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

In an attempt to identify causes of perinatal mortality and thence devise preventative strategies on the island of Jamaica, a study was made of the 1847 singleton perinatal deaths occurring over the 12-month period between 1 September 1986 and 31 August 1987. Complications of the pregnancy were elicited by questioning the mother as well abstracting data from the antenatal and clinical obstetric records. The deaths were classified using the Wigglesworth categorisation and the three largest groups were chosen for special study: antepartum fetal deaths, deaths of live birth from immaturity and deaths from intrapartum asphyxia. The medical features of the pregnancies were compared with data similarly obtained from 9919 women delivering singletons in the 2 months of September and October 1986 and who survived the first week of life. Unadjusted statistically significant associations were found with maternal syphilis, vaginal infection or discharge, bleeding in the first two trimesters, bleeding in the third trimester, lowest haemoglobin, highest diastolic and first diastolic blood pressures, highest level of proteinuria, diabetes and antenatal eclampsia. Logistic regression taking account of social, environmental and health behaviour variables showed the following significant relationships. Antepartum fetal death was associated with adjusted odds ratio (AOR) for syphilis 2.88 [95% confidence interval (CI): 1.91, 4.32], bleeding in third trimester 3.86 [2.73, 5.44], highest diastolic blood pressure (P < 0.0001), highest level of proteinuria (P < 0.0001), lowest Hb (P < 0.0001) and antenatal eclamptic fits AOR 4.62 [1.47, 14.50]. Deaths from immaturity were independently associated with bleeding < 28 weeks AOR 3.50 [2.39, 5.13], bleeding 28 + weeks AOR 1.93 [1.16, 3.22], highest diastolic blood pressure (P < 0.01) and highest level of proteinuria (P < 0.0001). Infection featured in deaths associated with intrapartum asphyxia, with syphilis AOR 2.17 [1.44, 3.26] and vaginal infection/discharge (P < 0.01) independently associated; other strong associations were bleeding < 28 weeks AOR 2.10 [1.57, 2.81], bleeding 28 + weeks AOR 2.32 [1.62, 3.33], highest diastolic blood pressure (P < 0.0001), first diastolic blood pressure (P < 0.0001) and antenatal eclampsia AOR 6.70 [2.63, 17.13]. For all perinatal deaths combined, independent features were syphilis AOR 2.06 [1.49, 2.85], vaginal infection/discharge (P < 0.001), bleeding < 28 weeks AOR 2.01 [1.60, 2.53], bleeding 28 + weeks AOR 2.65 [2.02, 3.48], highest diastolic blood pressure (P < 0.0001), first diastolic blood pressure (P < 0.0001), proteinuria (P < 0.0001) and antenatal eclampsia AOR 4.22 [1.76, 10.14]. The results help identify areas for monitoring and identifying pregnancies at highest risk.
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PMID:Medical conditions present during pregnancy and risk of perinatal death in Jamaica. 807 3

Various studies have provided evidence that peripheral T-cells from the diabetes-prone BB-DP rat are abnormal in function and cell surface phenotype. These characteristics have often been interpreted as indicators of immaturity and/or short life span. In this study, we describe a CD4-dependent signaling abnormality in BB-DP peripheral T-cells. In spite of the fact that CD4 plays a critical role in thymocyte development, the abnormal signaling does not appear to influence thymocyte development at the stage when the T-cell receptor is rearranged and the recombinase enzymes RAG-1 and RAG-2 transcripts are downregulated. Therefore, if a maturation defect leading to the seeding of the periphery with immature T-cells occurs in the BB-DP rat, it does not preclude the initial selection of the self major histocompatibility complex-restricted T-cell repertoire.
Diabetes 1994 Jan
PMID:Peculiar T-cell signaling does not preclude positive selection in the diabetes-prone BB rat. 826 16

