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

In this series of one hundred and twenty-eight adults with Down's syndrome nearly half (i.e. 42.2 per cent) developed a normal EEG. This would appear to bear out the findings of Gregoziades and Pampiglione (1966) that older children with this syndrome tended to have tracings similar to the normal child. The youngest age group of fifteen to twenty-four years developed a normal tracing in 38.9 per cent of cases. The most frequent abnormality was an excess of theta, in keeping with the suggestion of Godinova and Hirai and Izawa that this was due to immaturity. Neither the presence of congenital heart disease nor diabetes nor intercurrent illness appeared to have any effect on the development of seizures. Epilepsy developed at any time during adult life but, not surprisingly, the five cases developing it had shown sharp or paroxysmal activity previously. Two had suffered from fainting attacks. In one, the diagnosis was confirmed later by a typical grand mal seizure and the other by response to anticonvulsants. Neither suffered from congenital heart disease.
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PMID:The EEG and incidence of epilepsy in Down's syndrome. 15 92

Experiments were conducted on 162 female rats which had sustained alloxan diabetes during the period of sexual immaturity and had latent insular insufficiency (prediabetes and latent diabetes). Possibilities of chlorpropamide under conditions promoting decompensation development were studied. The animals were given propamide in daily doses of 100 mg per 1 kg of weight for one month, including the period of sexual maturation. Observation period--up to 5 months. A favourable effect of chlorpropamide was noted by the end of puberty and persisted in the course of further observation; the difference from control animals by the frequency of latent and manifest diabetes was intensified under the effect of glucose overfeeding during the perinatal period. Chlorpropamide improved the course of latent insular insufficiency in the rats and was capable of preventing its change into manifest diabetes.
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PMID:[The effect of chlorpropamide on the course of latent insular insufficiency in rats under conditions favorable for its transition to patent diabetes]. 125 24

Respiratory distress syndrome (RDS) is primarily caused by an immaturity in the synthesis and secretion of surfactant by the fetal lung type II cell. Fetal hyperinsulinemia associated with maternal diabetes places the newborn at an increased risk of developing RDS, and therefore, it has been hypothesized that insulin inhibits type II cell differentiation. We have previously shown that insulin inhibits the accumulation of surfactant-associated protein A (SP-A), the major surfactant-associated protein, in human fetal lung explants maintained in vitro. In the present study, we used Northern blot analysis to evaluate the effects of insulin on the content of SP-A messenger RNA (mRNA) as well as on the content of mRNA for the hydrophobic surfactant-associated proteins SP-B and SP-C in human fetal lung explants maintained in vitro. Lung explants were maintained in serum-free medium with or without added insulin (0.25-2500 ng/ml) for up to 6 days. We observed that insulin, at concentrations of 25-2500 ng/ml, significantly inhibited the accumulation of SP-A mRNA when compared to controls (P less than 0.01). The inhibitory effect of insulin on SP-A mRNA accumulation was dose dependent with an approximately 75% inhibition observed at 2500 ng/ml. Insulin, at the concentration of 2500 ng/ml, significantly inhibited the accumulation of SP-B mRNA by approximately 30% when compared to control levels (P less than 0.01) but had no effect at lower concentrations. Insulin had no significant effect on SP-C mRNA levels at any concentration tested. Our findings provide evidence that insulin may delay fetal lung development by inhibiting SP-A and SP-B gene expression. A deficiency of these proteins in pulmonary surfactant may account for the increased incidence of RDS in infants of diabetic mothers.
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PMID:Insulin regulation of messenger ribonucleic acid for the surfactant-associated proteins in human fetal lung in vitro. 163 13

