Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0424605 (developmental delay)
 8,158 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 7.5-month-old infant with failure to thrive, developmental delay, muscular hypotonia, a visible goitre and severe osteopenia is described. Laboratory examination revealed a markedly increased serum TSH with low free T4, severe iodine and carnitine deficiency. The infant was breastfed until the age of 2.5 months and was then given a mixture of almond extract in water. The mother is a strict vegan and the father a lactovegetarian. The nutritional intake of the child was severely depleted in calories (-46%), calcium (-73%) and iodine (-88%). The restrictive alternative nutrition was responsible for the various deficiency disorders.
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PMID:Risks of alternative nutrition in infancy: a case report of severe iodine and carnitine deficiency. 142 5

We describe two sisters with chronic hypernatremia, lack of thirst, and inappropriate osmoregulated vasopressin secretion. Only one sister, who presented with microcephaly and developmental delay, showed signs of dysplasia of the midline structures (ie, septum pellucidum and corpus callosum) and a large intracranial cyst. Neither sister showed any signs of thirst, even when osmolality exceeded 337 mmol/kg. In both patients, the vasopressin secretion did not respond to either osmotic or nonosmotic stimuli or was suppressed by a water load. Plasma osmolality values returned to normal after treatment with forced hydration and a vasopressin analogue, desamino-D-arginine vasopressin. These findings indicate a severe defect in the hypothalamic osmoreceptors that control thirst and vasopressin secretion. To our knowledge, this is the first report of such a disorder in two sisters.
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PMID:Adipsic hypernatremia in two sisters. 200 83

An on-line real-time computer system for the analysis of ultrasound vocalizations of rats is presented. The calls of young rats are recorded by an ultrasound microphone, transformed by an amplitude envelope and a frequency to voltage converter, digitized and stored by a microcomputer. The data management and analysis of the recorded vocalizations are entirely automated, allowing a high throughput of experiments in a routine laboratory. The frequency values are analyzed with respect to number, duration, base-interval, and mean frequency of the calls. Also, the frequency distributions of the call to call intervals, the call durations and the ultrasound frequencies, as well as the power spectra of the frequency modulations, are calculated. This system was used for the assessment of the behavioral teratogenicity of methylmercury chloride. Wistar rat dams were treated with 0, 1.5 or 5 mg/l in their drinking water from two weeks prior to pairing until the end of the experiment. The ultrasound vocalizations of two female and two male offspring per litter were recorded on days 5, 7, 9, 11, 13, and 15 for one minute in a clean glass beaker cooled to 20 degrees C. Methylmercury treatment resulted in a developmental delay and an overall reduction in the number of calls, a shortening of the base-interval and the call durations, a flattening and shift of the frequency distributions, and an alteration in the development with age of the frequency distributions. The frequency modulations of the calls also differed, their power being lower (smaller frequency variation) on several occasions.
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PMID:Microanalysis of ultrasound vocalizations of young rats: assessment of the behavioral teratogenicity of methylmercury. 231 62

On days 12 to 17 of pregnancy, B6D2F1 mice were pair-fed liquid diets containing either 25% ethanol-derived calories or an isocaloric amount of maltose-dextrin. During this period, half the mice in each dietary condition also underwent two daily one-hour periods of restraint stress. A fifth group, given lab chow and water ad lib, was left undisturbed throughout gestation. Neither treatment affected offspring body weight on days 22 or 32 postconception, but undernutrition produced by the pair feeding procedure reduced day 32 body weight in all groups relative to the ad lib-fed group. Both prenatal ethanol and pair feeding led to delayed neurobehavioral development on day 32, while prenatal stress significantly reduced the degree of developmental delay caused by these factors. In a second study, restraint stress significantly reduced blood alcohol concentrations in pregnant dams on day 15 of gestation while elevating plasma corticosterone concentrations, and this elevation was consistent regardless of the dietary condition of the dam. The pair feeding procedure also produced corticosterone elevations but the effect of ethanol was not significant. These results suggest that prenatal stress in the presence of other physiological insults may act to counter the actions of those insults.
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PMID:Prenatal ethanol and stress in mice: 1. Pup behavioral development and maternal physiology. 275 45

