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)

PRL secretion was evaluated in 30 human newborns during the early hours of life. Both levodopa and pyridoxine administration failed to suppress PRL release in all subjects. Synthetic TRH elicited a constant, prompt increase in PRL levels. No significant changes were observed after somatostatin injections. These results demonstrate normal pituitary PRL reserve in newborns. The failure to respond to levodopa and pyridoxine administration might reflect partial immaturity of the pituitary dopaminergic receptors.
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PMID:Dynamic evaluation of prolactin secretion during the early hours of life in human newborns. 12 39

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

In the ganglion cell layer of the adult cat retina, subgroups of displaced amacrine cells and alpha ganglion cells are immunoreactive for somatostatin or a somatostatinlike substance. Both types of immunoreactive cells are found preferentially in inferior retina. We studied the development of somatostatin immunoreactivity in the prenatal and postnatal cat retina to determine how such unusual distributions of immunoreactive cells arise. Somatostatin-immunoreactive profiles were first observed at embryonic day (E) 30, within the inner retina in a central region that included the optic disk and the area centralis. By E36, immunoreactivity had virtually disappeared from the central retina but was present throughout the periphery. The immunoreactive profiles could not be classified morphologically because of their immaturity but were most likely retinal ganglion cells, the earliest born cells of the inner retina. Of the two types of immunoreactive cell observed in the adult, the first to be recognized morphologically was the displaced amacrine cell, at E45. These cells were virtually adultlike in morphology and number by E51, two weeks before birth. In contrast, immunoreactive alpha ganglion cells were not apparent until five days after birth and did not achieve their mature numbers and immunoreactive staining characteristics until more than a month later. From the time they could initially be recognized, both immunoreactive displaced amacrine cells and alpha cells were distributed mainly in the inferior retina. A third type of somatostatin-immunoreactive cell was transiently observed in the superior and inferior retina during prenatal and early postnatal development. These cells were characterized by granular staining in irregular shapes and few, if any, faintly stained processes. Injections of retrograde tracers into retinorecipient targets revealed that many of these cells were retinal ganglion cells. They disappeared by postnatal day 38. Our results indicate that somatostatin immunoreactivity initially follows a central-to-peripheral pattern of development, as is typical of other developmental events in the mammalian retina. They also indicate that the two types of somatostatin-immunoreactive neurons present in the adult cat retina (displaced amacrine and alpha ganglion cells) attain their mature immunocytochemical properties with very different timecourses. Finally, the observation that somatostatin immunoreactivity appears transiently in the granular-staining ganglion cells, distributed throughout the superior and inferior retina, suggests that the peptide may play a regulatory role in the development of the retina and/or retinofugal pathways.
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PMID:Ontogeny of somatostatin immunoreactivity in the cat retina. 134 13

This is the first study investigating hormone secretion by the isolated perfused pancreas of the aged Fischer 344 rat. Nutrient-induced release of insulin, glucagon, and somatostatin in overnight-fasted rats aged 2, 10, 18, 24, and 30 mo was studied. After an equilibration period, the pancreas was perfused for 20 min with buffer A (containing 4.2 mM glucose plus a 3.5 mM mixture of amino acids) then for 20 min with buffer B (containing 8.3 mM glucose and 7.0 mM amino acids). When stimulated by buffer B, the amount of insulin secreted increased (P less than 0.05) from immaturity (2 mo) to adulthood (10-18 mo) because of growth of the organ. From adulthood to very old age an equal amount of insulin was released in all groups during the last 19 min of perfusion with buffer B. Fasting blood glucose levels remained constant throughout life, whereas pancreatic insulin stores and plasma insulin levels rose, reaching peak values at 18 mo. The alpha-cell appeared to be deemphasized relative to the beta-cell during development but not thereafter, as indicated by the findings that from immaturity to adulthood pancreatic glucagon stores expanded less than insulin stores and that glucagon release significantly decreased. Only minor changes in somatostatin release from the delta-cells were observed after the rat reached adulthood. We conclude that the endocrine secretory response of the pancreas is well maintained throughout life in the Fischer 344 rat.
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PMID:Hormone secretion by isolated perfused pancreas of aging Fischer 344 rats. 167 Sep 77

