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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delayed gastric emptying is a common problem in preterm infants. The factors underlying this gastroparesis remain unsettled but may involve immaturity of smooth muscle contraction. The present study was designed to test this hypothesis. Muscle strips from the gastric fundus of fetal and adult guinea pigs were studied in vitro for their contractile response to receptor activation (acetylcholine and bethanechol) and membrane depolarization (potassium chloride). The dose-response curves were analyzed for differences in active force development (kg/cm2). The role of extracellular calcium (Ca2+) in the contractile responses was determined by contracting the tissues in a zero-Ca2+ physiologic saline solution and in the presence of nifedipine, a voltage-dependent Ca2+ channel blocker. The results demonstrate the following: 1) tissues from adult animals developed significantly more active force when tested with acetylcholine, bethanechol, and potassium chloride; 2) tissues from the fetal animals were relatively unresponsive to contraction with potassium chloride compared with the adult; and 3) both nifedipine and incubation in a zero-Ca2+ physiologic saline solution had a significantly greater inhibitory effect on the contractions of adult than fetal muscle strips. Our data indicate that smooth muscle in the gastric fundus develops increasing force with maturation. The increased contractility in the adult fundus appears to be due to an increased involvement of extracellular calcium influx, in part through voltage-dependent Ca2+ channels.
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PMID:Developmental changes in gastric fundus smooth muscle contractility and involvement of extracellular calcium in fetal and adult guinea pigs. 787 85

The choice of anesthesia during pregnancy and fetal operations is controversial. Halothane frequently is used, but its direct effects on fetal cardiac performance are unknown. The effects of halothane on fetal cardiac mechanics were studied in 8 fetal lamb hearts (135 days' gestation) using a modified Langendorff model connected to a membrane oxygenator. The perfusate consisted of oxygenated maternal blood at a constant flow temperature, hematocrit value, and glucose level. Coronary blood flow, left ventricular systolic pressure, left ventricular end-diastolic pressure, and the developed left ventricular pressure at a fixed volume were evaluated at baseline and after the addition of incremental concentrations of halothane to the perfusate through the oxygenator. Perfusate halothane levels were maintained in a clinical range. Systolic and diastolic cardiac function were adversely affected by the administration of even low doses of halothane, despite a concomitant increase in coronary blood flow. Because of the immaturity of their calcium transport system, fetal hearts may be particularly sensitive to the known calcium channel-blocking properties of halothane.
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PMID:Effects of halothane on the immature lamb heart. 788 14

Patients undergoing bone marrow transplantation have a long-lasting defect of B cell-mediated immunity. Both quantitative (decreased blood B cell counts) and qualitative (decreased Ig production) abnormalities of B cells have been described. To better understand the mechanism of the qualitative defect and its potential relation to B cell immaturity, we studied the in vitro responsiveness of B cells to polyclonal stimuli in patients at 2-12 months post-transplant and in normal neonates. Several key steps of the B cell program were deficient in the patients while they were relatively normal in the neonates. These included (i) early activation as assessed by Ca2+ flux; (ii) late activation as assessed by the increase in cell size and upregulation of the activation antigens CD25 and CD71; and (iii) proliferation as assessed by the number of cycling cells after stimulation. We conclude that the functional B cell defect during the early (< 1 year) post-transplant period extends back to the level of early activation and cannot be simply attributed to the relative immaturity of post-transplant B cells.
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PMID:B cell dysfunction after bone marrow transplantation is associated with decreased Ca2+ flux upon membrane Ig crosslinking. 805 Jan 96

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

Intrinsically bursting (IB) neurons, responding with a burst of action potentials to just threshold intracellular depolarizing current pulses, are encountered in layer V of mature rodent sensorimotor cortex. We report the results of intracellular recordings performed on neocortical slices obtained from immature rats between postnatal day (P) 7 and P21, as compared to adult animals (above P60). The bursting properties are here reported to mature abruptly around P14. After this time a subpopulation of IB neurons was recognizable on the basis of both physiological and morphological characteristics (i.e. extensive apical and basal dendrites arborization, axon collaterals limited to layers V-VI). Maturational changes in number and distribution of Ca2+/K+ channels may account for this developmental step. The immaturity of IB neurons may be correlated with the poorly synchronized character of cortical activities in the very young animals.
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PMID:Expression of intrinsic bursting properties in neurons of maturing sensorimotor cortex. 812 30