Strict clinical management of a diabetic mother who is pregnant reduces the risk of neonatal complications. It also reduces the frequency of fetal macrosomia. Diabetic mothers have a heavier placenta than mothers who are not diabetic. Light microscopic placental changes associated with diabetes include villous immaturity and dysmaturity. We have examined the placentas of 27 diabetic mothers whose maternal hemoglobin A1c (HbA1C) levels were measured throughout pregnancy. None of these placentas had a trimmed weight in excess of 600 grams. Eighteen of 27 specimens had immature villi. Four had dysmature villi. Three placentas had fibromuscular sclerosis within the villi. Five had cholangiosis and there was one cholangioma. Villous immaturity was present in 16 of 18 mothers whose HbA1C was more than 5.6% of the total hemoglobin. We found villous immaturity in 2 of 5, within 5.1-5.5% HbA1C. There was no villous immaturity in four cases whose HbA1C was less than 5.0% total hemoglobin. Our findings indicate that maternal hyperglycemia during pregnancy is associated with placental immaturity and dysmaturity.
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PMID:[Correlation of placental villous immaturity and dysmaturity with clinical control of maternal diabetes]. 185 19

The effects of the cytokines tumor necrosis factor-alpha and interferon-gamma on the adult beta-cell have been well described: a reduction of insulin secretion and content and death of the cell. For this reason and because these cytokines may be released from activated lymphocytes and macrophages that infiltrate islets in insulin-dependent diabetes, they have been implicated in the pathophysiology of this form of diabetes. As to whether the human fetal beta-cell, which differs from the adult beta-cell in not releasing insulin in response to the nutrient glucose and not being adversely affected by the toxin streptozotocin, is similarly affected is unknown. To examine this question we cultured monolayers of a single cell suspension of human fetal pancreas in the presence or absence of 1000 U/mL of these cytokines for 7 days. Chronic insulin release was enhanced for the first 2 days of culture, but unchanged thereafter. Acute insulin release in response to the secretagogue theophylline (10 mM) was enhanced on day 7, but not earlier. There was an increase in the insulin content of the cells by the fourth day, probably due to an increase in the number of beta-cells present (45 +/- 5% vs. 22 +/- 3%). Microscopically, non-beta-cells also seemed to increase in number; there was an increase in both DNA and cell number by the seventh day. In contrast to these beneficial effects on the human fetal beta-cell, treatment of adult rat insulinoma cells, represented by RIN-m5F cells, resulted in inhibition of insulin secretion during the first day of culture and subsequent death of 86% of the cells by the sixth day of culture. It is hypothesized that the functional immaturity and lack of normal (adult) metabolic activity of the human fetal beta-cell somehow confers protection on these cells from the cytotoxic effects of tumor necrosis factor-alpha and interferon-gamma. Indeed, our findings suggest that these cytokines may be trophic for the developing beta-cell.
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PMID:Role of tumor necrosis factor-alpha and interferon-gamma as growth factors to the human fetal beta-cell. 193 17

The manifestations of endocrine derangements in the musculoskeletal system in infancy and childhood are disturbances in growth and maturation and in adulthood are disturbances in maintenance and metabolism. Hypercortisolism during skeletal immaturity suppresses growth. In the adult, hypercortisolism leads to osteoporosis, osteonecrosis, and muscle wasting. Deficiency of growth hormone during skeletal development results in short stature. An excess of growth hormone in a skeletally immature individual results in gigantism, an excess in a skeletally mature individual results in acromegaly. Patients with gigantism have extreme height with normal body proportions. Musculoskeletal manifestations of acromegaly include soft-tissue thickening, vertebral body enlargement, characteristic hand and foot changes, and enthesal bony proliferation. Hyperthyroidism causes catabolism of protein and loss of connective tissue, which manifest as muscle wasting. Deficient levels of thyroid hormone cause defects in growth and development. Severe growth retardation from congenital hypothyroidism is rare because neonatal screening recognizes the disorder and leads to early treatment. The skeletal manifestation of hypergonadism in children is precocious growth and early skeletal maturation. Although the initial precocious growth spurt results in a tall child, early closure of the growth plates results in a short adult. Hypogonadism in the prepubertal child results in delayed adolescence and delayed skeletal maturation. Diabetes mellitus in childhood results in decreased growth, a phenomenon presumed to be secondary to nutritional abnormalities. Generalized osteoporosis and short stature are common. In the adult, generalized osteoporosis may accompany insulin-dependent diabetes mellitus if obesity is absent. Calcification of interdigital arteries of the foot is common in diabetics and uncommon in other conditions. Additional skeletal manifestations relate to complications of diabetes such as peripheral neuropathy and diabetic foot disease.
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PMID:Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. 198 24

