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)

Autonomic regulatory mechanisms and some metabolic functions are predominantly influenced by the sympathetic nervous system. Premature and mature newborns show a high variability and a low adaptability of the sympathetic nervous system. In order to investigate whether sympathetic systems are completely developed at birth or underly a postnatal maturation process we have determined plasma levels of adrenaline and noradrenaline as well as the density and affinity of alpha- and beta-adrenoceptors on thrombocytes and lymphocytes in pre- and mature newborns and adults. Catecholamines were determined by means of a radioenzymatic method, number and affinity of adrenoceptors by use of the radioactive labelled antagonists 3-H-Yohimbine and 125-I-Cyano-Pindolol. Beta-adrenoceptor responsiveness was assessed by measurement of cyclic AMP in lymphocytes before and after stimulation of beta-adrenoceptors by isoprenaline. A linear relationship occurred between the gestational age and the number of adrenoceptors on lymphocytes, whereas the alpha-adrenoceptors on thrombocytes showed no age dependency. The basal content of cyclic AMP and the accumulation in response to beta-adrenoceptor stimulation by isoprenaline was significantly lower in newborns than in adults. Since noradrenaline and adrenaline plasma levels were not significantly different in newborns and adults it is assumed that the low density of beta-adrenoceptors in premature and mature newborns is due to a postnatal maturation and not to a "down regulation" by circulating catecholamines. Our results suggest that an immaturity of beta-adrenoceptors is involved in the poorly developed adaptive control in newborns.
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PMID:[Postnatal development of the sympathoadrenergic system in premature and newborn infants]. 301 54

Serum immunoreactive parathyroid hormone (iPTH), ionized calcium, the urinary cyclic AMP/creatinine ratio (cAMP/Cr) and some indices of bone turnover (alkaline phosphatase (AP), serum osteocalcin, and the urinary total hydroxyproline/creatinine ratio (OH-P/Cr)) were measured in 26 preterm infants during the first 4 weeks of life. Despite of stimulated parathyroid gland activity cAMP/Cr, AP, osteocalcin and OH-P/Cr were low during the first week. Thereafter iPTH decreased, whereas cAMP/Cr, and the indices of bone turnover increased, reaching high-normal values (in comparison to full-term infants) during the second and third week of life. Serum iPTH was negatively correlated to cAMP/Cr in the first week (r = -0.61, p less than 0.01), whereas the relationship became positive during the second (r = 0.47, p less than 0.05) and third (r = 0.54, p less than 0.05) week of life indicating maturation of the renal response to PTH. The study supports the concept that in premature infants a transient pseudohypoparathyroid-like state is present during the first week of life reflecting an immaturity of renal and possibly bone response to PTH. This may be an etiological factor in hypocalcemia of prematurity.
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PMID:Evidence for transient peripheral resistance to parathyroid hormone in premature infants. 303 25

It is now well established that human lymphoblastoid cell lines showing immaturity characters display ecto-5'-nucleotidase activities lower than normal levels. A recent paper (Sun, A.S., Holland, J.F. and Ohnuma, T. (1983) Biochim. Biophys. Acta 762, 577-584) mentioned that this phenomenon resulted from the presence of a 5'-nucleotidase inhibitor in these cell lines. We demonstrate here that the use of 5'-[3H]AMP as a substrate, and inadequate analysis of the products formed, led them to a misinterpretation. [3H]Adenosine derived from 5'-[3H]AMP hydrolysis was further transformed into [3H]inosine by the adenosine deaminase activity of the leukemic cell lines tested; [3H]inosine was precipitated with the excess substrate and was not taken into account in the ecto-5'-nucleotidase determination, which led the authors to confuse this adenosine deaminase activity with a 5'-nucleotidase inhibitor. We did not observe 5'-nucleotidase inhibition by leukemic cell cytosol when convenient assay methods were used and showed that the presence of such an inhibitor remains to be established.
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PMID:The proposed 5'-nucleotidase inhibitor in human leukemic cells is an artefact. 608 22

