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)

In adult monkeys, visual recognition memory, as measured by the delayed nonmatching to sample (DNMS) task, requires the interaction between inferior temporal cortical area TE and medial temporal lobe structures (mainly the entorhinal and perirhinal cortical areas). Ontogenetically, monkeys do not perform at adult levels of proficiency on the DNMS task until 2 years of age. Recent studies have demonstrated that this protracted development of visual recognition memory is due to an immaturity of the association areas of the neocortex rather than the medial temporal lobe. For example, lesions of the medial temporal lobe structures in infancy or in adulthood yield profound and permanent visual recognition loss, indicating that the medial temporal lobe structures operate early in life to sustain visual memory. In contrast, early lesions of area TE, unlike late lesions, result in a significant and long-lasting sparing of visual memory ability. Further evidence for neocortical immaturity is provided by studies of the development of opiatergic and cholinergic receptors, of the maturation of metabolic activity, and of the connectivity between inferior temporal areas TE and TEO and cortical and subcortical structures. Together these results indicate greater compensatory potential after neonatal cortical than after neonatal medial temporal removals. In support of this view, early damage to area TE leads to the maintenance of normally transient projections as well as to reorganization in cortical areas outside the temporal lobe. In addition, lesion studies indicate that, during infancy, visual recognition functions are widely distributed throughout many visual association areas but, with maturation, these functions become localized to area TE. Thus, the maintenance of exuberant projections together with reorganization in other cortical areas of the brain could account for the preservation of visual memories in monkeys that have had area TE removed in infancy.
Can J Physiol Pharmacol 1995 Sep
PMID:Development and plasticity of the neural circuitry underlying visual recognition memory. 874 86

SAMP1TA/Ngs, a substrain of senescence accelerated mouse, is a useful animal model for research on brain dysfunction due to senescence. In a previous study it was reported that the age-related changes in basal dendrites and spines of CA1 pyramidal neurons coincide with the behavioral characteristics found in SAMP1TA/Ngs. The goal of the present study was to investigate morphological changes in apical dendrites and dendritic spines of CA1 pyramidal neurons among 3-, 5-, 7-month-old SAMP1TA/Ngs. Pyramidal neurons of the hippocampus were stained by the rapid Golgi method, and the number of apical dendrites, the number of their spines and the density of the dendritic spines were evaluated. The number and density of the spines of apical dendrites were significantly higher at 5 months than at 3 or 7 months of age. We propose that the low number of dendritic spines in 3-month-old animals was caused by immaturity, while the changes in the density and number of dendritic spines in 7-month-old mice were due to accelerated aging. The data on the morphology of apical dendrites are a useful complement to the results reported previously. The findings of the present study also support the hypothesis that this model mouse demonstrates changes in respective developmental stages, i.e. immaturity, adulthood and senescence. This pattern of postnatal growth has special meaning because it indicates the usefulness of the strain in the study of geriatric disorders in humans.
Mech Ageing Dev 1996 Sep 09
PMID:Quantitative age-related changes in apical dendrites and dendritic spines of CA1 pyramidal neurons among senescence accelerated mice (SAMP1TA/Ngs). 884 49

The newborn immune system differs quantitatively and functionally from that of adults. Development of the immune system has important implications for childhood diseases. The immaturity of the immune system in the first years of life may contribute to failure of tolerance induction and in the development of allergic disease. T cell function is diminished, especially the capacity to produce cytokines; production of interferon (IFN)-gamma, and IL-4 is strongly reduced. IFN-gamma has been found to be even lower in cord blood of newborns with a family history of atopy. Differences in other cell types (natural killer cells, antigen-presenting cells, and B cells) could also play a role in the development of allergic disease. Current data suggest that irregularities in IgE synthesis, helper T cell subsets (Th1, Th2, CD45RA, and CD45RO), cytokines (IL-4, IFN-gamma), and possibly other cell types may play a role in the development of allergy in childhood. Moreover, the role of cell surface molecules, like co-stimulatory molecules (CD28, CD40L), activation markers (CD25), and adhesion molecules (LFA-1/ICAM-1, VLA-4/ VCAM-1) is also discussed. These variables are modulated by genetic (relevant loci are identified on chromosome 5q, 11q, and 14) and environmental forces (allergen exposure, viral infections, and smoke). The low sensitivity of current predictive factors for the development of allergic diseases, such as cord blood IgE levels, improves in combination with family history and by measurement of in vitro responses of lymphocytes and skin reactivity to allergens. New therapeutic approaches are being considered on the basis of our current understanding of the immunopathology of allergic disease, for instance cytokine therapy and vaccination with tolerizing doses of allergen or peptides.
Pediatr Res 1996 Sep
PMID:Development of immune functions related to allergic mechanisms in young children. 886 70

