Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of sodium- and potassium-stimulated ATPase (Na,K-ATPase) along the crypt-villus axis and crypt cytokinetics were examined in an infective model of celiac disease produced by infection of the rat with the nematode Nippostrongylus brasiliensis. In controls, levels of enzyme activity remained stable during enterocyte migration to the villous apex. In the jejunum of infected rats, the structural lesion of villous atrophy and crypt hyperplasia, observed at day 10 of infection, was associated with a three-dimensional expansion of the crypts. Cell cycle time was shortened and this resulted in a markedly increased crypt cell production rate. Enterocytes emerged from the crypts at a faster rate, and this functional immaturity was paralleled by decreased Na,K-ATPase activity. Further decreases in enzyme levels were observed during enterocyte migration along the villi. This may reflect enterocyte damage or increased enzyme turnover. In the ileum of these animals, enterocyte maturation was prolonged and enzyme activity was increased at the level of the crypt villus junction with further increases noted during enterocyte transit. These changes in ileal Na,K-ATPase appear to be adaptive.
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PMID:Alterations in quantitative distribution of Na,K-ATPase activity along crypt-villus axis in animal model of malabsorption characterized by hyperproliferative crypt cytokinetics. 131 Apr 59

In the term human and ovine fetus, plasma gastrin is elevated, but gastric acid secretion is below adult levels, suggesting a developmentally related immaturity in gastrin and gastric acid regulation. This study investigated a number of elements of the gastric acid regulatory system: gastrin and its glycine-extended precursor, somatostatin, and the H+/K(+)-ATPase. Measurements were made in blood, antrum, and fundus of the ovine fetus during the last half of gestation, of 15-day-old lambs, and of adult sheep at the level of mRNA synthesis, tissue storage, and secretion. Plasma amidated gastrin (gastrin-amide) was elevated at or above adult values from 125 days (term is 145 days) and steadily increased with development, peaking in the lamb. Similar changes occurred with plasma glycine-extended gastrin (gastrin-gly). The peak concentration of antral gastrin-amide was present in the lamb, while the maximum antral gastrin-gly level occurred 1 week before birth. Gastrin mRNA paralleled the changes in antral gastrin-gly. The proportion of higher mol wt species of gastrin decreased during gestation in both plasma and antrum. Low amounts of mRNA for the H+/K(+)-ATPase was present from at least 120 days of gestation and antedated gastric acid secretion. However, there was a 3-fold increase in H+/K(+)-ATPase mRNA from the 140-day-old fetus to the lamb, the period when the greatest reduction in gastric pH occurred (pH 5 to 2). Antral and fundic somatostatin increased rapidly in the fetus at 120 days gestation and were above adult values at term and in the lamb. Somatostatin mRNA changed in parallel to somatostatin peptide. Somatostatin-14 was the major species in antrum and fundus throughout development. The increase in circulating and antral gastrin-amide after birth may be the result of increased amidation of gastrin-gly as well as increased expression of gastrin mRNA. Amidation of gastrin may be a regulatory step in the production of biologically active gastrin during development. The major increase in gastrin and the H+/K(+)-ATPase that occurs in the week before and after gestation correlated with the onset of increased gastric acidity.
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PMID:Ontogeny of gastrin, somatostatin, and the H+/K(+)-ATPase in the ovine fetus. 134 9

Fetuses of streptozotocin-induced diabetic rats exhibited delayed lung maturation and a 40% reduction in the steady-state level of lung Na+,K(+)-ATPase alpha 1 subunit mRNA and Na+,K(+)-ATPase activity at 21 d of gestation. In in situ hybridization experiments the signal specific for Na(+)-pump alpha 1 subunit message was strongest above columnar epithelial cells of air-conducting structures. Strong labeling was also present above cuboidal cells lining the forming alveoli, but not above mesenchymal cells. Immunocytochemical localization of the protein paralleled the distribution of the mRNA. Mesenchymal cells were more abundant in fetal lungs of diabetic mothers, and thus the decreased overall levels of Na+,K(+)-ATPase may result from the observed morphological pulmonary immaturity. One day after birth there was no apparent difference in lung morphology at the light microscopic level, in the localization or the steady-state level of Na+,K(+)-ATPase alpha 1 isoform mRNA, or in enzyme activity. Na+,K(+)-ATPase has a likely role in the active phase of fluid absorption in the airways of newborns before the onset of breathing. Decreased fluid clearance and lack of thinning of the lung's connective tissue may contribute to the increased risk for respiratory distress in infants of diabetic mothers.
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PMID:Effects of maternal diabetes on fetal rat lung ion transport. Contribution of alveolar and bronchiolar epithelial cells to Na+,K(+)-ATPase expression. 184 38