The cause of the poor secretion of insulin in response to glucose by the beta-cell in the fetal rat pancreas is thought to be immaturity of the metabolism of glucose. Glucokinase (GK), a key enzyme in glycolysis, is the glucose sensor that maintains glucose homeostasis in the adult beta-cell; its role in the fetal beta-cell has not been determined. The aim of this study was to examine whether GK was functional in phosphorylation of glucose in the fetal islet, and if so, to determine what factors regulated this activity. Similar Km values were found in both fetal and adult islets: 7.4 vs. 7.7 mmol/l. The maximal GK velocity (Vmax) of the fetal islet and the contribution of GK to total glucose phosphorylation were also not significantly different from their adult counterparts. Western blot analysis of protein extracts from fetal and adult islets confirmed the presence of GK at 52 kDa. To determine if glucose had any effect on the Vmax of GK, islets were cultured for 7 days in medium containing low (1.4 or 2.8 mmol/l), normal (5.6 mmol/l), or high (11.2 or 16.8 mmol/l) concentrations of glucose. The maximal GK velocity increased linearly with increasing concentrations of glucose (r = 0.93; P < 0.01). To determine whether it was possible to up- and down-regulate Vmax of GK, islets were cultured in either a low (1.4 mmol/l) or high (30 mmol/l) concentration of glucose for 7 days and then switched to the opposite concentration for a further 3 days. The Vmax of GK in the fetal islet was upregulated 3.8-fold when the glucose concentration was raised. Conversely, the Vmax was downregulated 3.6-fold when the glucose concentration was lowered. The same phenomenon was also observed in the adult islet. These data indicate that GK is the glucose sensor for the fetal rat islet, just as it is for the adult islet. Since glucose did not cause insulin secretion from the fetal islet, it was important to examine whether this substrate had any effect on its own metabolism. Glucose utilization was estimated, and its Vmax was found to increase linearly with increasing concentrations of glucose (r = 0.96; P < 0.01). We conclude that the inability of the fetal rat beta-cell to secrete insulin in response to glucose cannot be explained by immaturity of GK or the glycolytic pathway.
Diabetes 1996 Aug
PMID:Glucose regulates the maximal velocities of glucokinase and glucose utilization in the immature fetal rat pancreatic islet. 869 Jan 54

Glucokinase (GK) is the glucose sensor in the adult beta-cell, resulting in fuel for insulin synthesis and secretion. Defects in this enzyme in the beta-cell are responsible for the genetic disorder maturity-onset diabetes of the young, with the beta-cell being unable to secrete insulin appropriately when challenged with glucose. The human fetal beta-cell is also unable to secrete insulin when exposed to glucose, but whether GK is present and functional in this developing cell is unknown. To determine the expression of GK in human fetal pancreatic tissue, cytosolic protein was extracted from human fetal islet-like cell clusters (ICCs) at 17-19 weeks gestation and examined for protein content and enzyme activity. On Western blots, a single band corresponding to GK was seen at 52 kDa, and this was similar to that obtained from human adult islets. The maximal velocity (Vmax) of GK was less in fetal ICCs than that in adult islets (8.7 vs. 20.7 nmol/mg protein x h); similar K(m) values were found in both ICCs and islets. No attempt was made to determine which cells in an ICC contained GK. Glucose utilization was determined radiometrically; the Vmax of the high K(m) component was less in ICCs than in islets (31.3 pmol/ICC x h vs. 101.4 pmol/islet.h). Culture of ICCs for 3-7 days in medium containing 11.2 mmol/L glucose resulted in a 3.7-fold increase in the Vmax of GK and a 1.8-fold increase in glucose utilization. These enhanced activities of glucose phosphorylation and glycolysis, however, did not lead to the beta-cell being able to secrete insulin when exposed to glucose. In conclusion, glucokinase is present and functional in human fetal ICCs, but the inability of the human fetal beta-cell to secrete insulin in response to an acute glucose challenge is not due to immaturity of this enzyme.
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PMID:Expression of glucokinase in glucose-unresponsive human fetal pancreatic islet-like cell clusters. 906 11

