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

The authors presented their own material of years 1974-1977. During this period 8788 children were born, in it 737 (8,3%) with low birth weight (below 2500 g). Retrolental fibroplasia was diagnosed in 4 children, it was 0,5% of newborns with low birth weight, and 0,04% of the all live-borns. The retrolental fibroplasia was diagnosed in: 1) the child born in 27 week of pregnancy with 1000 g of body weight, 2) in two children born in 32-33 week of pregnancy with 1450 g and 1350 g of body weight, 3) in a child born in 31 week of pregnancy with 1600 g of body weight. The infants were nursed in incubators with about 30% of oxygen during 36 to 46 days. Contemporary hypoglycemia, hypoproteinemia, atelectasia of lungs with respiratory insufficiency were diagnosed. In the discussion the authors underlined the role of immaturity and hypoxia of the premature baby, which play the role in the secondary injury of vessel's walls of retina. The disturbancy of carbohydrate and protein metabolism were certainly secondary pathogenic agent sin retrolental fibroplasia. There exists the necessity of oxygen therapy of premature baby, but to take cre of the infant in the incubator does not mean the necessity of oxygen therapy . Even with controlled oxygen dosage in incubator the retrolental fibroplasia may occur as a result of relative hyperoxydation induced by the constriction of retina vessels. The authors underlined the necessity of repeated ophthalmologic examination of premature babies in about every 2 weeks, what makes very early diagnosis possible.
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PMID:[Risk of damage to the organ of vision in low birth weight infants]. 26 40

Tiny babies have the potential problem of hypoglycemia due to diminished hepatic glycogen stores, which can be potentiated by conditions frequently present in this birth weight group: asphyxia, cold stress, hypoxia, polycythemia. Despite the early administration of fluid and feeding, tiny babies are still at risk for developing hypoglycemia. Their immaturity, expressed by their limited ability to tolerate parenteral glucose infusions, puts them at risk for becoming hyperglycemic as well. Hence careful glucose administration and frequent monitoring of blood glucose are essential during the first several days after birth, in anticipation of hypoglycemia as well as hyperglycemia.
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PMID:Perinatal glucose homeostasis: the unique character of hyperglycemia and hypoglycemia in infants of very low birth weight. 33 33

After having described in detail the pathophysiology, symptomatology, X-chromosomal inheritance and some laboratory methods in detecting G-6-PD-deficiency by demonstrating a case of favism (Schulz et al. 1977), the authors now discuss the particularities of the enzyme deficiency in the newborn. These are complicated by additional physiological and transient deficiency of the enzymes catalase, NAD-diaphorase, glutathione peroxidase, and glucuronyl transferase. Several chemical substances, acidosis, hypoxia, hypoglycemia, and immaturity may cause a severe hyperbilirubinemia in G-6-PD-deficient newborns. The development of a kern-icterus in these cases may be prevented by early exchange transfusion. From clinical findings and some observations in different regions of Greece an additional factor influencing the liver function has been postulated which favors the development of hyperbilirubinemias in G-6-PD-deficient newborns. The nature of this possible factor is discussed. The authors emphasize the necessity of screening for G-6-PD-deficiency during pregnancy in families of mediterranian descent.
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PMID:[Glucose-6-phosphate dehydrogenase deficiency of the mediterranean type B minus. 2. Etiological basis for severe hyperbilirubinemia in the newborn]. 63 93

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional immaturity' of the pancreas.
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PMID:Glucose tolerance and insulin release in malnourished rats. 81 69