The studies outlined in this review suggest that the immaturity of distal nephron segments may hinder urinary excretion of potassium early in life. Among the factors that may limit potassium secretion by principal cells in the neonatal cortical collecting duct are an unfavorable electrochemical gradient (reduced Ki, Na(+)-K(+)-ATPase activity and/or Vte), limited membrane permeability to potassium and sodium, low tubular fluid flow rate, reduced luminal sodium concentration, or increased paracellular backleak. Alternatively, enhanced potassium absorption by other relatively well-differentiated distal nephron segments may contribute in part to a reduced net potassium excretory rate in the newborn. It should be kept in mind, however, that the limited potassium secretory capacity of the immature kidney becomes clinically relevant only under conditions of potassium excess. Under normal circumstances, the tendency of the newborn to retain potassium is an appropriate and necessary condition for growth.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Maturation of renal potassium transport. 203 47

We performed an ultracytochemical study of Mg++-ATPase as a marker of maturation in circumventricular capillaries at the developmental stage of rats, from 19 gestational days to 18 postnatal day, comparing with hippocampal capillaries. During the course of perinatal development, the predominant site of the Mg++-ATPase activity in circumventricular capillaries was shifted from the luminal cell membrane to the antiluminal cell membrane and the total enzyme activity was markedly increased. In all hippocampal capillaries observed, the predominant site of the Mg++-ATPase activity was the antiluminal cell membrane. It was suggested that immaturity of circumventricular capillaries may be one of the causative factors leading to intraventricular and subependymal hemorrhages in neonates.
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PMID:[Mg++-ATPase activity in circumventricular capillaries during fetal development of rats]. 252 98

To assess the influence of immaturity on the responsiveness of enterocytes to specific pathogens, a dose-response curve for cholera toxin (CT)-induced fluid secretion was determined in the proximal small intestine of rats at 2 and 4 wk of age. The suckling rat was approximately 50 times more sensitive to CT in triggering the secretory response than the weaned rat, when estimated by the medium-effective dose (ED50, 0.8 vs. 38.9 nM). Cortisone, known to promote enterocyte maturation, when injected into suckling rats, decreased host sensitivity approximately 1,000 times. Neither age nor cortisone decreased the receptor binding of 125I-labeled CT to intestinal microvillus membranes. In contrast, cortisone treatment caused a threefold increase in receptor density from 14.5 to 43.0 pmol/mg protein. The enzyme responsible for the sodium pump, Na+-K+-ATPase, showed a threefold increase in activity both after weaning and after a cortisone treatment. These data indicate that the immature gut exhibited an increased host sensitivity to CT stimulation that was not correlated with initial receptor binding but was related to a lowered Na+-K+-ATPase activity, suggesting that an underdeveloped sodium pump may be partially responsible for the high incidence of secretory diarrhea in neonates.
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PMID:Age and cortisone alter host responsiveness to cholera toxin in the developing gut. 253 37

Nippostrongylus brasiliensis infection of the rat resulted, at day 10 of infection, in decreased levels of jejunal enterocyte sodium-potassium-activated adenosine triphosphatase (Na,K-ATPase) and potassium-activated p-nitrophenyl phosphatase (K-pNPPase) activities. Parallel decreases occurred in active sodium efflux from jejunal enterocytes in the presence and absence of actively transported monosaccharides. Ileal enterocyte Na,K-ATPase and K-pNPPase activities were significantly increased, as was active sodium efflux. In contrast to controls, the presence of monosaccharides produced a stimulation of active sodium efflux from ileal enterocytes derived from infected rats. Enzyme and sodium transport changes in the jejunal enterocytes probably reflect cellular immaturity. Functional changes in ileal enterocytes probably represent a compensatory phenomenon.
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PMID:Changes in Na,K-ATPase, sodium ion, and glucose transport in isolated enterocytes in an experimental model of malabsorption. 255 21

