fasting in the first postnatal week; however, its duration significantly increased with postnatal age (p< 0.03). Although fasting motor patterns changed with postnatal age. motor responses to feeding were present within the first few days of life. Motor activity was also recorded weekly in 11 newborn dogs for 6 wk. Intestinal motor quiescence was also absent during fasting for the first postnatal week but it significantly increased with postnatal age (p< 0.002). As in the human preterm infant, a motor response to feeding was present within the first few days of life. Plasma concentrations of gastrin and peptide YY during fasting were low in the preterm human and canine neonate during the first postnatal week but plasma concentrations of both peptides increased with postnatal age. Although plasma concentrations of gastrin were low during fasting for the first postnatal week, plasma concentrations of gastrin increased significantly postprandially compared with fasting (p< 0.05). We conclude that motor quiescence during fasting becomes a more prominent feature of newborn intestinal motor function postnatally. In addition the release of two peptides that regulate motor patterns also change postnatally. Thus, postnatal changes in motor patterns and peptide release change in a parallel fashion in human preterm neonates and canine neonates. We speculate that the postnatal change in intestinal motor quiescence reflects changes in inhibitory regulation by the enteric nervous system and that the neonatal dog will provide an excellent animal model to explore the mechanisms that regulate maturation of small intestinal motor function in the preterm infant.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Previous studies revealed that postnatally developing rats are resilient to the lethal effects of chlordecone (CD) + carbon letrachloride (CCI4) combination. The objective of this study was to investigate the underlying mechanism. We hypothesized that ongoing cell division and cell cycle progression as well as additional toxicant-induced stimulation of tissue repair help in restraining the progression of injury on the one hand, and in recovery through speedy healing on the other. Postnatally developing (20− and 45-d) and adult (60-d) male Sprague-Dawley rats were challenged with a nontoxic single dose of CCI4(100 μL/kg. i.p.) or corn oil after pretreatment with either dietary CD (10 ppm) or normal diet (ND) for 15 d. Hepatocellular injury was assessed by measuring serum enzymes [alanine transaminase (ALT), sorbitol dehydrogenase (SDH)], and bilirubin, as well as by histopathologic examination of liver sections during a time course of 0–96 h after the administration of CCI4or corn oil. Hepatocellular regeneration was assessed by [3H]thymidine ([3H]T) incorporation into hepatic nuclear DNA. In CD + CCI4treatment, ALT, SDH, and bilirubin levels peaked between 36 and 48 h after CCI4. All 20-d-old rats survived the challenge of CD + CCI4. CD-potentiated hepatotoxicity and lethality of CCI4begin to be manifested in 45-d-old rats at 48 h and later times (25% mortality), whereas adult rats experience progressive hepatotoxic injury and 100% mortality by 72 h. In contrast, regardless of pretreatment, 20-d-old rats recover fully from injury by 72 h after CCI4treatment. The rapid recovery of 20-d-old rats was associated with a combination of higher level of ongoing cell division and additional sustained stimulation of [3H]T incorporation from 24 to 72 h after the administration of CCI4. In the older rats (45− or 60-d-old) this response was significantly delayed and attenuated. Ongoing cell division and CCI4-stimulated regeneration were inversely related to postnatal development (20-, 45-, or 60-d). These biochemical, histopathological, and [3H]T incorporation studies suggest that the liver of younger rats has greater plasticity for repair after toxic injury whereas adult liver is much more quiescent in this regard.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