In the neonatal rat, the response of the hypothalamo-pituitary-adrenal axis to stressful stimuli is markedly decreased during the first 2 weeks of life. This peculiar period was named "stress hyporesponsive period." In this report, we studied the effect of insulin-induced hypoglycemia, known as a strong stimulator of the corticotroph function in the adult rat. Rats (8- or 20-day-old) were injected ip with 3 IU/kg synthetic insulin and were killed at various times. In 20-day-old rats, hypoglycemia induced a rapid drop in blood glucose concentrations accompanied by a stimulation of ACTH and corticosterone secretion which reached maximal values within 30 min. On the opposite, in 8-day-old rats, despite a rapid decrease in blood glucose levels, insulin injection induced a gradual rise of plasma ACTH and corticosterone concentrations which peaked at 90 min. This delayed response of the hypothalamo-pituitary-adrenal axis to hypoglycemia in the youngest rats does not seem to be due to a difference of sensitivity to insulin-induced hypoglycemia since injection of increasing doses of insulin (0.3, 0.75, or 3 IU/kg body wt) induced a dose-related decrease of blood glucose concentrations and a rise in plasma ACTH and corticosterone levels, comparable in the two age group studied. Basal or hypoglycemia-stimulated absolute corticosterone values were much lower in 8-day-old rats than in 20-day-old animals, suggesting an immaturity of the adrenal glands in the youngest animals. Daily ACTH injection, starting 3 days before the experiment, had a trophic effect on the adrenal glands leading to a more important increase of corticosterone levels after hypoglycemia in 8-day-old rats. Our results confirm that there is an immaturity of the adrenal glands in young rats, probably due to the low plasma ACTH levels during the neonatal period. To determine the respective role of the two major hypothalamic ACTH secretagogues, we studied the effect of passive immunization against CRF or arginine vasopressin (AVP) on plasma ACTH response after hypoglycemia. Passive immunization against AVP decreased significantly hypoglycemia-stimulated ACTH secretion in both 8- and 20-day-old rats, while no change of plasma ACTH response to insulin injection was observed after passive immunization against CRF. This results suggest that CRF does not seem to be involved in the regulation of ACTH secretion after hypoglycemia in the young rat while AVP seems to be the main hypothalamic stimulatory factor for anterior pituitary corticotrophs response to hypoglycemia during the postnatal period.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Stimulation of adrenocorticotropin secretion by insulin-induced hypoglycemia in the developing rat involves arginine vasopressin but not corticotropin-releasing factor. 131 56

We report a premature infant with severe hypoglycemia (serum glucose: 6 mg/dl) and cholestasis (serum total bile acids: 211.55 mumol/L) caused by hypoplasia of the interlobular bile ducts. This patient had developed intracranial hemorrhage and sepsis while undergoing treatment for hypoglycemia. As a result of endocrine evaluation, we made a diagnosis of idiopathic panhypopituitarism, congenital absence or hypoplasia of the pituitary gland. Moreover, we found abnormal bile acid profiles: The ratio of cholic acid to chenodeoxycholic acid was abnormally low in serum (0.04) and in biliary bile (0.33). However, 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestan-26-oic acid and bile alcohols were not detected. We therefore suspected that the severe cholestasis and abnormal bile acid profiles in the serum and biliary bile in this patient were related to physiologic immaturity of the enterohepatic circulation of bile acids and immaturity of hepatic 12 alpha-hydroxylation.
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PMID:Abnormal low ratio of cholic acid to chenodeoxycholic acid in a cholestatic infant with severe hypoglycemia. 207 33

The knowledge of various dysrhythmias and their prognostic value permits the selection of appropriate diagnostic and management strategies. The most frequent pediatric dysrhythmias are described: premature atrial and ventricular contractions, supraventricular tachycardias, preexcitation syndrome, long Q-T syndrome, sick sinus syndrome, A-V blocks congenital and acquired. These arrhythmias may be related to structural abnormalities of the conduction system or may reflect temporary cardiac immaturity, as in the newborn, or may occur after surgical repair of a congenital cardiac lesion. It is important decide if the arrhythmias is benign and likely to resolve spontaneously or if it is potentially dangerous. Sometimes an arrhythmias indicates underlying extracardiac disease such as central nervous system disease, sepsis, hypoglycemia, drug toxicity, severe tissue hypoxia, electrolyte abnormalities. In these instances the treatment of the underlying cause will correct the rhythm abnormalities.
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PMID:[Cardiac arrhythmias in childhood]. 245 Mar 37