Prepubertal years of insulin-dependent diabetes mellitus are protected from the nephropathic effects of this disease, yet this effect of immaturity has not been investigated in an animal model. Male Munich-Wistar rats were made diabetic with streptozocin at two ages: weanling (approximately 4 wk) and pubescent (approximately 10 wk). After 5 wk of untreated diabetes, weanling diabetic animals showed relatively greater growth of the medulla, whereas relative proportions of these areas were constant in the older animals. Glomerular volume increased by approximately 35% in older diabetic animals, but no glomerular enlargement was demonstrated in weanling rats with diabetes. Glomerular ultrastructure was not significantly altered during the short course of this study. The renal structural response to diabetes is age-dependent in the rat, with prepubertal animals protected from glomerular hypertrophy. Longer studies are needed to see if these differences will eventually parallel those demonstrated in patients with onset of diabetes before and after puberty. This model may ultimately prove to be valuable in determining the mechanism via which prepubertal kidneys are protected from the nephropathic effects of insulin-dependent diabetes mellitus.
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PMID:Age of onset of streptozocin diabetes determines the renal structural response in the rat. 916 8

So far, gestational diabetes treated with tolbutamide has never been associated with severe hypoglycaemia in the newborn when the mother's diabetes was well controlled. We report a case of a premature neonate, gestational age 34 weeks, with severe and long-standing hypoglycaemia from birth. The mother had well-controlled gestational diabetes, treated with tolbutamide from the 24th week of gestation until delivery. The neonate had inappropriately high levels of serum proinsulin, insulin and C-peptide relative to blood glucose concentrations. From day 19 after birth, the levels were normalized. Serum tolbutamide was 140.6 micromol/l (38 microg/ml) at 3 h after birth. Zero-order kinetics were seen during the first 90 postnatal hours. The half-life of serum tolbutamide decreased from 46 to 6 h. It is suggested that tolbutamide, when given to the mother until delivery, may cause severe and prolonged hyperinsulinaemic hypoglycaemia in premature neonates. The initially prolonged tolbutamide half-lives and zero-order kinetics suggest immaturity of hepatic elimination during the first 2 days of postnatal life.
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PMID:Prolonged elimination of tolbutamide in a premature newborn with hyperinsulinaemic hypoglycaemia. 967 39

The Diabetes Mellitus is the pathology that frequently is associated to the pregnancy and it is responsible for perinatal mobility specially by the respiratory distress syndrome since exists delay in the conversion of myoinositol-phosphatidyl inositol-phosphatidyl glycerol. To demonstrate the reliability of the DO tho 650 nm with standard of 20 in the determination of fetal lung maturity of the infant of diabetic mother. There were included 143 patient with pregnancy > or = 37 weeks with amenorrhea reliable and gestational age confirmed by ultrasound, of those 94 corresponded to gestational Diabetes Mellitus, 49 to pregestational (46 non insulin-dependent and 3 insulin-dependent). In all of them amniotic fluid studies was perform at 37 week and the resolution of the pregnancy was when DO to 650 nm showed fetal lung maturity. It was found a correlation among the DO to 650 nm of 20 and absence of RDS in 130 cases (true positive); there were seven cases with immaturity results by DO that they did not express RDS (false negative) and six cases with results that showed immaturity by DO and there were manifestations of RDS (true negative). We did not find results of false positive. The frequency of RDS was of 4.9% with a positive predictive value of the 100% an negative predictive value of 46%, a specificity of 100% and a sensitivity of 94%. An interesting finding was the fact that six cases true negative cases had poor maternal metabolic control of different degrees. For our results can be deduced that DO to 650 nm with standard of .20 it is reliable for the diagnosis of fetal lung maturity in the pregnancies complicated with Diabetes Mellitus, in addition to be an easy elaboration test and low cost.
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PMID:[Reliability of optic density at 650 nm in determining lung maturity in children of diabetic mothers]. 982 5

