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)

Mean urinary excretion values of some phenolic acids and alcohols have been measured by gas chromatography in 44 neonates (36 males, 6 females) during the first 2 days and days 3-7 of life, and the effect of prematurity and jaundice assessed. 4-Hydroxy-3-methoxymandelic acid (VMA) output rises immediately after birth in term but not in preterm infants. A similar increase in homovanillic acid (HVA) output was restricted to nonjaundiced term babies; in nonjaundiced preterm babies there was a steady rise during the first week. The ratio of HVA to VMA output was higher in these infants than in adults, suggesting a more rapid turnover of dopamine than adrenaline and noradrenaline. Unlike adult values, both HVA and VMA excretion values were directly related to urine volume, an observation perhaps related to renal immaturity. An unexplained reduction in HVA output in jaundiced as opposed to nonjaundiced infants was observed in the first 2 days of life. The ratio of 4-hydroxy-3-methoxyphenylglycol to VMA was about the same as in the adult. p-Hydroxyphenyl-lactic acid (p-HPLA), because of its superior stability, was measured in preference to p-hydroxyphenylpyruvic acid as an index of tyrosyluria. An output of 1 mg p-HPLA/24 h is proposed as the upper limit of normal. Prematurity was associated with a significant rise in p-HPLA output. A dramatic increase in excretion of this acid was noted in jaundiced, compared with nonjaundiced infants, presumably a manifestation of general enzyme immaturity.
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PMID:Urinary phenolic acid and alcohol excretion in the newborn. 120 Jun 75

Many centrally acting drugs which are prescribed for hypertension, depression, epilepsy, insomnia and asthma may also affect fetal brain neurotransmission and behavioral states. Nearly all these drugs enter the fetal circulation following maternal administration. The immaturity of the blood-brain barrier and greater accumulation in the developing brain make the fetal brain a major target of its mother's medication. Adverse effects that are seen in the fetus are not necessarily evident in its mother. We have shown that drugs like clonidine (an antihypertensive) and clomipramine (an antidepressant), which act on noradrenaline and serotonin neurotransmission in the brain, suppress rapid eye movement sleep in the developing rat. In adulthood, the neonatally treated rats showed hyperactivity, hyperanxiety, reduced sexual behavior, disturbed sleep patterns and reduced cerebral cortical size. Furthermore, such treatment induced an increase in voluntary alcohol consumption and a decreased adaptability of responses to changes in water deprivation in a Y-maze. Little is known about long-lasting consequences of centrally acting drugs used during late gestation in humans. Minor neurological disturbances, such as delayed visual motor performance, smaller head circumference, increased anxiety and disturbed sleep-wake patterns, have been reported in children born to hypertensive mothers treated with clonidine or alpha-methyl-dopa.
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PMID:Neurochemical and electrophysiological disturbances mediate developmental behavioral alterations produced by medicines. 287 4

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

Clinical and biological significance of increased urinary excretion of dopamine in Japanese children with neuroblastoma was investigated. There was an increase in dopamine excretion in 19 of 29 patients (66%) and 15 of 19 in stages III and IV (79%). When the ratio of noradrenaline and dopamine was divided into two at the value of 3.5 x 10(-2), the disease-free survival rate was four of 16 (25%) in the low ratio group and nine of 19 (69%) in the high ratio group. In five patients, the urinary analysis revealed that only the level of dopamine was elevated before initiation of the therapy. The common features of these patients were as follows: (1) the age at diagnosis was 1 to 4 years; (2) all originated from the suprarenal region; (3) stages were advanced III or IV; and (4) the prognosis was poor. N-myc oncogene of the primary tumor was evident in three, and all were amplified to 32, 37, and 112 copies. These observations suggested that the immaturity of catecholamine metabolism may correlate to the poor prognosis and that "dopaminergic neuroblastoma" may be a clinical subentity of poor prognostic neuroblastoma.
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PMID:Dopaminergic neuroblastoma as a poor prognostic subgroup. 338 88

1. After reaching its final destination the GnRH neuronal network develops under the influence of both excitatory and inhibitory inputs. 2. In the first 2 weeks of life, the immaturity of the GnRH neuronal system is reflected in sporadic unsynchronized bursts of the decapeptide, which determine the pattern of serum gonadotropin levels observed in female rats: high FSH levels and transient bursts of LH. The main inhibitory neuronal systems that operate in this period are the opioid and dopaminergic systems. A decrease in their inhibitory effectiveness may not be sufficient correctly to activate and synchronize the GnRH neuronal system. 3. There is a concomitant increase in excitatory inputs, mainly noradrenaline, excitatory amino acids, and NPY, which increase the synthesis and release of GnRH at the beginning of the juvenile period and participate in the coupling of GnRH neural activity to the ongoing rhythmic activity of a hypothalamic circadian oscillator. 4. The morphological changes of GnRH neurons which take place during the third and fourth weeks of life, and which are probably related to increasing estradiol levels, reflects the increasing complexity of the GnRH neuronal network, which establishes synaptic contacts to enable the expression of pulsatility and of the positive feedback of estradiol, both necessary components for the occurrence of puberty.
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PMID:Development of gonadotropin-releasing hormone (GnRH) neuron regulation in the female rat. 764 7