Renal handling of magnesium (Mg) has been incompletely studied during infancy and childhood due to the difficulty, until recently, of measuring the diffusible fraction of plasma Mg. In the present investigation this methodology has been used to assess Mg homeostasis in 45 healthy infants, aged 1 to 12 months, and in 63 healthy children, aged 1 to 15 years. When compared to children, infants had significantly higher plasma values (mean +/- SD) for both total (0.76 +/- 0.08 versus 0.70 +/- 0.06 mmol l-1; p < 0.001) and ultrafilterable Mg (0.51 +/- 0.07 versus 0.49 +/- 0.04 mmol l-1; p < 0.05). No significant correlations were present between values of plasma Mg and plasma concentrations of calcium, creatinine, total protein or albumin. The ratio Umg/Ucr, calculated in the second morning urine (median, 3rd-97th centiles), was also significantly higher during infancy (0.023, 0.009-0.07 versus 0.015, 0.006-0.04; p < 0.001). On the contrary, fractional excretion of Mg (median, 3rd-97th centiles) was identical in both age groups and did not correlate significantly with age (infants: 3.2, 1.0-7.8%, children 3.4, 1.6-8.1%; p = NS). During a Mg infusion, carried out in six children, we could establish an approximative value for renal Mg threshold (plasma ultrafilterable Mg = 0.50 mmol l-1) close to that found in adults. These results indicate that no functional immaturity is present during infancy for renal tubular reabsorption of Mg and that the high Umg/Ucr ratio observed in this age group is a phenomenon not dependent on a higher urinary Mg excretion but probably related to a lower urinary creatinine excretion per unit of lean body mass.
Acta Paediatr 1996 Sep
PMID:Renal magnesium handling in infants and children. 888 10

1. Systemic and intestinal antibody titres were measured in chickens following subcutaneous, intraperitoneal (i.p.), oral (p.o.) and combined i.p./p.o. administration of antigen, in soluble, emulsified or microparticulate form. Antigens tested included keyhole limpet haemocyanin (KLH), killed Campylobacter jejuni whole cells and purified campylobacter flagellin protein. 2. The effect of immunisation with purified flagellin protein or with killed C. jejuni whole cells in reducing intestinal colonisation was assessed. The ability of newlyhatched chicks to respond to immunisation was limited, possibly because of the immaturity of the immune system rather than maternal suppression of an immune response. Only 5 to 13 birds that were first immunised when 1-d-old with KLH showed a systemic response, even after 4 immunisations, whereas 10 of 11 birds that were first immunised at 24 d-old responded systemically. 3. In an immunisation and challenge experiment, birds that were immunised twice intraperitoneally, at 16 and 29 d-old, with killed C. jejuni whole cells, had fewer C. jejuni, in the caecal contents than unimmunised control birds. This reduction in intestinal colonisation, to less than 2% of bacterial numbers in control birds, was associated with an increase in specific IgG in intestinal secretions. There was no significant increase in specific IgA or IgM in intestinal secretions following immunisation and challenge. 4. These results indicate that immunisation can reduce the level of intestinal infection with C. jejuni. The protection may be enhanced by developing improved methods of immunisation that stimulate production of increased titres of specific antibody in intestinal secretions, particularly specific IgA antibody.
Br Poult Sci 1996 Sep
PMID:Immunisation of chickens to reduce intestinal colonisation with Campylobacter jejuni. 889 21

Noninfective acute respiratory disease develops in approximately 1% of all newborn infants and results in their admission to a critical care unit. Transient tachypnea of the newborn occurs as a result of a delay in the clearance of fetal lung liquid; however, respiratory distress syndrome, typically thought to be exclusively a problem of relative surfactant deficiency, is now suspected to be characterized by an even greater air space fluid burden from the inability to absorb fetal lung liquid. In vivo experiments have demonstrated that the lung epithelium secretes Cl and fluid throughout gestation and develops the ability to actively reabsorb Na+ only during late gestation. At birth, the mature lung switches from active Cl- (fluid) secretion to active Na+ (fluid) absorption in response to circulating catecholamines. Changes in oxygen tension augment the Na(+)-transporting capacity of the epithelium and increase gene expression for the epithelial Na+ channel (ENaC). The inability of the immature fetal lung to switch from fluid secretion to fluid absorption results, at least in large part, from an immaturity in the expression of ENaC, which can be upregulated by glucocorticosteroids. Both pharmacological blockade of the lung's epithelial Na+ channel and genetic knockout experiments using mice deficient in the ENaC pore-forming subunit have demonstrated the critical physiological importance of lung Na+ transport at birth. When Na+ transport is ineffective, newborn animals develop respiratory distress and hypoxemia, retain their fetal lung liquid and, in the case of the ENaC knockout mice, die. Bioelectrical studies of human infants' nasal epithelia demonstrate that both transient tachypnea of the newborn and respiratory distress syndrome have defective amiloride-sensitive Na+ transport. These results suggest that neonatal respiratory distress syndrome has, in addition to a relative deficiency in surfactant, defective Na+ transport, which plays a mechanistic role in the development of the disease.
Proc Assoc Am Physicians 1996 Sep
PMID:Immature epithelial Na+ channel expression is one of the pathogenetic mechanisms leading to human neonatal respiratory distress syndrome. 890 78