We investigated the expression of glutamine synthetase (GS), an enzyme involved in astroglial metabolism and marker of astroglial functional maturity, in a glioblastoma cell-line (GL-15) of clonal origin. In spite of their phenotypic immaturity, evidenced in a mosaic fashion by a poor glial fibrillary acidic protein (GFAP) expression, the level of GS-mRNA is high in GL15 cells and the considerable amount of GS biological activity can be further induced and stabilized by glucocorticoids. A correlation between the induction by dexamethasone of the GS-mRNA level and the GS biological activity suggests a transcriptional regulation of GS expression by the aforesaid hormone. Under this hormonal action, changes in cell morphology occur and they are correlated with an overexpression of the GFAP, a marker of astroglial differentiation. On the contrary, dibutyryl cyclic AMP (dbc AMP) down-regulates the GS-mRNA expression and decreases GS activity. These results suggest that GL-15 cells have a common glucocorticoid dependent mechanism able to induce GS and GFAP as well as morphological changes. However in these cells AMPc responsive elements are involved in the negative modulation of the GS expression, contrary to what occurs in normal astroglial cells.
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PMID:Glutamine synthetase gene expression in a glioblastoma cell-line of clonal origin: regulation by dexamethasone and dibutyryl cyclic AMP. 874 97

Bioactive peptides encrypted within the native milk proteins can be released by enzymatic proteolysis, food processing, or gastrointestinal digestion. These peptides possess a wide range of properties, including immunomodulatory properties. The first months of life represent a critical period for the maturation of the immune system because a tolerance for nutrient molecules should be developed while that for pathogen-derived antigens is avoided. Evidence has accumulated to suggest that milk peptides may regulate gastrointestinal immunity, guiding the local immune system until it develops its full functionality. Our data using the weaning piglet as the model suggest that several milk peptides can downregulate various immune properties at a time (one to two weeks after weaning) that coincides with immaturity of the immune system. The protein kinase A system and/or the exchange protein directly activated by cyclic AMP (Epac-1) are implicated in the mechanism through which milk peptides can affect immune function in the early postweaning period. Despite the fact that the research in this field is in its infancy, the evidence available suggests that milk protein peptides may promote development of neonatal immune competence. Milk contains a variety of components that provide immunological protection and facilitate the development of neonatal immune competence. Two main categories of milk compounds are thought to be associated with immunological activity. The first category includes cytokines, which neonates do not produce efficiently. Cytokines present in milk are thought to be protected against intestinal proteolysis and could alleviate immunological deficits, aiding immune system maturation (Kelleher & Lonnerdal, 2001; Bryan et al., 2006). The second category of milk compounds includes milk protein peptides. Milk peptides may affect mucosal immunity possibly by guiding local immunity until it develops its full functionality (Baldi et al., 2005). This chapter focuses on the effects of milk peptides on immune function and attempts to provide an overview of the knowledge available in this field.
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PMID:Milk peptides and immune response in the neonate. 1818 33

This review explores the potential for changes in dietary macronutrients to differentially influence mitochondrial bioenergetics and thereby the frequency of mtDNA haplotypes in natural populations. Such dietary modification may be seasonal or result from biogeographic or demographic shifts. Mechanistically, mtDNA haplotypes may influence the activity of the electron transport system (ETS), retrograde signalling to the nuclear genome and affect epigenetic modifications. Thus, differential provisioning by macronutrients may lead to selection through changes in the levels of ATP production, modulation of metabolites (including AMP, reactive oxygen species (ROS) and the NAD(+)/NADH ratio) and potentially complex epigenetic effects. The exquisite complexity of dietary influence on haplotype frequency is further illustrated by the fact that macronutrients may differentially influence the selective advantage of specific mutations in different life-history stages. In Drosophila, complex I mutations may affect larval growth because dietary nutrients are fed through this complex in immaturity. In contrast, the majority of electrons are provided to complex III in adult flies. We conclude the review with a case study that considers specific interactions between diet and complex I of the ETS. Complex I is the first enzyme of the mitochondrial ETS and co-ordinates in the oxidation of NADH and transfer of electrons to ubiquinone. Although the supposition that mtDNA variants may be selected upon by dietary macronutrients could be intuitively consistent to some and counter intuitive to others, it must face a multitude of scientific hurdles before it can be recognized.
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PMID:Review: can diet influence the selective advantage of mitochondrial DNA haplotypes? 2654 31