Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep disorders are classified in dyssomnias, parasomnias, sleep disorder associated with medical and psychiatric disorders and proposed sleep disorders. Only the parasomnias have been studied as such in the newborn period. The parasomnias that occur in this age group are infant sleep apnea, congenital central hypoventilation syndrome, sudden infant death syndrome, and benign neonatal sleep myoclonus. Infant sleep apnea includes three entities: (1) apnea of prematurity, (2), apparent life threatening episodes with apnea and (3) obstructive sleep apnea. Congenital central hypoventilation syndrome can be associated with other autonomic system illness, such as Hirschsprung disease (Haddad syndrome) and neuroblastoma. The implementation of the supine sleep position and smoking free homes has diminished the frequency of sudden infant death syndrome. Benign neonatal sleep myoclonus should be considered in all newborns with a normal exam between the episodes when they always occur during sleep. This entity may be mistaken for status epilepticus, because it is associated with increases in heart rate. Benzodiazepines prolongs the duration of the episodes.
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PMID:[Sleep disorders in the newborn]. 1842 81

Human ether-a-go-go-related gene (hERG) channels conduct delayed rectifier K(+) current. However, little information is available on physiological situations affecting hERG channel protein and function. In the present study we examined the effects of intermittent hypoxia (IH), which is a hallmark manifestation of sleep apnea, on hERG channel protein and function. Experiments were performed on SH-SY5Y neuroblastoma cells, which express hERG protein. Cells were exposed to IH consisting of alternating cycles of 30 s of hypoxia (1.5% O2) and 5 min of 20% O2. IH decreased hERG protein expression in a stimulus-dependent manner. A similar reduction in hERG protein was also seen in adrenal medullary chromaffin cells from IH-exposed neonatal rats. The decreased hERG protein was associated with attenuated hERG K(+) current. IH-evoked hERG protein degradation was not due to reduced transcription or increased proteosome/lysomal degradation. Rather it was mediated by calcium-activated calpain proteases. Both COOH- and NH2-terminal sequences of the hERG protein were the targets of calpain-dependent degradation. IH increased reactive oxygen species (ROS) levels, intracellular Ca(2+) concentration ([Ca(2+)]i), calpain enzyme activity, and hERG protein degradation, and all these effects were prevented by manganese-(111)-tetrakis-(1-methyl-4-pyridyl)-porphyrin pentachloride, a membrane-permeable ROS scavenger. These results demonstrate that activation of calpains by ROS-dependent elevation of [Ca(2+)]i mediates hERG protein degradation by IH.
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PMID:Calpain activation by ROS mediates human ether-a-go-go-related gene protein degradation by intermittent hypoxia. 2684 30