The pattern of ischemia-induced cell death was examined with histochemical methods in the striatum of adult gerbils 4 and 7 days after transient forebrain ischemia. The results showed a massive loss of immunoreactivity to enkephalin and tachykinins, peptides present in striatal efferent neurons. In contrast, neurons expressing acetylcholinesterase activity, or choline acetyltransferase immunoreactivity, as well as neurons immunoreactive for somatostatin, were relatively preserved in areas of severe neuronal loss. The selective vulnerability of subpopulations of striatal neurons to transient ischemia in the adult is similar to that observed in the neonate and after local injections of agonists of N-methyl-D-aspartate receptors, but not of agonists of other glutamate receptor subtypes. It also presents striking similarities to the pattern of neuronal death observed in Huntington's disease. The results further support a role for overstimulation of a subtype of excitatory amino acid receptor in ischemia-induced cell death and show that the selective sparing of subpopulations of striatal interneurons after ischemic injury is not related to immaturity of these neurons but also occurs in the adult.
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PMID:Ischemic damage in the striatum of adult gerbils: relative sparing of somatostatinergic and cholinergic interneurons contrasts with loss of efferent neurons. 197 9

In the neonatal period of the rat, pancreatic thyrotropin-releasing hormone content decreases and the sensitivity of insulin secretion to glucose increases. In adult rat islets, TRH inhibits glucose-induced insulin release. The aim of this study was to investigate whether a high TRH content and release can be part of the explanation for the functional immaturity of neonatal islets. For that purpose, we have measured the tissue content and the secretion of immunoreactive insulin, glucagon, somatostatin and TRH in islets from 21.5-day-old rat fetuses cultured for up to one week. Insulin, glucagon and somatostatin content increased during one week of culture in the presence of 11.1 mmol/l glucose. The TRH content decreased during culture, but did not equal adult values. Insulin, glucagon and somatostatin responses to glucose were present after one week of culture. Glucose had no effect on TRH release in cultured fetal islets, but inhibited TRH release in adult islets. We conclude that glucose can stimulate insulin secretion without inhibiting TRH release, but that a decrease in islet TRH content and a sensitization of TRH secretion to glucose may be important in the full maturation of fetal pancreatic islets.
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PMID:Insulin, glucagon, somatostatin, and thyrotropin-releasing hormone content and secretion by perifused fetal rat islets during culture. 197 58

A study on the development of biphasic insulin release and sensitivity to inhibitors has been performed using perifused rat pancreas at 19.5 days of gestation (3 days before birth) and at 3 days after birth. In the fetal pancreas, 16.7 mM glucose caused a marked stimulation of insulin release that did not, however, manifest a biphasic response and was not inhibited by verapamil, a Ca2+ channel blocker. This suggested that the immature response was due to either a lack of voltage-dependent Ca2+ channels or their failure to open in response to glucose. Depolarizing concentrations of KCl stimulated insulin release, which was inhibited by verapamil, demonstrating that functional Ca2+ channels were present. In the presence of 16.7 mM glucose, quinine, which blocks glucose-sensitive k+ channels, potentiated the response of the fetal pancreas that now became sensitive to verapamil, demonstrating that functional K+ channels were also present in the fetal pancreatic beta-cell. The immaturity of the response is not due specifically to a defect in glucose metabolism; rather the metabolism of nutrient secretagogues fails to couple with the K+ channel in the fetal islet and thus fails to depolarize the beta-cell membrane. Three days after birth the pattern of response to high glucose is biphasic. Insulin release in fetal pancreas was inhibited by epinephrine and somatostatin.
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PMID:Development of the biphasic response to glucose in fetal and neonatal rat pancreas. 289 70