Placentas associated with maternal diabetes are generally characterized by features of villous immaturity. We correlated the villous histology with the immunocytochemical distribution of four trophoblastic proteins: beta human chorionic gonadotropin (beta HCG), placental alkaline phosphatase (PLAP), pregnancy specific beta-1-glycoprotein (SP1), and human placental lactogen (HPL) in 14 third-trimester placentas associated with diabetes mellitus. Staining was increased for beta HCG and decreased for PLAP, SP1, and HPL in the diabetic placentas compared to control placentas of similar gestational age. This pattern was most prominent in areas of marked architectural villous immaturity within individual placentas and suggests concomitant functional immaturity.
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PMID:Placental protein distribution in maternal diabetes mellitus: an immunocytochemical study. 248 1

An important prerequisite for the management of high risk pregnancies is the accurate prediction of foetal lung maturity. A number of indices of foetal lung maturity based on the determination of surfactant constituents in the amniotic fluid have been proposed. Amniotic fluid contains phospholipids, including phosphatidylcholine (lecithin), sphingomyelin, phosphatidylinositol and phosphatidylglyerol (PG), some enzymes of the pathways of phospholipid synthesis, lamellar bodies, and lung specific apoproteins. The amount of these substances in amniotic fluid changes towards the end of gestation in a manner related to foetal lung maturity. Determination of the lecithin to sphingomyelin (L/S) ratio is by far the most widely used and accepted method. However, there is still controversy regarding the high incidence of false immature values, and the increased incidence of false mature values (from 1 to 15%) especially in pregnancies complicated by diabetes mellitus; an immature L/S ratio may predict respiratory distress syndrome (RDS) only in about 50% of cases. The incidence of false immature L/S ratio as well as other amniotic fluid tests depends upon patient variability, method employed, threshold taken for differentiating a normal from an abnormal condition, and on the fact that only few authors report their results in terms of sensitivity and specificity. Where laboratory facilities are minimal, it is advisable to perform the shake test or to measure the optical density of amniotic fluid. However, when these tests indicate immaturity, additional tests, such as determination of the L/S ratio or the lung profile (including PG), must be performed. The utilization of these tests is recommended for: 1) timing of delivery prior to elective caesarean section; 2) management of complicated pregnancies; and 3) recognizing indications for pharmacologic prevention of RDS in utero or at delivery.
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PMID:Assessment of foetal lung maturity. 266 95

Perinatal deaths were systematically investigated over a 25-month period in a Zimbabwean district and were classified into pathological subgroups according to Wigglesworth. There were 319 perinatal deaths (a rate of 30.6 per 1000) including 83 normally formed macerated stillbirths, 28 cases of congenital malformation, 79 deaths associated with immaturity, 111 due to asphyxial conditions developing in labour and 18 specific problems. Syphilis infection was a contributory factor among 27 cases, hypertension in 39 cases, amniotic fluid infection in 31 cases and diabetes in 11 cases. An avoidable factor was detected among 242 cases (75.6%) involving the mother in 120 cases, the maternity centres in 28 and the hospital in 94. These data suggest that educational programmes should try to convince all the pregnant women to attend an antenatal clinic at least once. A further perinatal mortality reduction might be obtained through treatment for syphilis, hypertension, diabetes and amniotic fluid infection, closer monitoring of the fetal condition during labour and skillful management of dystocia.
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PMID:Perinatal mortality audit in a Zimbabwean district. 278 80

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


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