The increase in the number and proportion of the elderly in Japan over the last 30 years has been faster than that in any other country. One of the measures we are compelled to take to deal with this drastic change in medicosocial circumstances is reform of the medical school curriculum. However, the necessary reforms are being implemented slowly and are still insufficient. We surveyed the present status of gerontology and geriatrics education in pathology, and the understanding, interest, and opinions on this matter among professors of pathology. Questionnaires were sent to 148 professors of pathology in 80 medical schools. Responses were received from 84 professors (57%) at 64 medical schools (80%). Of the 11 medical schools with a department of geriatrics 10(90%) included gerontology in the curriculum. In contrast, 43(80%) of the 53 remaining schools did not include gerontology in the curriculum, although education in geriatrics and gerontology has been given as part of pathology lectures in almost all medical schools. Many professors want to establish a department of geriatrics in their school, but feel it will be difficult because of lack of money and higher priority given to other fields. As other hindrances, most of the respondents noted the lack of money and higher priority given to other fields. As other hindrances, most of the respondents noted the lack of a good textbook of gerontology, ambiguity in the concept of the field, and the immaturity of gerontology as a science. Another major problem noted was uncertainty regarding the status of geriatrics as a clinical specialty. One professor mentioned that promotion of aging research would be the best way to solve these problems.
Nihon Ronen Igakkai Zasshi 1996 Sep
PMID:[University education in geriatrics--present status and future prospects of gerontology and geriatrics education in pathology]. 894 Aug 67

We studied changes during lactation in the relative concentration of individual gangliosides in human milk from mothers delivering preterm and term infants. The relative content of G(D3) was higher in colostrum than in mature milk, and tended to be higher in preterm colostrum than in term colostrum, whereas the relative content of G(M3) was higher in mature milk than in colostrum, and was also higher in term than in preterm milk. As G(D3) is usually detected in developing tissues whereas G(M3) is more abundant in mature tissues, these results suggest a relationship between the presence of individual gangliosides in human milk and immaturity of the mammary gland in mothers of preterm infants.
Biol Chem 1996 Sep
PMID:Changes during lactation in ganglioside distribution in human milk from mothers delivering preterm and term infants. 906 59

The possibility that infants' and young children's immature behaviors and cognitions are sometimes adaptive is explored and interpreted in terms of evolutionary theory. It is argued that developmental immaturity had an adaptive role in evolution and continues to have an adaptive role in human development. The role of developmental retardation in human evolution is discussed, followed by an examination of the relation between humans' extended childhood and brain plasticity. Behavioral neoteny, as exemplified by play, is examined, as are some potentially adaptive aspects of infants' perception and cognition that limit the amount of information they can process. Aspects of immature cognition during early childhood that may have some contemporaneous adaptive value are also discussed. It is proposed that viewing immaturity as sometimes adaptive to the developing child alters how children and their development are viewed.
Psychol Bull 1997 Sep
PMID:The role of immaturity in human development. 928 98

Mature myocardium utilizes calcium released by the sarcoplasmic reticulum (SR) for cell contraction. Transient exposure of mature myocytes to caffeine is known to directly trigger Ca2+ release from the SR. In contrast, neonatal rabbit heart cells rely on transsarcolemmal Ca2+ influx for tension generation. SR function is decreased in immature heart and appears to play a minimal role as a calcium source. Accordingly, we hypothesized that neonatal rabbit myocytes would not respond to a caffeine pulse. Isolated neonatal and adult myocytes were paced to load the SR with calcium and then exposed to a 1-s pulse of 10 mM caffeine. As previously described, adult myocytes exhibited a brisk contraction in response to caffeine. Unexpectedly, neonatal myocytes also exhibited a similar, brisk response. These caffeine-induced contractions were not dependent on extracellular Ca2+ but were dependent upon the loading of SR Ca2+ stores. When SR Ca2+ stores were depleted by exposure to caffeine, mature myocytes exhibited only small, slow contractions in response to electrical field stimulation. Replenishing the SR Ca2+ stores resulted in normal, brisk contractions. In contrast, electrically stimulated contractions in immature myocytes were largely unaffected by caffeine-induced SR depletion. Thus, although neonatal myocytes are capable of loading and releasing calcium from the SR, such SR calcium release is not normally required for contraction in the developing heart. The minor role of SR Ca2+ release in immature rabbit heart may not result from immaturity of the SR, but rather from an inadequate mechanism to trigger SR calcium release.
Pediatr Res 1997 Sep
PMID:Caffeine-induced contractions in developing rabbit heart. 928 67


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