Six infants with necrotizing enterocolitis were discharged after periods of prolonged hospitalization (two to nine months) with intact ileostomies. Their initial hospitalization was complicated by feeding difficulties, chronic diarrhea, sepsis, rickets, and developmental delay. All were rehospitalized within three months, with severe acidosis and dehydration after a presumed viral-type illness. Each had large-volume ileostomy output, which was rich in electrolytes and bicarbonate. A prolonged recovery phase (two to eight months) again was punctuated with episodes of diarrhea, problems in starting oral feeding, and sepsis. After reanastomosis of the remaining bowel, no infant has had a similar life-threatening episode. It is speculated that the infants' recurrent "salt-and-water-losing states" are secondary to either an anatomic or functional loss of the colon. This problem appears to be a poorly recognized sequela of bowel surgery and necrotizing enterocolitis, and early reanastomosis of discontinuous bowel should be of benefit.
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PMID:Importance of early ileostomy closure to prevent chronic salt and water losses after necrotizing enterocolitis. 709 91

Fostered rat offspring whose mothers had been administered 7.5% alcohol solution (4.85 g/kg/day) as drinking fluid during 0-17 days of gestation were compared with equivalent groups whose dams had given ad libitum and restricted volume of tap water in the following behavioral tests: reflex test, swimming behavior test, open-field test, radial-maze learning and two-way avoidance learning. The treatment with alcohol resulted in developmental delay in ear-flaps uncurling, placing reflex, swimming behavior, walking in addition to reduction in body weight at 1 and 7 days of age. The treated group also exhibited decreased open-field activity and deficit in the avoidance learning. The results show that maternal alcohol consumption produces developmental and behavioral deficits in offspring, which are comparable to the fetal alcohol syndrome (FAS) in man.
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PMID:Developmental and behavioral effects of maternal alcohol exposure in rats. 718 93

The expression of the neurofilament protein of the highest molecular weight (NF-H) is developmentally and spatially regulated. For example, the MAb RMO24.9, directed against a phosphorylated epitope in the tail domain of NF-H, immunohistochemically labels specific tracts within the rat brainstem prenatally, but does not label diencephalic tracts until after postnatal day 10 (P10). A diet providing 300 mg/kg/d Al (as Al lactate) to rat dams throughout gestation causes behavioral deficits in their offspring (Bernuzzi et al., 1989). We repeated this regimen by substituting 120 mM Al lactate (pH 6.5) for drinking water during gestation and lactation, and examined the distribution of immunolabeling by RMO 24.9 after exposure to Al. Tracts within the diencephalon that bind RMO 24.9 on P11 in control pups did not bind the MAb until P14 in Al-treated pups. In these preliminary experiments, Al seemed to have caused a developmental delay in the expression of phosphorylated NF-H in the pups of mothers that received Al during gestation. However, subsequent experiments showed that the neuropathology observed--and that reported by other investigators using similar Al levels--may not be the result of the direct effects of Al on the pups. Throughout lactation, treated dams appeared progressively more cachexic. Unlike the normal viscera of pair-watered controls, the stomachs of treated dams were ulcerated, and their kidneys had decreased cortical thickness and contained stones. Lesions such as these compromise a rat's ability to absorb nutrients, to excrete toxins, and to regulate water and electrolytes. In a lactating dam, these alterations could compromise the dam's ability to nourish her pups. Our experiments point out that the mechanisms of Al toxicity-- already complex in the adult--are further complicated in a system in which the pup is dependent on the mother for delivery of both nutrients and toxins. It is therefore impossible to determine the cause of any neuropathology in the pup in a system where Al delivery overlies a background of multisystem defect and altered maternal homeostasis.
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PMID:Oral aluminum administration during pregnancy and lactation produces gastric and renal lesions in rat mothers and delay in CNS development of their pups. 888 37