To focus attention on the problem of infant mortality in Lebanon, data were compiled on infant mortality from 1978 to 1986 at the American University of Beirut Medical Center. Causes of death are analyzed for 602 males and 398 females. 54.9% deaths occurred at 1 month of age and 77.4% died within the 1st year. Autopsies were performed on .7%. 37.7% of all neonatal deaths were due to neonatal diseases such as hyaline membrane disease, asphyxia neonatorum, immaturity, necrotizing enterocolitis, hemorrhage, hemolysis, meconium aspiration, and kernicterus. Better prenatal care would reduce this group, or the administration of corticosteroids to the mother 24-48 hours prior to delivery, as well as rapid resuscitation at birth and prevention of the 5 curses: hypoxemia, hypoglycemia, hypothermia, hypotension, and acidosis. Although unavailable in Lebanon, administration of surfactants through an endotracheal tube would also help. Infections constitute 25.1% of deaths; many are preventable through adequate public health measures and strict personal hygiene, i.e., diseases such as sepsis, pneumonia, meningitis, gastroenteritis, hepatitis, encephalitis, and 1-2 cases of the following: diphtheria, measles, peritonitis, tetanus, tuberculosis, cytomegalis inclusion, herpes, parathyphoid, pertussis, poliomyelitis, and shigellosis. Congenital diseases were 21.6%. In utero diagnosis could prevent some diseases and in utero treatment is possible for hydrocephalus and hydronephrosis. Screening programs postnatally could lead to treatment. 5.9% were malignancies such as leukemia, lymphoma, brain tumors, histocytosis, Wilm's tumor, Ewing sarcoma, and Hodgkin's disease. Early diagnosis is critical if mortality is to be reduced in this group, but medical advances are still needed. 2.9% are miscellaneous diseases such as poisoning, rheumatic diseases, marasmus, Reye's syndrome, nephrosis, rickets, and epilepsy. Most of these diseases are preventable, except for rheumatic inflammation of the heart. Recommended necessary steps to reduce infant mortality are: prenatal care, diagnosis and screening, intrauterine surgery; resuscitation and intensive care centers with modern equipment and trained personnel; national vaccination and screening programs; adequate public health measures and hygiene; parental education; and well-equipped hospitals to serve all regardless of income level.
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PMID:Pediatric mortality: an avoidable tragedy. 251 28

High plasma concentrations of C-terminal immunoreactive glucagon (IRG) have been found during early life in several mammalian species. We have analyzed the plasma IRG of 12 h to 60 day-old dogs in terms of the 4 peaks (IRG greater than 20,000, IRG9000, IRG3500 and IRG2000) obtained by gel filtration on Bio-Gel P-30. Significant changes with age and in response to administered agents were confined to IRG9000 and IRG3500. IRG9000 was 9-fold higher in 12-36 h old dogs than in adults (108 +/- 24 pg/ml pancreatic glucagon equivalents v. 12 +/- 3 pg/ml, mean +/- SEM) and showed a decline to 2-fold higher (27 +/- 5 pg/ml) at 31-60 days. IRG3500 was higher than in the adult only during the first 36 h of life (36 +/- 5 pg/ml v. 15 +/- 3 pg/ml). Arginine infusion (0.5 g/kg over 15 min) caused an increase in plasma levels of both IRG9000 and IRG3500 in the newborn, whereas in adult dogs only IRG3500 was increased. Insulin injection (0.2 U/kg intravenously) causing a marked hypoglycemia had no significant effect on the plasma level of any IRG component in newborn dogs. Dihydrosomatostatin infusion (10 micrograms/kg bolus +/- 90 micrograms/kg over 30 min) caused a decrease in both IRG9000 and IRG3500. The increased basal level and secretory response to arginine of IRG9000 in newborn dogs may reflect an immaturity of the A cells, whereby more of this component, which may represent a precursor of pancreatic glucagon, is secreted than in the adult. The immature A cells also appear to have an impaired secretory response to hypoglycemia.
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PMID:Plasma glucagon-immunoreactive components in early life in dogs. 286 2

In the mature rat, subcutaneous administration of insulin (0.02 IU/g body wt.) produced hypoglycemia and a profound activation of the sympatho-adrenal pathway, as indicated by a marked depletion of adrenal catecholamines. Cellular glucopenia caused by administration of 2-deoxyglucose also produced a sympatho-adrenal response. In contrast, in 2-day-old rats, the systemic injection of insulin evoked only a small depletion of catecholamines even though severe hypoglycemia was present, and 2-deoxyglucose also produced a diminished response. The central administration of insulin at an equivalent dose (0.02 IU/g brain) stimulated brain ornithine decarboxylase activity in both neonates and adults, but was ineffective in evoking hypoglycemia or adrenal catecholamine release. These results suggest that: (a) direct interaction of insulin with its receptors in the central nervous system is not required for activation of the sympatho-adrenal pathway, and (b) the lack of sensitivity of neonatal adrenal catecholamine release to subcutaneous administration of insulin is likely associated with immaturity of splanchnic neurotransmission rather than with absence of central insulin receptors or impaired peripheral responsiveness to insulin.
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PMID:Central and sympatho-adrenal responses to insulin in adult and neonatal rats. 331 47


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