The effects of diltiazem, a sarcolemmal Ca2+ channel blocker, and ryanodine, an inhibitor of sarcoplasmic reticulum function, were investigated in isolated newborn rabbit hearts (2 to 5 days old) subjected to ischemia and reperfusion. After cardioplegic arrest with St. Thomas' Hospital solution, global ischemia was induced at 37 degrees C (normothermia) for 45 minutes or at 20 degrees C (hypothermia) for 180 minutes. The hearts were then reperfused at 37 degrees C for 30 minutes. Diltiazem or ryanodine, at concentrations that have minimal to moderately negative inotropic effects under nonischemic conditions, was added to the cardioplegic solution. After normothermic ischemia, reperfusion of untreated hearts resulted in recovery of left ventricular developed pressure to 52.9% +/- 2.5% of the preischemic level. In hearts treated with diltiazem, recovery of left ventricular developed pressure was significantly improved (84.2% +/- 2.9% at 3 x 10(-8) mol/L; p < 0.01). Comparable improvement was achieved with ryanodine (90.5% +/- 4.1% at 10(-9) mol/L; p < 0.01). Creatine kinase leakage and structural derangement of mitochondria were also reduced by both agents. With hypothermic ischemia, left ventricular developed pressure recovered in untreated hearts to 72.7% +/- 3.3% of preischemic values. Treatment with diltiazem improved the recovery of left ventricular developed pressure to 96.9% +/- 3.5% at 3 x 10(-8) mol/L and reduced creatine kinase leakage and mitochondrial damage. Ryanodine also improved the recovery of left ventricular developed pressure and attenuated ultrastructural damage. These findings suggest that Ca2+ handling by the sarcoplasmic reticulum, like transsarcolemmal Ca2+ influx, plays an important role in the pathogenesis of myocardial ischemia-reperfusion injury in the neonatal heart despite the morphologic and functional immaturity of the sarcoplasmic reticulum in the neonate.
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PMID:Protective effects of diltiazem and ryanodine against ischemia-reperfusion injury in neonatal rabbit hearts. 832 Oct 5

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

Myocardial calcification has been rarely described in premature infants after myocardial infarction and myocarditis with coxsackievirus B1. In adults and older children, metastatic myocardial calcification has been reported in chronic renal failure. We report a case of myocardial calcification in a 680-gm preterm infant after a prolonged course of renal failure complicated by secondary hyperparathyroidism. Subclinical myocardial injury was evidenced by a high serum creatine phosphokinase MB band concentration, which probably provided a susceptible substrate for the deposition of calcium crystals, because the multiplication product of serum calcium and inorganic phosphorus levels transiently exceeded 75 mg x mg/100 ml, indicating serum saturation during the course of secondary hyperparathyroidism. We report this case as an unusual complication of renal immaturity in extremely low birth weight infants and an indication of a relatively intact parathyroid glandular function in them. Hypoxia, myocardial dysfunction, and renal failure are common complications in such infants, and in the presence of renal failure, the serum levels of calcium and inorganic phosphorus should be maintained below the pathologic level to avoid ectopic calcification of the tissues, including the myocardium.
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PMID:Myocardial calcification in an extremely low birth weight infant with chronic renal failure and secondary hyperparathyroidism. 851 2

Effects of beta-agonists isoproterenol (Isp) and adrenaline (Adr) and beta-adrenoblocker obsidan (Obs) on the voltage-dependent calcium currents in cultured embryonic skeletal myocytes were studied at various stages of development ranging from day 2 to 10, using the whole-cell patch-clamp technique at 19-21 degrees C. Adr (or Isp) in concentrations 0.1-10 mumol/l increases the amplitude of both the slow dihydropyridine(DHP)-sensitive calcium current (ICa) and the fast-activated DHP-insensitive ICa. From day 2 to 6 after myoblast plating, Adr and Isp did not change the amplitude of ICa at all or slightly increased it. Obvious strong positive effects (an approximately twofold amplitude increase) on the calcium channels have been observed in 7-10-day-old myocytes only. beta-adrenoblocker obsidan known to abolish the positive beta-agonist effect, had a positive effect on membrane calcium currents. It may have been a result of the immaturity of the beta-adrenergic regulatory system of the myocytes. It is concluded that the beta-adrenergic regulatory complex can stimulate the activity of the fast and the slow voltage-dependent calcium channels of the frog skeletal myocytes, and that there is a distinct developmental stage at which a functioning beta-adrenergic regulatory complex appears in the membrane of skeletal myocytes.
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PMID:Beta-adrenergic regulation of voltage-dependent calcium currents in cultured skeletal myocytes of the frog Rana temporaria. 877 93

Renal handling of magnesium (Mg) has been incompletely studied during infancy and childhood due to the difficulty, until recently, of measuring the diffusible fraction of plasma Mg. In the present investigation this methodology has been used to assess Mg homeostasis in 45 healthy infants, aged 1 to 12 months, and in 63 healthy children, aged 1 to 15 years. When compared to children, infants had significantly higher plasma values (mean +/- SD) for both total (0.76 +/- 0.08 versus 0.70 +/- 0.06 mmol l-1; p < 0.001) and ultrafilterable Mg (0.51 +/- 0.07 versus 0.49 +/- 0.04 mmol l-1; p < 0.05). No significant correlations were present between values of plasma Mg and plasma concentrations of calcium, creatinine, total protein or albumin. The ratio Umg/Ucr, calculated in the second morning urine (median, 3rd-97th centiles), was also significantly higher during infancy (0.023, 0.009-0.07 versus 0.015, 0.006-0.04; p < 0.001). On the contrary, fractional excretion of Mg (median, 3rd-97th centiles) was identical in both age groups and did not correlate significantly with age (infants: 3.2, 1.0-7.8%, children 3.4, 1.6-8.1%; p = NS). During a Mg infusion, carried out in six children, we could establish an approximative value for renal Mg threshold (plasma ultrafilterable Mg = 0.50 mmol l-1) close to that found in adults. These results indicate that no functional immaturity is present during infancy for renal tubular reabsorption of Mg and that the high Umg/Ucr ratio observed in this age group is a phenomenon not dependent on a higher urinary Mg excretion but probably related to a lower urinary creatinine excretion per unit of lean body mass.
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PMID:Renal magnesium handling in infants and children. 888 10


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