The aim of this study was to assess the impact on neonatal neurobehavioral development of methimazole (MMI)-induced in-utero hypothyroxinemia and of correction by maternal-fetal thyroxine (T4) transfer in the rat. Two groups of pregnant Sprague-Dawley rats received MMI as drinking water from gestation day 10 until birth. From day 16 until parturition, one of these groups received daily intraperitoneal injections of L-T4 and the other received saline injections. A third (control) group drank tap water and received saline injections. From day of birth, offspring from all groups were raised by untreated foster dams. Their neurobehavioral development was monitored, on postnatal days 5-14 (N = 3/litter, from 30 litters) by experimenters blind to treatment group. Prenatal T4 treatment resulted in correction of MMI-induced delayed appearance of three different reflexes. Body-weight gain of treated pups was similar to that of controls and more rapid than development of rats treated with MMI-alone. T4 treatment did not prevent, however, MMI-induced delay in maturation of physiological landmarks (e.g. ear opening). At least a portion of the developmental delay resulting from prenatal (maternal) MMI administration may be reversed by maternal-fetal transfer of T4 administered to the gravid dam.
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PMID:Neurobehavioral development of neonatal rats after in-utero hypothyroxinemia: efficacy of prenatal thyroxine treatment. 889 55

Antiepileptic drugs (AEDs), such as phenytoin (PHT), carbamazepine (CBZ), trimethadione (TMD), and phenobarbital (PB), have all been associated with a similar pattern of malformations, as well as growth retardation and developmental delay. Valproic acid (VPA) has been associated with a different pattern of malformations. Recent studies suggest that PHT's fetal adverse effect is related to its membrane stabilizing pharmacological properties (blockage of voltage-dependent ion channels). During a restricted sensitive period, this results in induction of concentration-dependent bradyarrhythmia in the embryo and episodes of hypoxia/reoxygenation. The aim of this study was to compare the potential of PHT, CBZ, PB, TMD, and dimethadione (DMD; the active metabolite of TMD) to cause bradyarrhythmias. All of these AEDs exert mainly their pharmacological effect via blockage of ion channels. VPA and vigabatrin (VGB), which are pharmacologically active mainly by other mechanisms, were also tested. C57 Bl/6J mouse embryos were cultured in vitro on gestation day 10 in vitro (in 20% rat serum). The drugs were suspended in either water or dimethylsulfoxide and administered into the culture medium in increasing concentrations up to 20 times the human therapeutic plasma concentration. A scoring system was employed in order to rank the drugs based on their potential to cause bradycardia, ventricular arrhythmia, and cardiac arrest in relation to human therapeutic concentrations. Based on this system, the drugs were ranked as follows: DMD = PHT >> PB = CBZ > TMD = VPA >> VGB (no potential). The results correlate well with the available clinical/experimental data of the tested AED's potential to induce hypoxia-related fetal adverse effects, such as oral clefts, distal limb defects, growth retardation, and developmental delay. The results support the idea that adverse fetal effects after in utero exposure to PHT, PB, CBZ, and TMD (via the active metabolite DMD) are initiated via a common pharmacological mechanism: blockage of ion channels in the developing heart in the early embryo resulting in bradyarrhythmias, hemodynamic alterations, and hypoxia/reoxygenation damage.
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PMID:Pharmacologically induced embryonic dysrhythmia and episodes of hypoxia followed by reoxygenation: a common teratogenic mechanism for antiepileptic drugs? 958 65

In an effort to assess potential ecological hazards to amphibian species in selected regions within New Hampshire, the traditional Frog Embryo Teratogenesis Assay-Xenopus (FETAX), a 14-/21 day tail resorption thyroid disruption assay and >30 day limb development tests were conducted with representative surface water and sediment samples. Two separate sets of samples collected from five sites were evaluated. The primary objectives of the study were to determine if samples were capable of inducing early embryo-larval maldevelopment, to determine if maldevelopment included limb defects, to determine if thyroxine co-administration altered the rates of limb malformation and to evaluate the impact of the samples on growth rates, developmental progress and metamorphic climax. Results from these studies suggested that pond water and sediment extract samples, but not whole sediment samples, from B2, FW, LP and W ponds were capable of inducing abnormal early embryo-larval development. In addition, water samples from B2 and W ponds induced significant abnormal hindlimb development. Some abnormal forelimb development was noted in the tail resorption studies, but not to the same extent as the hindlimbs. Each of the water samples induced appreciable developmental delay, including the paired reference site B1, which could be reversed by the addition of exogenous thyroxine.
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PMID:Effects of pond water, sediment and sediment extract samples from New Hampshire, USA on early Xenopus development and metamorphosis: comparison to native species. 1140 31


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