Fetuses of diabetic mothers who were exposed to excessive glucose show delayed maturation. Under these conditions, altered growth factor expression or signaling may have important regulatory influences. We examined the role of epidermal growth factor (EGF) in lung development and maternal diabetes in the rat. In order to evaluate the possible role of glucose for the expression of EGF and the growth of lung tissue, we performed in vitro studies with organotypic cultures of fetal alveolar cells obtained from control rats. Compared to pups of normal rats, the newborn rats of untreated diabetic rats had reduced body weight, but normal lung weight relative to body weight. The air:mesenchyme ratio and the average size of alveoli per mm(2) lung tissue were reduced. The immunoreactivity (IR) of EGF, which was quantified using a computerized image analysis system, appeared with increased intensity and was associated with a reduced intensity of surfactant protein A-IR. The only difference observed between pups of treated diabetic rats and controls was a decrease in the lung weight:body weight ratio. In organotypic cultures, the presence of 13 mmol/L glucose in the cell media increased immunoreactive staining against EGF, but decreased the incorporation of thymidine as compared to the results obtained with alveolar cells grown in a normophysiological concentration of glucose (3 mmol/L). Addition of EGF increased the thymidine incorporation only in cells grown in 3 mM glucose. These findings may indicate immaturity of the lungs of pups of untreated diabetic rats, and subtle alterations in the lungs of pups from treated diabetic rats. The results also suggest that glucose plays a role in the expression of EGF, and that cells exposed to high concentrations of glucose are less responsive to EGF.
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PMID:Epidermal growth factor and lung development in the offspring of the diabetic rat. 1063

A light microscopy study was carried out on 48 placentae. Seventeen placentae were obtained from non-diabetic mothers while the other 31 placentae were from both women with controlled diabetes and women who had an abnormality of the glucose tolerance test. All the women delivered at 38-40 weeks of gestation. Placentae from diabetic patients showed immaturity of the villi, hypertrophy of the capillaries and thickening of the basement membrane of the trophoblastic villi (3.2 +/- 0.35 microns) and the amniotic membrane (1.8 +/- 0.3 microns). Focal fibrinoid necrosis, an increase in the number of Hofbauer cells and dilatation of villi capillaries were also commonly observed in placentae from diabetic mothers, and the normal cuboidal cells lining the amniotic membrane tended to become tall columnar (17.6 +/- 6.3 microns) with distally located nuclei. Similar findings were observed in patients who had a potentially abnormal glucose tolerance test, which suggests the possibility of primary lesion in origin. Therefore, control of hyperglycemia may only partially prevent the development of placental abnormalities.
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PMID:Basement membrane thickening in the placentae from diabetic women. 1084 57

Neonatal diabetes mellitus is defined as hyperglycemia detected in the first month of life of more than 2 weeks' duration, requiring insulin treatment. It is extremely uncommon (1/500,000 neonates) and is permanent in only 30% of cases. Several hypotheses concerning its etiology have been postulated, such as pancreatic immaturity, paternal uniparental isidisomy of chromosome 6, and the existence of a gene located in the 6 q 22-23 chromosome region subjected to imprinting and exclusively of paternal expression. The management of these patients is usually difficult. These neonates are underweight for their gestational age, and neither anti-insulin antibodies nor anti-islets are detected. We studied a neonate hospitalized because of low weight for his gestational age with dimorphic features and hyperglycemia since the 17 th day of life. Clinical and anatomical follow-up has been periodically performed to the present date. The child presents permanent neonatal diabetes with negative antibodies. Although various insulin patterns have been used since the onset of the syndrome, management remains difficult. The child presents hypothyroidism, bilateral neurosensory deafness, bilateral congenital cataract, myopia, dimorphic features, congenital stridor and slow weight-stature curve. The results of muscle biopsy and metabolic studies were normal. Wolfram's syndrome and mitochondrial diabetes were ruled out. This is an exceptional case of permanent neonatal diabetes associated with other malformations corresponding to no known syndromic patterns.
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PMID:[Permanent neonatal diabetes associated with other anomalies]. 1133 81


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