To investigate the effect of pubertal development on serum levels of IGF binding protein-3 (IGFBP-3) and IGF-1, and the relationship between IGFBP-3 levels and height, weight, weight for height and age (WFHA), and IGF-1 levels, a cross-sectional study was performed in a Spanish basic education school in Vigo (NW Spain). The study was made up of 181 girls with a mean chronologic age of 11.03 ± 0.22 y and 173 boys with a mean chronologic age of 10.9 ± 0.23 y. The pubertal development was graded into three groups according to estradiol and testosterone concentrations for girls and boys, respectively. All subjects were in good health and among the 5th and 95th percentile for height. Serum IGFBP-3 and plasma IGF-1 concentration was determined by RIA. Pubertal development was significantly associated with IGFBP-3 and IGF-1 concentrations in girls and boys, respectively (p< 0.0001, analysis of variance). Multivariate regression analyses between IGF-1 or IGFBP-3 with age, sex, and estradiol or testosterone show significative correlation in prepubertal children for IGF-1 (r= 0.545,p= 0.0001 andr= 0.574,p= 0.0001 for girls and boys, respectively) and only in prepubertal boys for IGFBP-3 (r= 0.336,p= 0.0012). The linear correlation between IGF-1 and IGFBP-3 was significant in both prepubertal (r= 0.25,p< 0.0001) and pubertal (r= 0.40,p< 0.0001) girls, but only in prepubertal boys (r= 0.30,p< 0.0001). Stepwise regression analysis between SD score (SDS)-IGFBP-3 or SDS-IGF-1 as independent variables and height-SDS, weigh-SDS, WFHA, and age as dependent variables, show that IGFBP-3 or IGF-1 are significantly correlated to WFHA only in prepubertal children. Present data suggest that interpretation of IGFBP-3 concentrations during adolescence requires knowledge of gonadal steroid levels, and the determination of IGFBP-3 level is a useful parameter for clinical proposes mainly in prepubertal children.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Bile acids and bilirubin are synthesized by the fetal liver very early on during intrauterine life. The main fate of these compounds is to be transferred to the mother. This excretory role of the placenta is primarily determined by the ability of the trophoblast to transport them, which is believed to occur mainly by carrier-mediated processes. The aim of this study was to investigate the role of the cholephilic organic anion exchanger located in the fetal-facing plasma membrane of the human trophoblast in placental “biliary-like‘’ function. No relationship between the magnitude of transplacental gradients for total bile acids and bilirubin was found. However, transport studies, which were carried out by using perified plasma membrane vesicles derived from the fetal-facing pole of the human trophoblast, revealed that [14C]taurocholate transport was affected by both another bile acid (taurochenodeoxycholic acid) and a non-bile acid cholephilic organic anion (bromosulfophthalein). On plotting the ability of different major bile acid species to inhibit radiolabeled taurocholate uptake by these vesiclesversustheir concentrations in fetal serum or the magnitude of their transplacental gradients, inverse relationships were found. Lower fetal serum concentrations and transplacental gradients were found for bile acid species with higher abilities to affect this transport and presumably to interact with the carrier. By contrast, the magnitude of the transplacental gradient for bile acid species was not correlated with their hydrophobic/hydrophilic balance, as would be expected if diffusion across the lipidic structures of the placental barrier would be the major pathway for the flux of bile acid across this organ. In summary, these results indicate that carriers located in the basal plasma membrane may play an important role in the control of the qualitative and quantitative fetal-maternal bile acid exchange. Moreover, they suggest that although both bile acids and bilirubin may share this pathway for access to the trophoblast, other additional mechanisms are probably responsible in part for the control of the magnitude of their transplacental gradients.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Several epithelial ion transporters are developmentally regulated in the preweaning period, at the time when the ciculating levels of glucocorticoid and mineralocorticoid hormones increase. The specific role of glucocorticoids and mineralocorticoids in the maturation of epithelial ion transporters is still disputed. In this study, we investigated the effect of corticosteroids on the mRNA expression of ion transporters in the infant rat colon, a glucocorticoid- and mineralocorticoid-sensitive organ. The expression of the Na,K-ATPase, the H,K-ATPase and the amiloride-sensitive Na+channel mRNA was investigated in control rats from fetal to adult life. We found that the mRNA of the three transporters is temporarily up-regulated in the preweaning period. Rats were then injected with a single dose of betamethasone or aldosterone at 10 d of age. The main effect was the glucocorticoid stimulation of the Na,K-ATPase mRNA within 6 h (4-fold). Glucocorticoids did not alter H,K-ATPase nor Na+channel mRNA within 6 h. Aldosterone moderately (1.7-fold) stimulated Na+channel within 6 h, but did not alter Na,K-ATPase nor H,K-ATPase mRNA. Twenty-four hours after injection, both glucocorticoids and mineralocorticoids had less pronounced and distinct effects. In tissue with lower aldosterone receptor abundance (renal cortex) or with no aldosterone receptor (stomach), glucocorticoids induce a similarly rapid increases in Na,K-ATPase mRNA (4-fold within 6 h), whereas aldosterone had no effect within 6 h. However, glucocorticoids did not stimulate Na,K-ATPase mRNA in the brain, a tissue rich in glucocorticoid receptors.This study indicates that Na,K-ATPase is a primary target for glucocorticoids in the preweaning period, and suggests that glucocorticoid induction of Na,K-ATPase mRNA may play an important role in the maturation of epithelial ion transport capacity. The effect is probably mediated by glucocorticoids and not by mineralocorticoid receptors. However, it seems that an auxiliary factor is required for glucocorticoid-dependent stimulation of Na,K-ATPase mRNA.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Infants of diabetic mothers have an increased risk for thrombosis. The etiology of their hypercoagulable state is unknown. To examine the effects of hyperinsulinemia on the development of coagulation during fetal life, 10 sets of chronically catheterized fetal lambs were studied. One twin from each pair of 120-d gestation lamb fetuses was infused with insulin at a rate of 2.5 U/h for 48 h, whereas its twin sibling was infused with an equal volume (20 ml.) of dextrose 5% in water Changes in coagulation factor activities were measured before and after the infusions, and differences were analyzed by pairedttests. There was a significant decrease in protein C after insulin treatment in the insulin-treated twins. There were relative increases in fibrinogen factors V, VII, and XI when the insulin-treated group was compared with the controls. The changes are consistent with an increased risk of thrombosis and may explain, in part, the higher incidence of thrombosis in infants of diabetic mothers.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

