Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apnea of prematurity in the majority of the cases becomes evident during the nonREM phases of sleep. Aminophylline, one of the most commonly used xantines in prevention, seems to reduce the incidence of these crises, increasing the duration of the REM phase and of the wakefulness of the newborn. It is possible that the serotonin, neuromediator of the REM phase, represents an important element in determining the crises of apnea, conditioned by variation in the serum levels of tryptophan that regulates the synthesis and liberation of cerebral serotonin. Our data demonstrate how aminophylline increases the post-natal physiological diminution of total tryptophan in the preterm. Therefore we can deduce, from our results, that an increased synthesis and liberation of serotonin may to increase the duration of the REM and to reduce the incidence of apnea.
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PMID:[Serum levels of total and free tryptophan in the premature newborn infant treated with aminophylline]. 409 10

The spectral transmittance and non-tryptophan fluorescence of human crystalline lenses were evaluated. Eleven eye bank lenses and three lenses of prematurity of retinopathy patients were investigated. All lenses absorbed the short wavelength light below 430 nm strongly. The transmission of the short wavelength visible light decreased gradually with age. There was a positive correlation between the fluorescence intensity ratio of non-tryptophan to tryptophan fluorescence and the logarithm of age. It was thought that the generation of non-tryptophan fluorescence might be a first-order chemical reaction.
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PMID:[Spectral transmittance of normal human crystalline lens]. 782 4

The brain is unusual among organs in that the rates of many of its characteristic enzymatic reactions are controlled by the local concentrations of their substrates, which also happen to be nutrients that cross the blood-brain barrier. Thus, for example, brain levels of tryptophan, tyrosine, or choline can control the rates at which neurons synthesize serotonin, dopamine, or acetylcholine, respectively. The rates at which brain cells produce membrane phospholipids such as phosphatidylcholine (PC) are also under such control, both in adult animals and, especially, during early development. If pregnant rats are fed the 3 dietary constituents needed for PC synthesis- docosahexaenoic acid, uridine, and choline-starting 10 days before parturition and continuing for 20 days during nursing, brain levels of PC, and of the other membrane phosphatides (per cell or per mg protein), are increased by 50% or more. In adult animals, this treatment is also known to increase synaptic proteins (eg, synapsin-l, syntaxin-3, GluR-l, PSD-95) but not ubiquitous proteins like beta-tubulin and to increase (by 30% or more) the number of dendritic spines on hippocampal neurons. Docosahexaenoic acid currently is widely used, in human infants, to diminish the negative effects of prematurity on cognitive development. Moreover, docosahexaenoic acid, uridine (as uridine monophosphate), and choline are all found in mother's milk, and included in most infant formulas. It is proposed that these substances are part of a regulatory mechanism through which plasma composition influences brain development.
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PMID:Synapse formation and cognitive brain development: effect of docosahexaenoic acid and other dietary constituents. 1880 68

Excitotoxicity plays a key role during insults to the developing brain such as neonatal encephalopathy, stroke, and encephalopathy of prematurity. Such insults affect many thousands of infants each year. Excitotoxicity causes frank lesions due to cell death and gliosis and disturbs normal developmental process, leading to deficits in learning, memory, and social integration that persist into adulthood. Understanding the underlying processes of the acute effects of excitotoxicity and its persistence during brain maturation provides an opportunity to identify mechanistic or diagnostic biomarkers, thus enabling and designing possible therapies. We applied mass spectrometry to provide metabolic profiles of brain tissue and plasma over time following an excitotoxic lesion (intracerebral ibotenate) to the neonatal (postnatal day 5) mouse brain. We found no differences between the plasma from the control (PBS-injected) and excitotoxic (ibotenate-injected) groups over time (on postnatal days 8, 9, 10, and 30). In the brain, we found that variations in amino acids (arginine, glutamine, phenylananine, and proline) and glycerophospholipids were sustaining acute and delayed (tertiary) responses to injury. In particular, the effect of the excitotoxic lesion on the normal profile of development was linked to alterations in a fingerprint of glycerophospolipids and amino acids. Specifically, we identified increases in the amino acids glutamine, proline, serine, threonine, tryptophan, valine, and the sphingolipid SM C26:1, and decreases in the glycerophospholipids, i.e., the arachidonic acid-containing phosphatidylcholine (PC aa) C30:2 and the PC aa C32:3. This study demonstrates that metabolic profiling is a useful approach to identify acute and tertiary effects in an excitotoxic lesion model, and generating a short list of targets with future potential in the hunt for identification, stratification, and possibly therapy.
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PMID:Persistently Altered Metabolic Phenotype following Perinatal Excitotoxic Brain Injury. 2849 60