Recently described techniques for separating myosin isoenzymes have been adapted for analysis of myosins from diseased and developing human skeletal muscle. The method is highly suitable for analysis of human myosins because only 2 - 3 mg of muscle are required for routine analyses. Human embryonic/foetal myosins are electrophoretically distinct from mature skeletal myosins, and are not normally detected beyond the first month of post-natal life, except in premature infants. They have a high alkaline calcium-activated ATPase activity. This would account for the histochemical classification of foetal fibres as "Type II", although physiological differences between adult fast-twitch muscle and foetal muscle are well recognized. Foetal myosins are also synthesized in human skeletal muscle under certain pathological circumstances. Their presence in Duchenne dystrophy probably reflects the associated marked muscle regeneration, with immaturity of some muscle cells. The large amounts of foetal myosin present in many cases of infantile spinal muscular atrophy is evidence that innervation is necessary for the normal cessation of foetal myosin synthesis.
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PMID:Embryonic and foetal myosins in human skeletal muscle. The presence of foetal myosins in duchenne muscular dystrophy and infantile spinal muscular atrophy. 731 Apr 40

We studied muscle biopsies from 36 Becker muscular dystrophy patients, and correlated dystrophin negative fibers with regenerating and degenerating myofibers. Dystrophin immunohistochemistry was used to identify dystrophin-negative and dystrophin-positive fibers. Immunohistochemical staining for fetal myosin and acid ATPase identified regenerating fibers, and calcium glioxalate and beta-spectrin staining identified necrotic fibers. All Becker biopsies contained detectable dystrophin in the majority of muscle fibers. 13 cases (36%) showed no dystrophin negative fibers, 9 cases (25%) showed a generalized, markedly decreased immunostaining pattern, and 14 cases (39%) showed a subset of dystrophin negative fibers (0.3-8% of total). Most dystrophin-negative fibers in Becker muscle were judged to be in the process of regeneration, and not in degeneration. No correlation was observed between the age of the patients and number of dystrophin negative fibers. We conclude that the absence of dystrophin and spectrin labeling in some BMD myofibers is associated with regeneration, probably due to incomplete expression of dystrophin secondary to myofibers immaturity. Our results might be explained by a developmental delayed expression of these two proteins, or by abnormal assembling in membrane's components during regeneration in dystrophy. Furthermore, our results rationalize the recently reported finding of some dystrophin-negative fibers in polymyositis.
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PMID:Absence of dystrophin and spectrin in regenerating muscle fibers from Becker dystrophy patients. 806 27

The newborn has a limited ability to regulate H+/HCO3- homeostasis, due in part to immaturity of the intercalated cells in the distal nephron. We traced the postnatal differentiation of the intercalated cells of the rabbit cortical collecting duct (CCD) and outer medullary collecting duct (OMCD) using MAb to the 31-kD subunit of the vacuolar H(+)-ATPase, membrane portion of erythrocyte band 3, and apical surface of B-intercalated cells (peanut agglutinin [PNA], MAb B63). In the most superficial CCD of the newborn there was no binding to these probes, although deeper in the cortex there was faint apical staining with PNA and MAb B63 and a few patterns of H(+)-ATPase and band 3 labeling of neonatal intercalated cells. The OMCD showed mostly apical H(+)-ATPase and both cytoplasmic and basolateral band 3 labeling but B-intercalated cell markers were not seen. By 3 wk of age the staining of the CCD and OMCD was more polarized, resembling those in the adult. Band 3 positive cells (as a percentage of total cells) in the CCD increased from 13 to 17% during maturation, and in the OMCD they increased from 22 to 37%. Some basolateral band 3 and apical H(+)-ATPase staining was also seen in the inner medullary collecting duct of 3-wk-old rabbits to a greater extent than in newborn or adult rabbits. Labeling of intercalated cells in the CCD and OMCD was weakest and least numerous in the newborn, greater in the 3 wk old, and greatest in the adult. Most maturing cortical intercalated cells bound both PNA and H(+)-ATPase MAb, comparable to what has been observed in the adult CCD. PNA-negative cells showing apical H(+)-ATPase labeling, consistent with the classic A-intercalated cell phenotype, comprised only 5% of identified intercalated cells in the newborn CCD compared with 12% in older animals. In or near the developing renal vesicles and ampullary structures were occasional cytoplasmically staining PNA- and B63-positive cells. Whether these cells are precursors of specific renal tubular cells cannot yet be established. Staining for principal cells (ST.9) was less intense in the neonatal cortex than in more mature cortex, but the deep cortex and outer medulla were heavily labeled at all ages. These data indicate that immature intercalated cells, in the CCD and OMCD, may undergo significant postnatal proliferation and differentiation, acquiring mature phenotypes during the first month of life. The A-intercalated cell appears more differentiated than the B cell during the 1st wk of life, suggesting that A-intercalated cells contribute more than B cells to the maintenance of acid-base homeostasis in the newborn.
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PMID:Postnatal differentiation of rabbit collecting duct intercalated cells. 882 79


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