A randomized, investigator-masked trial determined the effects of oral recombinant human transforming growth factor-α (TGFα) on jejunal mucosal recovery in 75 piglets with rotavirus diarrhea. Rotavirus inoculation of artificially reared piglets induced subtotal (∼50%) villus atrophy and watery diarrhea. Dietary TGFα was associated with significant restoration of villus surface area by 4 d postinoculation (p.i.) and complete restoration by 8 d p.i., whereas saline-treated animals required 12 d for recovery. Jejuna segments from clinically recovered TGFα-treated piglets showed an increase in electrical resistance across the epithelial barrierin vitrowhich was proportional to villus height. TGFα treatment for 12 d also produced a 30–50% increase in jejunal mucosal mass (protein content and wet weight), compared with the corresponding values in salinetreated piglets and in uninfected controls. However, oral TGFα did not hasten the resolution of diarrhea, enhance the specific activities of jejunal mucosal digestive enzymes, or increase jejunal glucose-stimulated Na+absorptionin vitro.We conclude that dietary TGFα stimulates jejunal mucosal hypertrophy, improves barrier function, and enhances regrowth of villi in rotavirus enteritis; however, it does not facilitate the restoration of functional activity or mucosal digestive enzymes. Oral TGFα can facilitate intestinal epithelial recovery in diseases associated with mucosal damage.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Based on the observation that children with a history of atopic disease show significantly increased levels of cleaved secretory lgA in nasopharyngeal secretions, we have previously formulated the hypothesis that bacteria-induced local deficiencies of the immune barrier of the upper respiratory tract may be a contributing factor in the development and perpetuation of atopic diseases. To evaluate this hypothesis, 25 infants were subjected to clinical, bacteriologic, and immunologic examination at the age of 18 mo, 30 mo, and 5 y. The 11 infants, who showed clinical and immunologic evidence of atopic disease at the age of 18 mo, harbored significantly higher proportions of lgA1 protease-producing bacteria (median, 36%; range, 14–64%) than the 14 healthy infants (median, 5%; range, 0.4–14%). No statistically significant differences were observed at the two subsequent examinations, but healthy children showed a statistically significant increase in proportions of lgA1 protease-producing bacteria in the pharynx with increasing age. lgA1 protease-producing bacteria detected includedStreptococcus mitis biovar1.Hoemophilus influenzae, Haemophilus parahaemolyticus, Streptococcus pneumoniae, andNeisseria meningitidis, of which the first mentioned species was mainly responsible for the difference observed at the 18-mo examination. Percentage proportions of lgA1 protease-producing bacteria were significantly related to passive smoking which may stimulate the premature and more pronounced pharyngeal colonization of the atopic infants with the lgA1 protease-producing variant ofS. mitisbiovar 1. The results of the study support the hypothesis that lgA1 protease-producing bacteria colonizing the upper respiratory tract jeopardize the local immune barrier and, thereby, may facilitate the penetration of potential allergens resulting in atopic disease.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Children with asthma usually become asymptomatic by the time they reach age 20 y. To clarify the immunologic mechanisms responsible for this phenomenon, we studied patients in remission and others who still had frequent asthma attacks. Patients were grouped by clinical status, and three variables were measured: serum levels of lgE, production of 11.4 and interferon (IFN)-γ, and the activation of T cells induced byDermaophagoides farinae(DF) antigen. Df-induced activation of T cells (as measured by antigen-induced 11.2 responsiveness) or 11.2 synthesis itself was induced in patients with active asthma but not in normal subjects. These responses were much weaker in patients in remission. When stimulated by Df antigenin vitro, lymphocytes from patients with active asthma produced much more 11.4 than did the cells from normal subjects, and cells from patients in remission produced only a small amount. In contrast, under similar conditions lymphocytes from patients with active asthma produced less IFN-γ than did the cells from normal subjects. Production of IFN-γ stimulated by Df antigen was high in patients in remission but not in normal subjects. Thus, up-regulated IFN-γ production after exposure to Df antigen might reduce 11.4 secretion, which would suppress IgE production and would improve clinical status. Df antigen may suppress Df-induced allergic responses in patients with asthma in remission.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The purpose of this study is to describe the pain experienced by children with juvenile rheumatoid arthritis. A patient sample composed of 33 children, 7–16 y of age, with juvenile rheumatoid arthritis was included in the study. The children, their parents, and the attending rheumatologist assessed the child's pain using the Abu-Saad pediatric pain assessment tool. In addition, a disease activity index was used by the physician. All children reported pain. This was most often described as hurring, sitting, warm, and uncomfortable. Significant correlations were found for present pain between the child, parent, and physician. The worst pain of the child for the previous week, and not the present pain, correlated with the disease activity as rated by the physician. These findings indicate a need for pain assessment in patients with juvenile rheumatoid arthritis and emphasize the importance of longitudinal studies in this area.

ISSN:0031-3998    

出版商:OVID    

年代:1995

数据来源: OVID