Twin fetuses experience much higher rates of perinatal mortality/morbidity than age- and weight-matched singletons. Across species, the prepartum increase in fetal plasma cortisol is responsible for maturing a number of systems in preparation for birth and the immediate postnatal period. In sheep, it is known that basal adrenocortical function is delayed in twins relative to singletons. Thus, it could be argued that relative immaturity in twins may explain their increased susceptibility to stress in the perinatal period and their relatively poor perinatal outcome. However, whether adrenocortical responsiveness to stress is also diminished in the twin fetus and whether the fetal cardiovascular, metabolic and endocrine defences to acute stress are comparatively weak in the twin fetus is unknown. This study investigated the effect of twinning on adrenocortical responsiveness to either the physiological stress of acute hypoxaemia or to an exogenous ACTH test, and on the fetal cardiovascular, metabolic and endocrine responses to acute hypoxaemic stress. Twenty Welsh Mountain sheep fetuses were chronically instrumented (1-2% halothane) at 121 +/- 3 days of gestation (term is ca 145 days) with amniotic and vascular catheters and with a transit-time flow probe around a femoral artery. The animals were divided into two groups based upon fetal number (singletons, n= 10; twins, n= 10), as determined at surgery. At 130 +/- 2 days, a 1 h episode of acute, isocapnic hypoxaemia (to reduce carotid P(O(2)) to 12 +/- 1 mmHg) was induced in all fetuses by reducing the maternal inspired O(2) fraction (F(IO(2)); 9% O(2) in N(2)). Fetal cardiovascular variables were recorded at 1 s intervals throughout the experimental protocol and arterial blood samples taken at appropriate intervals for biophysical (blood gases, glucose, lactate) and endocrine (catecholamines, vasopressin, cortisol, ACTH) measures. At 133 +/- 2 days a 2.5 microg bolus dose of synthetic ACTH (Synacthen; Ciba Pharmaceuticals, UK) was injected i.v. into eight of the singleton and six of the twin fetuses to determine adrenocortical steroidogenic sensitivity to exogenous ACTH. Under basal conditions, twins had lower plasma cortisol concentration, arterial blood pressure and femoral blood flow relative to singleton fetuses. Twins responded to acute hypoxaemia with similar pressor and vasopressor responses compared to singleton fetuses. However, the rate pressure product, an index of myocardial work, tended to decrease during hypoxaemia in twins, in contrast to the increase observed in singletons. Similar increases in the fetal plasma concentrations of ACTH, AVP, noradrenaline and adrenaline were observed during hypoxaemia in both groups; however, both the increments in fetal plasma concentration of cortisol in response to acute hypoxaemia and to exogenous ACTH were blunted in twins relative to singletons. This study shows that basal adrenocortical function as well as adrenocortical responsiveness is blunted in the twin relative to the singleton fetus. Further, the mechanism for adrenocortical blunting resides at the level of the adrenal cortex rather than higher up the axis. Relative adrenocortical immaturity in the twin fetus may reflect a specific endocrine adaptation to prolong gestation in multiple ovine pregnancies; however, such an adaptation does not affect the cardiovascular, metabolic or endocrine defence responses to acute hypoxaemia in the twin fetus.
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PMID:Adrenocortical responsiveness is blunted in twin relative to singleton ovine fetuses. 1507 82

There is evidence for the efficacy of noradrenaline and serotonin reuptake inhibitors treating attention-deficit hyperactivity disorder (ADHD). In this open trial, we checked St. John's wort, a serotonin and noradrealine reuptake inhibitor, and actually used as an antidepressant, for this indication. Three 14-16-year-old male psychiatric outpatients, diagnosed with ADHD have been rated at baseline and while taking St. John's wort or a placebo, respectively, by the Conner Scale and by the Continuous Performance Test, to determine its efficacy as a treatment option for ADHD. Patients' mean scores improved for Conners' hyperactivity, inattention and immaturity factors. Although the sample size is very small and therefore generalisation is very difficult, this observation indicates that St. John's wort might be a slightly effective treatment for ADHD also.
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PMID:St. John's wort may improve some symptoms of attention-deficit hyperactivity disorder. 2014 Jul 99

The existence of putatively painful situations to the fetus demands a careful evaluation of the issue of fetal pain. Several indirect approaches are used to evaluate the existence of fetal pain. Neurobiological studies showed that from the 30th week on, the anatomical and physiological system for pain transmission is already developed, with the connections from the periphery to the cortex being successively established. Stress responses to a painful stimulation are complex but they can be detected from the 16th week on. There is activation of the hypothalamus-pituitary-adrenal axis, autonomic nervous system and hemodynamic changes in response to nociceptive stimulation. In prematures exposed to pain there are significant increases of adrenaline, noradrenaline and cortisol, hemodynamic changes, motor reflexes and facial reactions. The changes induced by strong nociceptive stimulation of newborns have important postnatal consequences since they affect future reactions to noxious stimuli. Central sensitization and immaturity of the pain inhibitory system are the main neurobiological explanations for the increased pain. Detailed studies of the neurobiological mechanisms of the transmission of painful stimuli along with follow-up studies of the consequences of exposure to pain during the development of the fetus are necessary to fully understand fetal pain.
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PMID:[Fetal pain - neurobiological causes and consequences]. 2065 61