The ontogeny of insulin, glucagon, PP and somatostatin in the mammalian fetal pancreas has been examined in recent years largely by immunocytochemistry and in some instances by radioimmunoassay. Complete ontogenic data are available only for the rat, human, pig and sheep. Figure 3 compares the time of appearance of the endocrine cell-types within the fetal pancreas when the periods of gestation of the four species are converted to a uniform scale. The striking ontogenic difference in the rat probably reflects the immaturity of the rodent fetus at birth compared with the human, pig and sheep. In the fetal pancreas, differences in cell number of glucagon and PP cells in the dorsal and ventral lobes become apparent from an early gestational period. Factors responsible for the functional and structural maturation of the fetal pancreatic endocrine cells and the processes involved in pancreatic organogenesis are poorly understood. Studies in these areas would have clinical implications since it may be possible in the future to employ agents for selective replication of fetal beta-cells for transplantation in patients with Type I diabetes, bearing in mind that such cells must have the capacity to respond to normal stimuli and repressors when transplanted. The presence of the other islet cell-types may be obligatory for these appropriate responses. This would require a more complete knowledge of those factors which produce the normal selectivity of the four hormonal cell-types.
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PMID:Ontogenic development of peptide hormones in the mammalian fetal pancreas. 289 13

Six extragonadal teratomas that contained pancreatic tissue were retrieved from archival material at the University of Minnesota Hospital, Minneapolis. The neuroendocrine cells were studied immunohistochemically for insulin, glucagon, somatostatin, pancreatic polypeptide, vasoactive intestinal polypeptide, gastrin, chromogranin, and synaptophysin. Pancreatic tissue from autopsies of 10 stillbirths (20 to 40 weeks' gestational age) was evaluated similarly. The features of the teratomatous pancreatic tissue were compared with those of the fetal pancreata and with data from previous studies of normal pancreatic development and adult pancreata. The pancreatic tissue in all six teratomas contained abundant mature islets that contained beta, alpha, delta, and pancreatic polypeptide cells; however, they also showed widespread nesidioblastosis with the same cell types, resembling third-trimester fetal and neonatal pancreata. Increased proportions of alpha and delta cells were observed in three and five cases (relative to those of adult tissue), respectively, providing further evidence of immaturity. Two cases showed a lack of alpha cells. None of the teratomas contained pancreatic cells that were positive for vasoactive intestinal polypeptide or gastrin. Mechanisms that regulate neuroendocrine cell differentiation in the normal pancreas also seem to operate in the teratomatous pancreas; they may eventuate in features similar to those of the late fetal and neonatal pancreas. Abnormal differentiation in teratomas may result in deficient hormone production.
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PMID:Immunohistochemical characterization of teratomatous and fetal neuroendocrine pancreas. 831 55

To study possible age-related differences in the role of neuronal histaminergic pathways in the control of GH secretion, the effects of alpha-fluoromethylhistidine (alpha-FMH), an irreversible inhibitor of histamine (HA) synthesis, were examined on basal and opioid-induced GH release in neonatal and adult rats. The mechanisms involved in such effects were evaluated by measuring pituitary GH mRNA levels and hypothalamic levels of GH-releasing hormone (GHRH) and somatostatin (SRIF) mRNAs. Daily injection of alpha-FMH (20 mg/kg, s.c.) in pups of either sex, from birth until 10 days of age, caused a significant increase in baseline plasma GH and potentiated the GH response to the [Met5]-enkephalin analog FK 33-824 (1 mg/kg, s.c.) administered 3 h after the last alpha-FMH injection. GH and SRIF mRNA levels were significantly higher in alpha-FMH-treated pups than in controls, whereas no difference was observed in GHRH mRNA levels. In young adult male rats, acute administration of alpha-FMH (100 mg/kg, s.c., 3 h before) did not change significantly basal GH levels but potentiated FK 33-824 (0.3 mg/kg, intracarotid)-induced stimulation of GH secretion. Repeated administration of alpha-FMH (200 micrograms/rat, i.c.v., for 3 days) failed to modify basal and FK 33-824-induced GH secretion, caused a significant reduction in hypothalamic GHRH mRNA levels and left SRIF and GH mRNAs unchanged. These findings indicate that HA exerts an inhibitory effect on GH secretion in both neonatal and adult rats. The different effects of short-term HA depletion on hypothalamic and pituitary indices of somatotropic function observed at the two age periods may be ascribed to the immaturity of the HA system in early postnatal life and to a different functional role of GH-regulatory factors during ontogeny.
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PMID:Role of the neuronal histaminergic system in the regulation of somatotropic function: comparison between the neonatal and the adult rat. 895 79


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